Talk:Cancer/Archive 1

"-oma"

"Benign tumors are named using -oma as a suffix. For instance, a benign tumor of the smooth muscle of the uterus is called leiomyoma (the common name of this frequent tumor is fibroid). This nomenclature is however somewhat inconsistent, since several "malignant" tumor growths also have this suffix in their names, e.g. neuroblastoma, lymphoma and melanoma."

This paragraph doesn't make sense to me. Surely all tumours end in -oma whether they are benign or malignant. Maybe this paragraph needs to be reworded to start "Benign tumours are also named using -oma as a suffix". Radstudent 11:29, 15 November 2006 (UTC)

Mechanism Section

The section on oncogenes is rather outdated and simplistic. For example "proto-oncogenes" can do a lot of other things besides "promote growth" and "mitosis". For example the genes abl and TrkA are tyrosine kinases which become oncogenes through translocation-induced mutation, causing the constitutive activation of the kinase. Also, a myriad of other gene types can cause cancer when mutated. It may be better to caveat the section, and give examples of typical oncogenes, rather than make sweeping statements. If you like, I could do this edit. Gacggt 16:55, 4 June 2006 (UTC)

Cure for cancer...

I was attending science class when our class had a discussion about cancer cells and the whole mitosis thing. Turns out, my science teacher was at a workshop at the local university and there is an acutal cure for cancer... the only catch is, is that 1. the price of the substance is approximatly $10,000 (Canadian Funds) per micro-gram (0.001 gram). The substance would stop cell reproduction in a certain stage of mitosis, therefore eliminating the spread of cancer in the body. The only downfall is that it has a low percentage of success. It would either cure the cancer completly, or kill the person immediatly. Can anyone explore this further and add it to the page. Im sure a lot of people would be interested in finding out

I'm not sure what you are specifically talking about, could you provide more details? The general strategy of stopping cell reproduction during mitosis, to prevent the formation of new cells, is one used by many anti-cancer drugs. See Taxol or chemotherapy, for instance. The two major problems with these approaches are (1) it is not specific to cancer cells, causing many side effects and (2) cancer cells can evolve resistance to the drug, see multi-drug resistance.

The costs that you mention are probably not a significant barrier. Almost any unique compound would cost as much as you quote. These costs drop quickly once mass production begins. --- Jpbrody 17:47, 15 May 2006 (UTC)

"Killing the person immediately" sounds like a non-trivial side effect of this dubious "cure for cancer." Andrew73 18:21, 15 May 2006 (UTC)

That "cure you or kill you" should ring all bells on your BS detector. This is rumor transformed into nonsense. alteripse 18:32, 15 May 2006 (UTC)

The China Study

I think a mention the China Study should be included in the prevention/diet area. Colin Campbell was able to statistically show the correlation between animal protein and cancer.

Flow of article

I rearranged the article chapters to facilitate reading for someone not interested in molecular biology or the (excrutiatingly detailed) mechanism of carcinogenesis. I hope everyone likes it. Emmanuelm 19:30, 23 December 2005 (UTC)

This article on cancer is not well written. From a lamens point of view, this article is over detailed, and the English is of poor quality. From an experts point of view, the article is incorrect in so many instances that citing them would take longer than writing the article again. The molecular biology section is overly biased towards the P53 pathway. People are confusing the terms protein expression and gene expression. The section on the causes of cancer is diabolical. Any article written on this should include diagrams to illustrate the text. Really the article would be better arranged by having separate sections for the various aspects of cancer. 129.67.4.64 (talk · contribs)

With due respect, your edits did not make the intro much better. Please work on your spelling. Please correct whatever expert material appears incorrect. There are already various sections about the various aspects; what are you suggesting? Do you own the copyright to useful diagrams that could be included? JFW | T@lk 02:20, 12 March 2006 (UTC)

I am in agreement with Jfdwolff's comments.Jellytussle 05:15, 12 March 2006 (UTC)

Carcinogenesis

Include some information about the definition of carcinogenesis, please.

Carcinogenesis can be divided conceptually into four steps: tumor initiation, tumor promotion, malignant conversion, and tumor progression.

Mesothelioma

There should be an entry for Mesothelioma under "Forms of Cancer". There could be a link to Asbestos in the "Carcinogenesis" section of the Cancer article. There is no need for "Cancer of mesothelium: Mesothelioma - Information about cancer which results due to exposure to asbestos" in the "External links" section of the Cancer article; that link is already at the Mesothelioma article. JWSchmidt 13:45, 13 Apr 2004 (UTC)

Done for mesothelioma in the classification. Emmanuelm 19:28, 23 December 2005 (UTC)

prevention and screening

I thought the prostate screening was controversialErich 03:15, 30 Jun 2004 (UTC)

I think an important topic to introduce into the "Prevention and screening" section is lead-time bias. This expression describes the phenomenon by which early detection of a cancer may in some cases falsely appear to be associated with improved outcomes. Imagine for example, a person develops a cancer in the year 2000. With no screening program, the cancer does not become symptomatic or otherwise clinically apparent until 2003. Treatment is initiated but ultimately the patient dies in 2006. Thus this patient lived three years after the diagnosis was made. Imagine another patient in the setting of a screening program. They develop the cancer in 2000, and it is detected by screening in 2001. Treatment is initiated, but ultimately the patient dies in 2006. The patient lived 5 years after the diagnosis was made, but in fact they lived the same time after developing the cancer in the first place. This spurious increase in survival is lead-time bias.

The concept of stage migration, which is mentioned in an entry on the Will Rogers phenomenon, is also pertinent to prevention and screening.--128.163.110.72 22:16, 26 August 2005 (UTC)

Please edit the article accordingly if you feel this should be covered. JFW | T@lk 07:29, 28 August 2005 (UTC)

Throat cancer

As I write, the link above to throat cancer is red. Given all the coverage on cancer we have, this seems quite odd. Is there a better name to redirect it to - or is there a gap here? Pcb21| Pete 22:40, 28 Jul 2004 (UTC)

• Head and neck cancer - Nunh-huh 22:45, 28 Jul 2004 (UTC)

Sentence moved from cancer

"Also recent studies have found a very close relation betwen obesity and cancer, the main reason for that is that your lever can't process all the toxins of your body."

I agree this is a bit short. The relation between obesity and cancer has been proven in many tumours, but hepatic detoxicication is hardly an issue. Elevated concentrations of insulin and estrogens have been blamed, especially for breast cancer. The relation is not "very close". JFW | T@lk 16:08, 21 Oct 2004 (UTC)

There should be something in the article about obesity; "we estimate that overweight and obesity now account for one in seven of cancer deaths in men and one in five in women in the US" [1]. JWSchmidt 05:15, 24 Dec 2004 (UTC)

Cancer as a name

I was looking for information and the name "cancer": exactly why it is so called and when it was first given that name (what exactly about it looks like a crab?). Is the information here and did I miss it? If not could someone include it somewhere? Thanks. -R. fiend 00:16, 7 Nov 2004 (UTC)

It's the same in German (Krebs). It has to do with the shape of some malignant processes: they may be star-shaped or have tentacles (while benign tumors are often round). On mammography, malignant lesions suggestive of breast cancer indeed may resemble a crab. The etymology is doubtful; it is claimed to have originated in the 17th century[2], but some put it to Galen[3]. Alternatively, it has nothing to do with crab but is due to the Middle-English canker (hardening)[4] - which is also a name for the typical lesions of syphillis (chancre in French). JFW | T@lk 00:47, 7 Nov 2004 (UTC)

Cool, thanks. Should this be added to the article in some way? -R. fiend 06:18, 7 Nov 2004 (UTC)

de:Krankheit als Metapher.--Nerd 12:10, 7 Nov 2004 (UTC)

I would certainly write something about the etymology. The conclusion is of course that we don't know. JFW | T@lk 12:45, 7 Nov 2004 (UTC)

The word "cancer" itself comes from the Latin word for crab (just like the constellation), and is so called on account of early physicians noticing the similarity in the shape of a tumor to a crab. This shape, as I understand it, is on account of angiogenesis, the growth of outward-sprawling blood vessels to feed the tumor, looking like the legs of a crab. That’s my understanding. Martschink

After 12 years of looking at tumors every day with the naked eye and under the microscope, I can tell you that the star-like, white, pointy "crab legs" surrounding the tumor are bands of scar tissue, the so-called desmoplastic reaction of healthy tissue in response to invasion by abnormal cells. Blood vessels would look red or purple, not white. Emmanuelm 19:38, 23 December 2005 (UTC)

what does the root 'carcin' mean? i see it in 'carcinogenic' as well as 'carcinization' meaning "becoming a crab" is this a related word for crab that somehow managed to affix itself to both meanings of 'cancer' ?

My dictionary says that carcinogen comes from the Greek word karkinos which literally means "crab." —Brim 03:30, Mar 9, 2005 (UTC)

I rewrote this section. Ideally, I want to find photos of a tumor and a crab side by side. Let me know if you have one. Emmanuelm 19:38, 23 December 2005 (UTC)

Graph

I'm not at all happy about the graph showing the connection between smoking and lung cancer. Where does it come from? Was it plotted by a Wikipedian? If so, where did that person get their data from? No sources are cited, which leads me to suspect that this graph has just been fabricated. If so, that's a terrible deception. I don't doubt the link between smoking and cancer, but the lines on the graph look conveniently and improbably similar. Somebody please clarify. Palefire 22:24, Dec 8, 2004 (UTC)

I was not the Wikipedian who uploaded the graph, but a simple Google search revealed that the graph is published on the NIH website. No references were given on that particular web page, so I'm not sure how the graph was generated, but I would believe that the data are valid if they're from the NIH. — Brim 01:52, Jan 22, 2005 (UTC)

It doesn't look that unlikely to me. Of course there are other factors affecting Lung Cancer, but only smoking continually increased in this period, the others are unlikely to have changed, so a corresponding increase 20 years later is what you'd expect.

Exile 11:21, 28 January 2007 (UTC)

Deleted sentence fragment

Original paragraph:

<<Mutations can also be inherited. Inheriting certain mutations in the BRCA1 gene renders a woman much more likely to develop breast cancer., chronic inflammation from any cause.>>

Deleted fragment: <<, chronic inflammation from any cause.>> ---Rednblu | Talk 10:21, 12 Dec 2004 (UTC)

When Healing Becomes a Crime article

192.80.65.234 [5] and 63.164.145.198 [6] — please stop adding the section Articles containing:

• When Healing Becomes a Crime from Tikkun (link now broken; archived here)

The article When Healing Becomes a Crime: The Surprising Facts Behind 'Unproven' Cancer Therapies by Kenny Ausubel is not an important reference in the encyclopedic article about cancer. Rafał Pocztarski 02:28, 22 Dec 2004 (UTC)

Why should this be NOT added?? Or maybe it should be put in it's own section or referenced to at least in some way. As a cancer patient, I am painfully aware of the politics at play because of all the money at stake. I live in the DC suburbs, and PERSONALLY heard a PhD. Pharmocologist that had his Pharmacy nead the HQ of NIH say, "NIH is OWNED by the drug companies! I know many people that work there and that is what they would tell you, if it would not cause them to loose their jobs."

Your argument suffers from the logical fallacy of 'Appeal to Authority' and even in that it fails. You cite some person that you do not name and attribute a statement to them that is purely opinion. If you think the article should be included, say so (you do), but make a better argument than the one you made. I too am a cancer patient (Hodgkins, stage 3B) and I believe it's very important that the information in this article either be verified as factual or clearly labled as unproven.

Why not have a section devoted to all the alternative medicine thearopies that have been advanced by different people over the years. It need not endorse them,nor condem them. Certianly the case of of Harry Hoxsey is one of public record, after all it is said that there were court cases, etc. so why can't it be documented as part of the history of the search for a cancer cure?

This article is a good example of something that is not a valid reference - it contains a huge number of outrageous claims, provides no references to support them (it has no references at all!), and is in a source that has been criticized for fabrications [7].

anerobic glycolysis

I wandered "in here" looking for information on the metabolism of cancer cells. I have found a reference to anerobic glycolysis in cancer cells but cannot find additional supporting information in the form of refered journal articles. HELP! Please. Thank you.

I added a section on the Warburg effect addressing the glycolysis issue and how p53 maybe involved from a Science Article.

NON PROVEN NOVEL THERAPIES

(Unconventional Medicine) I need guidance as to were to put on the Wikipedia an article on Alternative Cancer Treatments, or at least non-proven novel therapies (for example patents on treatments). Any Ideas? Dr. Gabriel Gojon 22:03, 23 December 2005 (UTC)

• I think such an article is a great idea. Here is a start: Unproven cancer therapies. I would recommend beginning the article with an explanation of the differences between (a) new cancer treatments proposed or tested by establishment oncologists or scientists but not yet proven effective, (b) cancer treatments proposed by established oncologists or scientists but proven ineffective in trials, (c) unproven cancer treatments that are offered by unorthodox practitioners as an alternative to mainstream treatment (this is what some would call cancer quackery; and (d) unorthodox treatments offered as a complement to scientific treatment rather than a substitute. Go to it and thanks. alteripse 07:13, 24 December 2005 (UTC)

• Yes, that should be a subsection of the treatment section in the main cancer article. A whole section would be overkill (as we are writing about cancer, not the dangers of quackery), but then we could use template:main to link it to unproven cancer therapies.

Jfdwolff reversion of 68.108.100.105 link addition

Jfdwolff,

Was your reversion of the link addition by the anonymous 68... due to the low value of adding a link to a link farm page?

Courtland {2005-01-27 USA ~8PM EST}

GENERAL QUESTION: What is a "benign" tumor?

What, exactly, is a "benign" tumor? Sure, it's not dangerous and all that, but is it going through uncontrolled cell reproduction or not? Do the cells of a benign tumor go through apoptosis or not? (And for that matter, what do we mean when we say "tumor"? Is it just a fancy word for "ugly clump of cells"?) Do the cells in a benign tumor function properly? Does anyone know where I can find out more about benign tumors beyond the uninformative contrast with their malignant counterparts? And while we're on the subject, there's some recent news about carrots affecting somthing called "pre-cancerous tumors." (See e.g., http://www.sciam.com/article.cfm?chanID=sa003&articleID=000948D4-3498-1209-B49883414B7F0000) Does anyone know what a "pre-cancerous" tumor is? Is that like a pre-pregnant girl, a pre-shut door, or a pre-caught fish? The National Cancer Institute gives the following ho-hum definition: "A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant." Not so helpful, really. And why does it seem that so many cancer studies (like the above-mentioned carrot study) are premised on correlation rather than causation? Martschink

A benign tumor is certainly a neoplasm, but it does not invade other tissues. It still arises from uncontrolled mitosis. Premalignant are benign tumors that are statistically likely to degenerate. The word precancerous is rubbishy; don't use it. JFW | T@lk 22:41, 9 Feb 2005 (UTC)

Benign tumors lack the ability to invade other tissues and lack the ability to metastasize. However, being benign does not mean they're not potentially dangerous. A decent definition for a tumor is "a clump of cells that grow uncontrollably." So, benign tumors still grow uncontrollably. That answers your question "Do cells in a benign tumor function properly?" No, they do not, since they grow uncontrollably. They lack the function that normal cells have which is to be able to recognize their bounds and to stop growing when they become crowded. "Pre-cancerous tumors" are tumors that are pre-invasive — they haven't yet invaded beyond the basement membrane of the epithelium. Since they haven't invaded beyond the epithelium, they therefore lack the ability to metastasize. You might be tempted to call these tumors benign, but in practice that is not usually done. The obvious conclusion that you can come up with when something is called "pre-cancerous" is that someday it will become cancerous. That is our basic understanding of the development of cancer, that a few mutations in the genes which regulate cellular growth lead to tumors that grow but lack the ability to invade (pre-cancerous), then more mutations take place which give them the ability to invade tissue (malignant) but as of yet haven't metastasized, then additional mutations give them metastatic potential and they invade into the lymphatic system or into capillaries. It's a rather simplistic view (especially considering the hundreds upon hundreds of genes and the interplay of multiple cellular signalling pathways) but it does a good job of describing what happens. Your last question is the most difficult one to answer. Basically, studies of causation are inherently difficult because one can never see inside the "black box" of a system; we can only observe inputs (conditions, treatments) and outputs (results: dying from cancer or a tumor shrinking). In most scientific experiments, conditions are highly controlled. For example, for a chemical reaction reaction where chemical A is combined with chemical B to produce chemical C, you can vary the concentrations of both chemical A and chemical B to see the effect on the kinetics of the reaction. Since everything else is controlled for, you can conclude that "increasing the concentration of A leads to an increase in the reaction rate". This doesn't necessarily prove causation, but since all other variables are controlled for, you can conclude that it's the only reasonable explanation. In humans, however, we obviously can't do experiments like that. All we can do is get a bunch of people (example: people with lung cancer), try an intervention (a new cancer drug), and look for a specified results (tumor shrinkage, time until death). However if people who get Drug X live longer than those who don't get the drug, you can't really conclude that Drug X caused them to live longer since it's not a controlled experiment. Your groups of people are not exactly the same. They're NEVER exactly the same. One group or the other will have older patients, they might metabolize the drug differently, they have different stages of disease and different tumor types (not all lung cancers behave the same way), etc. There are infinitely many variables. Even after all the statistical tests we do to eliminate the effects of random differences between groups causing differences in outcome, all we can safely conclude at the end is "Yes, Drug X is associated with a better outcome" or "No, Drug X is not associated with a better outcome." We can't say Drug X caused the outcome to happen. — Brim 05:44, Feb 10, 2005 (UTC)

Thanks for the answers, Brim. I'd like to rephrase one question, the one about whether cells of a benign tumor function properly. Other than their growth problem, do the cells do the stuff they're supposed to do? That is, do the cells of a benign tumor in the liver do the work of non-cancerous, non-malignant, non-tumorish, plain-vanilla liver cells? Martschink 07:57, 11 Feb 2005 (UTC)

That's a tough question to answer. I'm definitely not the most authoratative person on this subject, but I think I can give you a rough answer. It depends on the type of tumor. It also depends on how you define function—are you looking only at gross functional abnormalities or biochemical changes? Most common malignancies are of epithelial tissue, which have no real function other than to serve as a barrier. A good example of a tumor that can lose its function is a pituitary adenoma. The normal function of cells of the anterior pituitary gland is to produce one of the several pituitary hormones. Adenomas of the pituitary are usually classified as "functional" or "non-functional". The functional tumors continue to manufacture hormone and actually lead to an excess of hormone, causing symptoms. However the non-functional tumors don't produce hormones. So this is an example of how a tumor can continue to function "normally" or stop its normal function. By the way, while a pituitary adenoma is a benign tumor, this applies to malignant cancers as well. For example, in malignant germ cell tumors of the testis or ovary, the cancerous cells continue to secrete hormones like B-HCG. However, as I alluded to earlier, there may still be biochemical derangements within the cell, so even cells that continue to have part of their normal function have other abnormalities. Oncogenesis in a complicated process with several changes occurring in the cell. We know that most tumors have defective DNA repair processes, which in part is responsible for how they turned into neoplasia in the first place. I hope this answers the main part of your question. It's a fairly complicated topic to be able to talk about if a cell is "normal" or not. Someone with more of a cell biology background might be able to give you a more in-depth answer. — Brim 19:41, Feb 11, 2005 (UTC)

I wanted to clarify something in the example of pituitary adenomas. While functional adenomas produce pituitary hormones like normal pituitary cells, they are not really normal since the process is not properly regulated. Adenomas will continue to produce pituitary hormone even when the hypothalamic signal is inhibited. — Brim 20:28, Feb 11, 2005 (UTC)

A benign tumor can certainly invade an adjacent structure. Benign pituitary adenomas, for example, can invade through the sella turcica (a small depression in the skull, so named because it resembles a Turkish saddle). Benign tumors in general do not carry out all the normal functions of the cell type from which they arose. However, they may carry out some vestiges of function. A pituitary adenoma, for example, might secrete abnormal quantities of a hormone. Benign tumors are best understood as tumors that do not metastasize. They may not truly be benign in the colloquial sense of the word if their location is such that local growth of the tumor threatens physiologic function. Desmoid tumors of the abdomen, for example, are histologically benign, but may result in the death of the patient eventually. Pituitary adenomas, as another example, can compress the optic chiasm and cause derangement of vision. --originally unsigned comment by 12.203.233.125

Incorrect. Pituitary adenomas grow through the sella, which is a hole, and may indeed compress the optic chiasm, but do not "eat into" those tissues. Malignant tumors eat their way into healthy tissue, blood vessels and lymph vessels, and this is a crucial property as it enables them to reach the bloodstream and metastasise. JFW | T@lk 16:04, 26 August 2005 (UTC)

The sella turcica is not a hole, it is a depression in the base of the skull in which sits the pituitary gland. (I am in fact looking at a human skull on my desk as I type this. I encourage dissenters to at least google an image of the anatomic structure in question.) Pituitary adenomas can perforate this bony structure, and the definition of a stage III lesion in this context is "localized perforation of the sellar floor." Stage IV is defined as "diffuse destruction of the sellar floor."

Pituitary adenomas are perhaps poor examples for debating benign vs maligant lesions since, as David Huang, MD and Francine Halberg, MD write in their chapter on the subject in Leibel & Phillips' Textbook on Radiation Oncology (Pituitary Tumors, chapter 24, page 533), "cytologic characteristics that are typically used to assess growth in malignancy, including hypercellularity; variations in nuclear size, shape and chromatin content; presence of multinucleated cells; and so on, are unreliable in pituitary tumors. Pituitary tumors cannot be classified as benign or malignant on the basis of pathological criteria."

They do add, however, that "Local invasion of bone and soft tissue is common with benign adenomas, and cellular pleomorphism does not correspond with clinical malignancy." This does suffice to refute the statement that no benign tumor can invade a local structure. Of note, the authors comment in the same chapter on page 534 that "Pituitary carcinomas [i.e. malignant tumors of the pituitary] are exceedingly rare, with only 36 cases reported in the past century."

Regarding desmoid tumors, also known as aggressive fibromatoses, I present the following paragraph from chapter 58 of the same textbook, authored by Quynh-Thu Lee, MD, Theodore Phillips, MD and Steven Leibel, MD, entitled Sarcomas of Soft Tissue:

Desmoid tumors -- also known as aggressive fibromatoses -- are rare, slow growing benign fibrous neoplasms that arise from fascial or musculoaponeurotic structures. They are commonly associated with Gardner's syndrome. Although first described as tumors of the anterior abdominal wall in post-partum women, they may arise from any anatomic location, most commonly the shoulder girdle and thigh areas. Histologically, they appear as well-differentiated fibrous neoplasms without associated cellular pleomorphism or mitotic activity. These tumors rarely metastasize. Their natural history consists of slow, progressive invasion and destruction of contiguous structures by finger-like projections. This infiltrative behavior results in a high incidence of local recurrence (occasionally fatal) after conservative surgery. Posner described 11 deaths from locally uncontrolled tumors of 138 patients treated at MSKCC [Memorial Sloan-Kettering Cancer Center]. Factors predictive of local failure were age between 18 and 30, recurrent disease, incomplete resection, close or microscopic positive margins, and no adjuvant radiation for gross residual disase.

I feel that the above passages from the oncology literature sufficiently support my original statement that benign tumors can indeed invade local structures (although certainly many benign tumors do not do so), and that they are not necessarily "benign" in the colloquial sense of the word. --originally unsigned comment by 12.203.233.125

You've just cited exceptions to prove a point (and verbosely so). Can we agree on the phrasing "most benign tumors do not invade surrounding structures". That covers it, doesn't it? JFW | T@lk 07:30, 28 August 2005 (UTC)

Verbosely? Your huffy tone borders on a lack of civility and gives the impression that I am intruding on "your page." Secondly, my original post that you disagreed with was brief. I'm sorry if my efforts to offer comprehensive support for statements relating to medical matters are not welcome here. Citing exceptions is the valid way of disproving a blanket statement such as "All X are not Y." You show that there exists an X that is Y. I stand by the original statement that benign tumors are best understood as tumors that do not metastasize.--12.203.233.125 04:07, 29 August 2005 (UTC)

You seem to be attempting to play a game of "gotcha" with one of our better-tempered contributors. You nitpicked past his patience and then complained that his reply seems "huffy". Try something different. Offer an alternative description of benign and malignant that helps people understand what doctors mean by those terms-- how the use resembles the ordinary senses of the words but there are important exceptions. Do it in a way that accurately reflects the probabilities and reasons why the concepts have been deemed useful for most of the last century. Then explain the limitations of the terms-- few useful generalities map exactly to the real world. That would be a more constructive use of your knowledge and talents than what you have been doing on this page. alteripse 04:28, 29 August 2005 (UTC)

Thanks Alteripse. Do you agree that most benign tumors do not invade? JFW | T@lk 08:14, 29 August 2005 (UTC)

Alteripse I think if you read my original contribution to this Talk section ("A benign tumor can certainly invade an adjacent structure. Benign pituitary adenomas...") you will agree that it satisifies your suggestions. The inability to metastasize is the hallmark of a benign tumor ("alternative description of benign and malignant that helps people understand what doctors mean by those terms"). An attempt to "explain the limitations of the terms" did run a little long and hence the nitpicking charge. Even I agree that benign tumors tend not to be invasive, but there are sufficient counter-examples in which they are invasive and so I would not use lack of invasiveness to define a benign tumor. As to "a more constructive use of your knowledge and talents than what you have been doing on this page"... I am offering concrete knowledge, citing authoritative sources on the subject and correcting misinformation where I see it. I'm not clear on what grounds I am being reproached, other than a not-very-subtle hint to remember my place.

My impression was that you were perseverating with a great deal of effort and energy on a minor aspect of a still useful broad concept. My suggestion was that you use this effort contribute to our article. If you tried to explain why millions of people have found benign and malignant a useful distinction you would probably get your questions answered and produce something more balanced and useful than simply complaining that there are exceptions.

IANAO (I am not an oncologist), but my understanding of this concept is roughly: Traditionally physicians have classified tumors as benign or malignant, as a rough guide to expected tumor "behavior." Benign tumors tend not to spread by distant metastasis. While they may cause problems by expansion against adjacent normal tissue and bone, they rarely infiltrate and invade normal tissue the way many malignant tumors do. Removal is far less likely to be followed by recurrence. In most cases the principal clinical criteria for characterizing an individual tumor as benign or malignant are aspects of the microscopic appearance of the tissue. There are occasional exceptions to these broad generalizations but they continue to be clinically useful.

There is no question that many of us are more patient with users with accounts who are contributing to the project. Don't take offense, join us. 159.14.249.236 Damn logouts alteripse 12:58, 29 August 2005 (UTC)

OK, I will explain my response. When a tumor (e.g. a colorectal adenoma) is studied microscopically, its relationship to surrounding tissues is one of the criteria by which it is declared benign or malignant. If lymphovascular invasion is seen, the tumour is decidedly malignant, while the absence of this phenomenon argues in favour of a benign neoplasm. This applies accross pathology. I am not a pituitary endocrinologist, but it may be true that the resorption of bone is due to tumour hypervascularity and pressure, rather than through direct resorption by the tumour. Again, you have been relying on exceptions to generalise a point. I do not mind having this discussion, but I do mind excessively long posts and personal attacks. JFW | T@lk 20:58, 29 August 2005 (UTC)

Wording of the first paragraph

The first paragraph begins "Cancer is a group of diseases". Is this completely true? Would you say "melanoma is a member of cancer" or "melanoma is an example from cancer". No, you always say "melanoma is a cancer" or "melanoma is an example from the cancer family". The reason I post this here rather than boldly editing is that I think I'm wrong. So, what do people think? Anyhow, it seems to me that if you introduce it as a group of diseases, to say that that group is caused by DNA damage (later in the paragraph) is to slightly miss the point. Its the members that are caused by this. Does anyone think that this would make the paragraph easier to read if changed? --Mike C | talk 08:00, 27 Apr 2005 (UTC)

I think it is prudent to refer to the various cancers as different diseases, together forming the group of malignancies. If cancer was one disease, how come skin cancer is curable and mesothelioma patients all die? The intro should firmly unseat the public perception that all cancers are similar. They are not; they only share their pathogenesis, and even in that respect they differ wildly (e.g. hematological malignancy is a different kettle of fish altogether). JFW | T@lk 20:42, 27 Apr 2005 (UTC)

PS I would refer to melanoma as a "form of cancer" in the same way I would refer to angina as a form of cardiovascular disease.

I haven't made myself very clear, sorry. Of course the different cancers are different diseases. My question is one of semantics. It is made very clear by your PS. If we take as example of a group: "a flock of birds" where a parrot is a member, we would never say "a parrot is a form of a flock of birds". This leads me to question whether cancer is not "a group of diseases", but rather a noun referring to any member of the group of cancers (hmm kinda cyclical sounding, but it is the group that is dirivative and the members that are defined). Do you see what I'm getting at? Its a rather silly point and I'm still not sure it warrants changing. --Mike C | talk 01:39, 28 Apr 2005 (UTC)

Your new form sounds odd. Cancer is a group, and the various forms (e.g. oesophageal carcinoma, soft-tissue sarcoma) are its members. You can refer to those diseases as a cancer like you would refer to myocardial infarction as a cardiovascular disease. JFW | T@lk 06:02, 28 Apr 2005 (UTC)

I agree the alternative form sounds odd. But I'm now convinced that the current version doesn't quite make grammatical sense. You wouldn't, if writing an article "tree", start off "Tree is a group of tall perenial woody plants". If you wanted to phrase it like this, you would have to say "The trees form/are a group of...". Do you see what I'm getting at? I'll concede to you, though, if no-one else supports me. I'm open to the fact that I'm just plain wrong. I'd accept instantly if you can give an example where "cancer", in that exact wording, is used a group. But, in your above case, you're reffering to a cancer, a member of that group. Most groups I know have an article in front, either "a football team" or "The Star Alliance". However, I can't see how an article can be put in front of "cancer" to make it a group. I'm really confused, now. Please help tease this out. --Mike C | talk 13:03, 28 Apr 2005 (UTC)

To my (non-native speaker) ears the present form is not wrong. Perhaps you feel the word "group" should be associated with a plural term, but some groups do go by their singular. Perhaps the village pump is a nice place to discuss this. I will settle for "cancer refers to a group of diseases", which should resolve the problem. JFW | T@lk 20:51, 28 Apr 2005 (UTC)

I think you're right. The present form sounds fine. Lets leave it for now. --Mike C | talk 11:54, 29 Apr 2005 (UTC)

Geopathic Stress as a cancer risk factor?

I'm quite doubtful that geopathic stress is accepted in mainstream (non-alternative/complementary) medicine as a component cause of carcinogenesis. Perhaps someone could correct me / correct the article? Thanks.

--Guohao 14:26, 2 May 2005 (UTC)

It's raving pseudoscience. JFW | T@lk 19:21, 2 May 2005 (UTC)

Blood Vessel Supply Within Tumors

Something that isn't perfectly apparent to me is why the body supplies tumors with a full supply of blood vessels, for keeping the tumor alive, as it were. One can easily understand how a mutation can cause a single group of cells to reproduce in an unhealthy manner, but what is it that causes the body to grow a complete circulatory system for the tumor? And, along these lines, does the body also supply the tumor with nerves? And lymphatics?--McDogm 15:52, 6 May 2005 (UTC)

A tumour requests the new blood vessels using the same methods as any non-cancerous bodily tissue. A protein called vascular endothelial growth factor VEGF is secreted by most cells which are not being supplied with enough oxygen. there is a clever and not-fully-understood control mechanism involving mRNA stability and a gene called HIF-1 that stimulates VEGF gene transcription. VEGF stimulates the growth of nearby blood vessels into the tissue.

This process is known as angiogenesis and there is some useful information on the relevant page. A fast growing tumour is going to use up a lot of oxygen, so VEGF would be secreted anyway. However, in cancers, the genes coding for chemicals such as VEGF are permanently switched on, as these mutants are favoured by the "clonal selection" process described in the cancer article. Thus, very large amounts of these angiogenins are produced, and blood vessels form. Of course the body wouldn't "want" to supply cancers, but it cannot distinguish the tumour from a healthy tissue short on O2. Angiogenesis is a critical process in the generation of malignancy. Without it, fast growth is not possible and critically, metastasis will not occur. For these reasons, it is a key target of anti-cancer research.

Nerve cells are very reluctant to grow in adults (unfortunately for spinal injury victims) and their growth would not be beneficial to the tumour cells, so would not be selected for. Lymph, again, is not very important to the tumour, as it is there to deal with the osmotic physiology of the entire organism and its lack would not prevent growth. See teratoma for some tumours in which strange cell differenciation (including nerve cell and presumably lymph tissue) occurs, although for completely different reasons. I hope this has answered your question. If not, explain your concerns and I'll try and work it through with you. I'll also put some of this onto the angiogenesis page. --Mike C | talk 22:11, 6 May 2005 (UTC)

Thanks; I have a sneaking amateurish suspicion that lymphatics and their development may be some kind of an adjunct of angiogenesis but since we are talking about tumors here that might not make sense from a canonical mRNA science standpoint. I'm just a solid amateur but I like lymphatics and I am sure I remember that lymphatics are essential for capillary function. A tumor without lymphatics would be undrainable as a mass of tissue. I knew that nerve doesn't really grow very much in the body after a very early stage. In terms of bedside manner and DRG days it seems to me that for the cancer patient it would be good for the doctor to be able to say something helpful about oncoangiogenesis to the patient and their family. Is that word good? Personally I think the oncoangiogenesis, as it were, is a very vulnerable part of the tumor in terms of effecting cures. It makes a lot sense to me that it is a critical topic of study. On a mundane basis oncoangiogenesis goes culturally to the paradigm of economics, in which resources are allocated quite carefullly. It really makes sense to the patient, in other words, to gain leverage over the disease through understanding the negative cultural aspects of oncoangiogenesis as compared to ordinary personal relations and current events. In other words, there is usually a quid pro quo for services rendered, or in even more colloquial terms, one has to pay the (utility) bills. That's just common sense and it is really easy to explain in lamen's terms.

The mRNA mechanisms et al are of course the core of continuing study of the cancer problem.--McDogm 15:49, 7 May 2005 (UTC)--McDogm 19:44, 7 May 2005 (UTC)

Oncoangiogenesis is not a very current term. There is also very little point in discussing it with cancer patients - all treatments in this respect are experimental (although it is one of the underpinnings of radiation therapy). I must say that the role of lymphatic drainage is not crucial to tumorigenesis, as lymphatics usually bear a close relation to the arterial supply of any tissue and probably form together with the blood vessels.

Tumors have no nerve supply apart from the autonomous nervous system branches that come with the blood vessels. JFW | T@lk 22:26, 7 May 2005 (UTC)

What are the genetics of tumorangiogenesis and tumorlymphiogenesis? As I understand the reading, tumors cannot grow more than 3 cubic millimeters w/o angiogenesis. What exactly does angiogenesis, or more descriptively, capillariogenesis, have to do with whether a tumor is malignant or benign, at the nuts and bolts level?--McDogm 16:20, 13 May 2005 (UTC)

Is the commencement of angiogenesis the moment of change from benign to malignant? Of course, if there is no angiogenesis, the tumor will not generally grow bigger than 3 cubic millimeters, so angiogenesis is important. But is it the central factor in malignancy? Is angiogenesis the door to curing cancer?--McDogm 13:24, 14 May 2005 (UTC)

Hmmm. Expression of collagenases and MMPs is more likely the defining factor - metastasis can occur when the cells can invade other tissues. I suspect proangiogenetic mutations probably occur earlier rather than later. Inhibiting angiogenesis as a cancer cure is the premise of the Folkman hypothesis. Malignant cells will develop, but will be starved of nutrients as they cannot command adequate angiogenesis. Some antiangiogenic drugs (including thalidomide) are undergoing trials, so I suppose the experimental evidence will tell us if antiangiogenetic therapy will cure cancer. JFW | T@lk 19:31, 22 May 2005 (UTC)

Acrylamide

I was wondering what other health professionals around the globe believe about Acrylamide, whether it is Carcinogenic or not.

In vitro it appears to be a carcinogen, but cancer indicence due to the consumption of acrylamide-rich foods is not as shocking as has been suggested. JFW | T@lk 19:31, 22 May 2005 (UTC)

Frequency of different cancers

Please can we have some information of the relative frequency of different types of cancer. Even a simple pie chart would be useful.

Hmm, these are different in each country. Are you asking for worldwide statistics? There may be obtained from the WHO. If you provide an URL, I'll gladly make an OOo pie chart! JFW | T@lk 12:48, 24 May 2005 (UTC)

Article Length

This article is getting a little on the long side. Does anyone have any ideas about shortening it? --Mike C | talk 11:00, 28 May 2005 (UTC)

I think this is just about right. You can't make such a major topic much shorter than this. You may want to find redundancies, and some sections may be shortened with more information added to subarticles, but on the whole I don't think you can slim this down any more. JFW | T@lk 06:41, 29 May 2005 (UTC)

I felt the molecular biology section was a little long, perhaps it could be trimmed down if anything. The explanations are excellent, but it could be simplified a bit allowing the reader to go into more detail if they wish to read the main article. Richard001 08:05, 15 January 2007 (UTC)

Featured article?

This article needs to become a featured article. With all those nice graphics and most subpages written it should be worked on to become a WP:FA. JFW | T@lk 05:25, 6 Jun 2005 (UTC)

I agree. I made a few changes to improve things, and I see you did too. Here's some things that are still bothering me. We should fix some of this before starting it onto the featured article road.:

1. The origins of cancer section. It is incomplete, I don't know if it should be expanded or replaced or deleted.
2. "Adult cancers are usually formed in epithelial tissues" is followed by a list that includes many non-epithelial cancers
3. The list following "Childhood cancers include, from most frequently occurring to least" includes a mixture of cell types (germ cells, epithelial) and cancers (neuroblastoma)
4. the immunotherapy section gives me problems. Herceptin is not using the patient's immune system against the cancer, it uses a mouse's immune system. I think this section should be lumped into chemotherapy unless it goes into a discussion of cancer vaccines, which are still pie-in-the-sky, except for the hepatitis B virus vaccine.
5. "Contrary to expectation, randomized trials found no benefit" begins a string of confusing statistics about diet and cancer. I believe the basics are: diet has some affect, smoking tobacco much more of an effect. Specifics about diet are not yet well established.
6. the statement about cancer being the leading cause of death is incomplete, in the united states, at least, it is only true for people under the age of 85. Note 2, the reference, is now pointing to a dead page.
7. the Cancer research section is weak. Just a grab bag full of things.

Jpbrody 22:17, 7 Jun 2005 (UTC)

To elaborate on each point:

1. The section "origins of cancer" should be merged with the "causes and pathophysiology" section, if no-one objects. DONE.
2. Adult cancers are mainly epithelial, but there are many rare types which are nonepithelial but still worth mentioning (e.g. melanoma, sarcoma). Perhaps we should rephrase that awkward line. DONE.
3. "Childhood cancers" should be reviewed. Perhaps a reference is in order here. It should be clear that when a cell type is mentioned, all its tumors are intended. DONE.
4. I disagree that trastuzumab/Herceptin® does not use the human immune system. The antibody is only one part in a complex process, which involves complement-mediated cell lysis. The fact that the antibody is murine is extra. Perhaps we should replace "immune system" with "immune mechanisms". As for cancer vaccines, some good results have been booked with vaccination for cervical carcinoma, but we should warn that all is still experimental. DONE.
5. The diet section needs overhaul, preferably with a recent systematic review in hand. There is so much news-fuelled nonsense going round about diet & cancer that we need a very clear-headed section on this subject. DONE.
6. The vast majority of the population are <85, so correcting for that will still make cancer the #1 cause of death. A good journal reference will be needed. HELP NEEDED.
7. The research section overlaps with the pathophysiology section higher up. Most of that stuff should be on subpages (e.g. carcinogenesis, oncogene, tumor suppressor gene, Knudson hypothesis - a red link!) DONE - removed the research section. JFW | T@lk 23:30, 7 Jun 2005 (UTC) Keeping tabs on myself - JFW | T@lk 21:15, 9 Jun 2005 (UTC)

Trials and experimental treatments paragraph

I don't think this paragraph is required. A sentence elsewhere (beginning of treatments?) could provide links to clinical trials and experimental cancer treatment. But as it stands, it is just information about clinical trials and not cancer related, particularly. I have removed the experimental treatments bit from the title, as it had nothing about this and I think that is best left to a sub-page anyway. --Mike C | talk 13:33, 10 Jun 2005 (UTC)

Mike, a very large proportion of cancer treatment takes place in the context of clinical trials, as ideal treatment is simply not yet established in many scenarios. I think we should distinguish between clinical trials, which are usually with established agents, and those with newly-developed treatments (such as the TK inhibitors) which are yet in their Phase II or Phase III stages. JFW | T@lk 15:40, 10 Jun 2005 (UTC)

Brilliant. You know how I'm concerned about the size. But you've convinced me. People are going to come here wanting information about the reality of cancer as well as the theory. Clearly treatment in trials is important to someone wanting to know about the implications of having cancer. --Mike C | talk 22:26, 10 Jun 2005 (UTC)

Categorisation

Contrary to the guidelines on the Wikipedia:Categorization page, this page is currently a member of a category (Cancer) and its sub-category (Oncology). Should this stay this way? --Mike C | talk 16:06, 11 Jun 2005 (UTC)

You're right. JFW | T@lk 11:35, 12 Jun 2005 (UTC)

When people categorize things, they normally do not use a linear chain of subcategories. Different people use different, overlapping categorizations. It is futile for Wikipedia to try to enforce a single linear chain of categories and subcategories. Too strict enforcement of this rule (avoid using a category and one of its subcategories for the same article) can weaken the power of Wikipedia that grows out of the flexibility of hypertext. Rational arguments could be made for making "cancer" a subcategory of "oncology". --JWSchmidt 13:26, 12 Jun 2005 (UTC)

In that case, is there really a need for these two categories "Cancer" and "Oncology"? Having the two is potentially confusing. What content should belong in "cancer" that shouldn't belong in "oncology"? See here Category Talk:Cancer--Mike C | talk 15:54, 12 Jun 2005 (UTC)

I try to think of categories in terms of causality. Oncology is the consequence of cancer (not vice versa - no cancer means oncologists go looking for other work). I think "cancer" alone is fine, although Mike is right that easy access to the oncology category would be nice for the reader. JFW | T@lk 19:40, 12 Jun 2005 (UTC)

Peer-review

Okay guy's, let's do it again. Can we identify problems with the article, and how we should go about solving them? What sections, in particular, need attention?

Another question is: how are we going to make good references and external links? I want to keep these sections concise and very to the point. I'd like to limit the references to 3-4 papers on cancer incidence & epidemiology, mechanisms, and directions in treatment. This will be hard to find - no author will attempt to tackle the whole field of oncology in one paper. Nonetheless, these may still be available.

Concerning history: what is the etymology of cancer, when was it first recognised as a disease, and who identified such crucial concepts such as dysplasia, invasive growth, metastasis, etc. Was it just Virchow? JFW | T@lk 09:20, 15 Jun 2005 (UTC)

After the peer review process in WikiProject Clinical medicine, I recommend going through Wikipedia:Peer review for review by the general nonclinical people. "This page is for nearly Featured-standard articles that need the final checking by peers before being nominated as Featured article candidates." Petersam 19:27, 18 Jun 2005 (UTC)

I agree. JFW | T@lk 22:52, 18 Jun 2005 (UTC)

Since p53 plays such a significant role in a number of different cancers may I suggest a specific section dedicated to this alone.

Where do cancers rank in cause of death worldwide?

I added to the intro paragraphs that cancer is the #2 cause of death in the US and in the UK, but we need a worldwide number instead, which I can't seem to find. The WHO statistics are helpfully divided between the low/middle income countries and the high income countries, which would be useful to discuss with some precision, but unfortunately WHO lists each cancer as a separate disease, so the highest ranking one, lung cancer, is rated #10 overall. Can someone find a better reference? Tempshill 23:27, 16 Jun 2005 (UTC)

Look further down tha page. JFW | T@lk 23:34, 16 Jun 2005 (UTC)

Malignancy

I want to put in a line defining malignancy early on in this article, probably in the first paragraph or two. It's referred to a lot during the article and for the first time in that second paragraph. However, I'm having trouble actually defining the term. Malignant is often used instead of "cancerous" by most doctors and academics when referring to cells or tissues, but is it quite as simple as being synonyms? I don't think so, but I can't put my finger on it. --Mike C | talk 22:56, 18 Jun 2005 (UTC)

Yes, it is synonymous. alteripse 23:05, 18 Jun 2005 (UTC)

I find it a horrible term (cancerous, that is). JFW | T@lk 23:17, 18 Jun 2005 (UTC)

Yes. Its sounds wrong in almost all circumstances. --Mike C | talk 22:12, 19 Jun 2005 (UTC)

I once caught myself searching for the term in Wikipedia and eradicating it... JFW | T@lk 22:55, 19 Jun 2005 (UTC)

We don't have to use it beyond making it explicitly clear that it is a synonym for cancerous-- precisely because Mike needed to ask. alteripse 04:27, 20 Jun 2005 (UTC)

disjointed presentation

The presentation of the article is very disjointed and the article doesn't flow. I'll attempt to correct it. For one thing, the key principles should be defined within the first few paragraphs, with general references even in diagnosis, etc. then slowly becoming more specific, then branching off. -- Natalinasmpf 02:26, 22 Jun 2005 (UTC)

I'm not sure what you mean by "disjointed". The organisation of the article is certainly correct, and I think we shouldn't be moving paragraphs about anymore. As for the flow of the text, this requires copyediting (that's what you get when hundreds of editors follow their own style when inserting a few words...)

General references are extremely hard to find. I would be unhappy with the mention of niche references in such a general article. There are numerous textbooks about cancer, but even these works classify diagnosis by specific cancers. This is actually a result of the general readership treating cancer as "one disease", while doctors have the habit of seeing every form of cancers as its own entity (most oncologists rarely treat skin cancers, unless it's melanoma, as this is the domain of dermatologists).

The article now focuses on the principles of cancer. We should avoid getting too specific, and concentrate on those things that are germane to all cancers (e.g. uncontrolled cell division and its mechanisms, principles of screening, palliative care for incurable cancer causing symptoms). JFW | T@lk 08:57, 22 Jun 2005 (UTC)

Oops, Jfdwolff, I already re-organized the chapters before reading your comment! Frankly, I agree with Natalinasmpf. Have a look at what I did and let me know. I also added a chapter at the top of this page about this subject. Emmanuelm 19:43, 23 December 2005 (UTC)

Are these true?

I went through the article again and spotted some problems. Fixed some wording, added some text, and flagged these statements as potentiallly not true. Jpbrody 21:20, 22 Jun 2005 (UTC)

• Proto-oncogenes are involved in signal transduction by coding for a chemical "messenger", produced when a cell undergoes protein synthesis.
• Tumor suppressor genes code for chemical messengers that command cells to slow or stop mitosis in order to allow DNA repair

I know this is true for some oncogenes/tumor suppressors, but I don't believe it is true for all.

• • Its a generalisation, which is good for a subject as broad as cancer - I mean, I could go type up the function of every single tumor suppressor, but that is its general ability. The idea to "suppress" a tumor, is when triggered by cell damage is to stop mitosis, evaluate any damage - if its repairable, activate some enzymes to fix it (through a complex pathway), or tell the cell to undergo apoptosis. Proto-oncogenes are involved in stimulating growth...they enzymes they make send growth signals, and as enzymes they are activated by say, triggered by growth hormone or internally (ie. like the genes activated in human germination), starting a pathway for growth. Tumor suppressor send opposite signals, to halt mitosis. One notices for example, that cancer cells tend to be irregular and smaller than normal cells because they undergo mitosis faster than normal - there are so much mutated proto-oncogenes that overexpress themselves - ie. they were only supposed to activate under certain conditions, like a certain hormone, and such, but now they do it constantly, and are insenstitive to signals that tell them to stop, and there the usual regulation (tumor suppressors) are mutated, providing little resistance - cancer. -- Natalinasmpf 21:48, 22 Jun 2005 (UTC)

• A mutation to only one tumor suppressor gene would not cause cancer either, due to the presence of many "backup" genes that duplicate its functions.

I believe this is speculation, not established.

How is it not established? The p53 gene isn't the only tumor suppressor gene, for example, and there are duplicates throughout the genome. "backup" is colloquial. Its not really a backup, just addition tumor suppressor genes to "cover for it" in case its mutated. If we only had a few tumor suppressors on hand we'd be having cancers while we're in the prime of youth. Poorly worded, perhaps. Natalinasmpf 21:48, 22 Jun 2005 (UTC)

Isn't Retinoblastoma the classic case? All you need to develop it are mutations in both copies of Rb-1. No other mutations in "backup" genes. Jpbrody 18:15, 23 Jun 2005 (UTC)

No, not really - just that if you already have pre-developed mutation, your chances for retinoblastoma is very very high - especially in something like Rb1. From what I read here [8] " in heritable form one allele is already mutated" - seems like its "to get a higher chance of acquisition", not that its the only mutation you need. -- Natalinasmpf 23:32, 23 Jun 2005 (UTC)

Is this about a mutation of one gene? or the mutation of one copy of one gene? Every gene in the body (just about) has two copies per cell (one per chromatid) so a mutation in one copy of a tumour suppressor gene doesn't cause cancer as the second allele is still producing the protein - the mutation is recessive. However, in an oncogene, only one copy needs to be mutated - it is dominant because any production of the incorrect protein, or over expression of it, can cause cancer. --Sinkingpie 16:34, 1 February 2006 (UTC)

Knudson’s two hit model has recently been challenged by several investigators. Their studies show that a mutation or loss of a single allele may be sufficient to exert a cellular phenotype that leads to tumorigenesis without inactivation of the second allele. This gene-dosage effect is called haploinsufficiency and has been demonstrated by a number of experimental approaches. Tumors influenced by haploinsufficiency usually have a later age of onset when compared with those by a two hit process. This is from a Science article. I can cite if necessary.

One section mention 15% of cancers maybe caused by viruses and then downplay that fact. I cited a Science article that says 15% of world wide cancers are viral in etiology and then say that is second only to tobacco usage.

• Faster rates of mitosis increasingly leave less window space for repair enzymes to repair damaged DNA during DNA replication, increasingly the likelihood of a genetic mistake.

Again speculation.

Not really, for example, you notice DNA replication in the cell cycle (phase S) nearly takes a third of the entire cycle, because making changes to, or replicating DNA is an energy intensive process that takes a long time. In order to repair DNA, you have to halt mitosis. How is it speculation? I mean, take a look at polymerase - it comes it with tons of enzymes to repair DNA during replication itself, and they are not there for no reason. This already doesn't count the factors that are involved outside of replication. Natalinasmpf 21:48, 22 Jun 2005 (UTC)

Perhaps faster rates of mitosis lead to more genetic mistakes due to other reasons like: more DNA replication (I would argue this is the primary reason, not less window space to repair DNA). Maybe you don't have to halt mitosis to repair DNA, these could occur simultaneously. Jpbrody 18:15, 23 Jun 2005 (UTC)

Uh, you can, just that mitosis occurs before DNA repair can be completed. The idea is that DNA repair is a lengthy process - thus you halt mitosis to prevent it from escaping to the next generation, repair the DNA first, otherwise if DNA repair doesn't occur until after mitosis it could well be too late, as mutations after mitosis becomes permanent. That is why it is crucial to stop mitosis for repair. If you see the link I posted above, it says one of the tumor suppressors "arrest cell division in response to radiation damage", hence... -- Natalinasmpf 23:32, 23 Jun 2005 (UTC)

• A cell that degenerates into a tumor cell does not usually acquire all these properties at once, but its descendant cells are selected to build them. This process is called clonal evolution. A first step in the development of a tumor cell is usually a small change in the DNA, often a point mutation, which leads to a genetic instability of the cell.

This is the textbook multi-hit model hypothesis. It is not fully established, especially in the details of (clonal selection).

It is quite established, well, just as natural selection is....its just extending natural selection to explain how a cancer cell manages to acquire to accumulate mutations within a person's lifetime. A cell doesn't acquire these mutations all at once - it takes generations of cells to do it. How this develops is natural selection, to explain otherwise, what would be a very small probability, ie. one in a trillion. However, since those 30% of those who lived over 70 have got cancer in their lifetime (a rough statistic, but you can get my point when you see how common it is for the elderly, and not so much for the youth), natural selection reconciles this. Natalinasmpf 21:48, 22 Jun 2005 (UTC)

Heard a talk by a respected UCSF professor, Joe Gray. He is pushing the idea that in breast cancer, mutations occur suddenly rather than gradually, contrary to the multi-hit model. He had convincing data suggesting that this is triggered by telomere crisis. I'm not saying that clonal evolution is wrong, just that it isn't well established and universally true for all cancers. Jpbrody 18:15, 23 Jun 2005 (UTC)

For example, notice how a benign tumor can become malignant later on life? That is due to evolution - first, uncontrolled growth trait, then acquiring the metastasis trait - the genes controlling motion that are normally inactivated (ie. usually activated on only mobile cells, like white blood cells), thus enabling to metastasize. I think there's strong evidence that its gradual. Leukemia, for example, some of the cells already have the ability to metastasize as that was a normal trait to be mobile. -- Natalinasmpf 23:32, 23 Jun 2005 (UTC)

• It [chemotherapy drugs] interferes with cell division in various possible ways, e.g. with the duplication of DNA or the separation of newly formed chromosomes.

this is again a generalization, not true for all chemotherapy drugs.

Thanks for pointing all that out. I think most of these rather bold statements can be toned down with "many", "some", "a large proportion" etc etc. On the whole, many of these statements should not even be in this article but in carcinogenesis (to be written). This article should mention that cancer is due to cumulative damage (bar a few examples) and that there are oncogenes and tumor-suppressor genes. If we elaborate too much (1) the article flow stops, (2) it becomes too thick a read for the casual reader, (3) it will attract scientific controversy for unestablished facts. Hence, I suggest we trim the pathogenesis section to bare bones. The chemo comment is actually very balanced. JFW | T@lk 21:32, 22 Jun 2005 (UTC)

Natalinasmpf, please understand that what we're presently presenting as solid truths are actually scientific controversies. These should NOT be elaborated on in depth over here. Let's stick with what is known. JFW | T@lk 07:00, 23 Jun 2005 (UTC)

How are they "controversies"? These are generally accepted facts in oncology. It is a known fact there are duplicate (well sort of wrong word), well a vast array of both proto-oncogenes and tumor suppressor genes, that activate at different times, such that if one gene gets mutated, cancer prevention takes a setback, but doesn't get devastated, even if p53 goes out (although its very very major), that is huge set back, but still doesn't cause cancer, as it removes a key check (most of the apoptotic pathway) - which there is generally consensus on. Apoptosis itself is a fresh discovery, in terms of discovering the pathways, but its not so much a "controversy", but rather, new discovery. Seeing how as its been at least a decade, I think its safe to establish as fact. I mean, after all, there hasn't been an alternative model of cancer either. DNA repair is known, and tumor suppressors' role in halting mitosis in order to conduct DNA repair is an established fact, I don't see any scientific opposition against it. Apoptosis is known. Apoptosis is also related to signal transduction, which the process itself relies on tumor suppressor genes. Proto-oncogenes code for growth signals, by triggering the pathway for growth (which counts as a "signal", lets call it a "trigger", here), and that has been established what they do. What do you expect proto-oncogenes to do, provide some miraculous protein that speeds up growth other than being a chemical messenger that starts a cascade? Not really. Even growth hormone is a chemical messenger - and the stuff it affects are also chemical messengers, ie. it comes into contact with the cell membrane, which the enzymes on the membrane when receiving the hormone, trigger another messenger, or a cascade of them, which leads to say, faster acquisition of nutrients, faster replication and mitosis...of course what they exactly do isn't known, but to "speed up growth" generally the idea is that the speed up the processes involved in growth, that are usually well timed.

These are controversies because the precise details are not understood. To see what I mean, contrast this with something like the citric acid cycle, where the precise details are all worked out. In your examples, DNA repair, apoptosis, etc have been definitively established, but the role that they play in cancer is not well established. Jpbrody 18:15, 23 Jun 2005 (UTC)

Not clearly established, but I already generalised the role. The "window space for mitosis", for example, is hardly speculation, as yes, faster rates of mitosis means a higher chance of mistakes, but DNA repair tends to solve it if there's enough time. Unless of course, mitosis occurs so fast after synthesis that it lacks the time to repair it fully, thus the mutations become permanaent (because originally it could tell which was the template strand and which was a mutated strand, if say, it was a mismatch) - if this is passed to the next generation before it can be repaired, the next generation can't tell anymore, because the mutated strand then becomes the template strand. -- Natalinasmpf 23:31, 23 Jun 2005 (UTC)

hmmmm -- Unsigned comment by User:TTLightningRod

Biopsy Section

Isn't there a logic to moving the biopsy section to below the screening section, on the basis that screening would always happen before biopsy, if at all? --Mike C | talk 10:33, 23 Jun 2005 (UTC)

As you are the second person to propose this, we should try to clarify that the section is saying that there are 3 basic roads to diagnosis: (1) presenting symptom to biopsy to dx; (2) accidental finding to biopsy to dx; (3) screening test to biopsy to dx. Nearly every case takes only one of those three paths. Since the first path is the most common, Dr JFDW and I thought it most logical to put the biopsy after the presenting s&s, rather than after listing all three initial steps, but perhaps you have a suggestion for making this message clearer? alteripse 11:06, 23 Jun 2005 (UTC)

I moved the biopsy section after screening to follow the introductory paragraph.

Most cancers are initially recognized either because signs or symptoms appear or through screening. Neither of these lead to a definitive diagnosis, which usually requires a biopsy. Some cancers are discovered accidentally during medical evaluation of an unrelated problem.

I understand the argument for biopsy first and I won't change it again, but could someone rewrite the above paragraph to fit the following section. I couldn't think of how to do so. Jpbrody 18:22, 23 Jun 2005 (UTC)

Good. Just checking for good logic. It makes sense like that --Mike C | talk 20:32, 23 Jun 2005 (UTC)

Protection

I have protected the page for a little while in response to tasteless vandalism from various IPs. If there are pressing matters on the page content, please propose them here. Otherwise let's wait a day or two for the vandalism to die down. JFW | T@lk 22:10, 26 Jun 2005 (UTC)

Can someone unprotect it now? It should be all over by now. -- Natalinasmpf 28 June 2005 08:26 (UTC)

Sure. JFW | T@lk 28 June 2005 15:03 (UTC)

Molecular biology problems

I just made a few edits to the introduction paragraph, which I thought was difficult to read. Do people like the rewrite? I think this is an important paragraph to get down perfectly, since many people with little knowledge of biology will be reading this to understand exactly what cancer means.

The molecular biology section really needs to be re-written. Lots and lots of statements are disjointed, and the whole section has no flow at all. A few examples of confusing or irrevelant information:

• Jpbrody pointed this out earlier: "Proto-oncogenes are involved in signal transduction by coding for a chemical "messenger", produced when a cell undergoes protein synthesis."

This sentence is generalized to the point that it means nothing, even to a specialist. Also, cells don't "undergo protein synthesis" - protein synthesis is a continuous process.

• "Frustratingly, the chance of cancer cannot be reduced by removing proto-oncogenes from the human genome as they are critical for growth, repair and homeostasis of the body. It is only when they become mutated, that the signals for growth become excessive."

This statement is based on a naive assumption that if something is bad, you should just get rid of it. I think this needs to be re-stated.

• "Other types of mutations can be caused by chronic inflammation, as neutrophil granulocytes secrete free radicals that damage DNA."

Assumption: the reader knows what neutrophil granulocytes have to do with inflammation.

• "Tumor viruses ... usually carry an oncogene or a gene inhibits normal tumor suppression in their genome."

Assumption: the reader understands the mechanisms of viral infection and how a virus with an oncogene could turn a normal cell into a cancerous one.

• "It is impossible to tell the initial cause for any specific cancer."

This is quite a blanket statement. It's hard to tell the initial cause, but not impossible. Just before, the article listed many mutagens that have been proven to lead to certain cancers.

Last but not least, the last paragraph of the section reiterates what has already been said (how a cell becomes cancerous), but in a different way. For instance:

• "A first step in the development of a tumor cell is usually a small change in the DNA, often a point mutation, which leads to a genetic instability of the cell." - oops, haven't we said that already?

Mr.Bip 20:06, 1 August 2005 (UTC)

New to editing, but I think the old Molecular Biology of cancer is pretty messed up. For instance, point mutations do not lead to genetic instability, as many are silent, any edits need to be more specific. There are too much stuff to say about molecular biology of cancer, do you think new article is nessary? I cleaned up and rewrote some paragraphs, any suggestions are welcome!

Peregrine Falcon 08:41, 17 November 2005 (UTC)

Restructuring

Does this make more sense to people? 1-5 are about cancer itself, 6-9 about impact of cancer.

1 Diagnosing cancer

2 Types of cancer

3 Causes and pathophysiology

4 Treatment of cancer

5 Prevention

6 Epidemiology

7 Social impact

8 Coping with cancer

• I think Cancer research should just be a link with a brief explanation to another article. It is a much more technical topic, and the page could become quite detailed when someone decides to take the topic on. I think this article should just focus on defining what we know for sure, and let the research article describe current research areas and controversies.

Mr.Bip 20:06, 1 August 2005 (UTC)

I wholly agree that Cancer research should be a link rather than a paragraph. I've had concerns for a while that this article, although of a reasonable current size, could be expanded greatly in other articles.

As to the order of contents, I have a concern. I see in the list above three sorts of section:

Those about cancers, the diseases themselves: sections 2 and 3

Those about the clinical medicine surrounding cancer: sections 1,4,5

Those about the human impact: sections 6,7 and 8

The proposed structure nearly has a separation of these, with the exception of the diagnosis section. I can see some arguments for putting diagnosis first, but this is an article about cancer so it makes sense to me to jump in with a description of what cancer is and run 23145678, with the diagnosis before treatment. I've tried moving the article around in rough, and it seems to flow better with a clear patient progression from presentation to outcome without a wad of molecular biology in the middle. Does anyone agree? --Mike C | talk 10:46, 29 August 2005 (UTC)

Statistics

As it stands, the information presented regarding the incidence of various cancers is completely US-centric; this needs to be altered, as this is NOT a US-specific reference work, but rather one which is used by English-speaking persons all over the world. The information in this section should be altered to reflect the incidence of various cancers worldwide, and could perhaps link to a separate article giving a breakdown for specific nations. Just a thought. Spider Jerusalem 22:36, 10 Aug 2005 (UTC)

Well, go ahead. The American stats were just 1000x easier to find, and cancer numbers in Europe are not much different. JFW | T@lk 23:42, 11 August 2005 (UTC)

List of genes

I move that adding a large list of genes is not conducive to this article. Saving certain translocations etc in haematology, mutations have little bearing on the care of the bulk of cancer patients. This should be on cancer research or cancer genetics, but certainly not on this page. JFW | T@lk 16:58, 8 September 2005 (UTC)

How does cancer kill people?

This article goes into a lot of detail about what cancer does at a cellular level, and then says that cancer is a very prominent cause of death. But it doesn't seem to explicitly state how cancers kill people, or why they're dangerous. Do tumors produce toxins? On House, M.D. they talked about blood clots once; is that a common method of death from cancer? Are all cancer deaths caused by post-metastasized cancers? Are the exact causes of cancer death unknown? I mean, I find it very unintuitive that a disease in the skin, breast, or testicles is often fatal. This information seems really fundamental to the topic; I think that it should be mentioned in the first few paragraphs of the article, and in later sections in more detail. I'd appreciate information about this. Thanks. -- Creidieki 03:12, 29 September 2005 (UTC)

This needs elaborating in the article. The main causes of death are infection, malnutrition, any problem due to organ failure (e.g. liver failure from hepatic metastasis) etc. Breast cancer etc is generally metastatic by the time it kills. JFW | T@lk 07:43, 29 September 2005 (UTC)

Although perhaps it needs to be emphasised more, the thing is that it's not one cause, than your cells revolting against you (to describe it poetically). They no longer obey what your body tells them to. That is, not only do you now lose function from those cells, they now work against you. It's the same thing with germs - not necessarily toxins they produce, but loss of function, production of waste material, fast growth and thus deprivation of nutrients from healthy cells, and invasion. Remember, it's a biological disease, not a chemical one. What matters in biological diseases are the allegiance of the cells, and how to kill rebel or hostile cells (ie. bacteria, or perhaps viruses, although they are not cells), whereas in say, poisoning or chemical related problems it deals with it more directly. Again, cancer is harmful depending on the cell's ability as a now disobedient biological unit. For example, what's wrong if say, there was a coup d'etat against the United States at this moment? Will it result in rape, plunder, change of government, more taxes? These can vary according to how the perpetrators intend to seize power or their objectives, but remember, the most clear danger of cancer is the fact that these cells have the power, through some means of other, by refusing to obey your body's cellular signals through signal transduction, hormones, apoptosis or otherwise, to threaten your well-being in some way. This is why cancers also take time to have effect. At first the cells are not that ambitious, just a bit rowdy, but within a decade, you get full-fledged revolution. Just to describe it in poetic terms, perhaps it is something to relate to. -- Natalinasmpf 00:03, 30 September 2005 (UTC)

Morphine?

I'm puzzled how a huge encylopedic article on cancer and the discussion that followed does not have a single reference to the most powerful drug to counter the illness' most devasting effects.

"This needs elaborating in the article. The main causes of death are infection, malnutrition, any problem due to organ failure (e.g. liver failure from hepatic metastasis) etc. Breast cancer etc is generally metastatic by the time it kills"

Incidently my father died 'whilst suffering from cancer' recently and the cause of was a chest infection. He underwent several blood transfusions prior to his death, his immune system was clearly weakened by his lack of bone marrow, and consequently white blood cells, as the cancer spread into his bones.

If his immune system wasn't so weak at the time he might not have died. However he was in such awful pain it was just as well.

There are three mentions of 'pain' in the whole article, all in the same small paragraph. I think some of you are forgetting what cancer actually is.

A large proportion of cancer patients never needs morphine. To push this point too much adds to the misunderstanding and stereotype that all cancer patients are in wrenching pain and spend their last months drugged up. Yet, a mention of opioids is a good idea. JFW | T@lk 10:34, 23 October 2005 (UTC)

I wrote cancer#symptom control to address these points. You were quite right that this important dimension of cancer medicine was missing from the article. JFW | T@lk 10:45, 23 October 2005 (UTC)

Do you have any evidence that "a large number of cancer patients never need morphine". I'm under the impression that if cancer spreads, then this will eventually result in severe pain.

Do these other people die from related illness and therefore not experience the real pain of cancer or are you suggesting that such severe pain as my father suffered is rare in cancer patients and if so do you have the evidence to back this up?

My father was on opioids for ten months prior to his death. He experinced pain on a regalar basis throughout those ten months. He got used to it but the pain was often so severe that he was almost unable to speak even whilst on morphine as the drug didn't always work properly.

The pain definately got worse throughout those ten months and his last month was particularly bad, his last week we wanted him to die. I don't think his experience is unusual in cancer sufferers.

It depends completely on the type of cancer and where it has spread. Melanoma patients with cerebral metastasis may not have pain at all. I'm trying to explain that you shouldn't generalize on the basis of your own personal experience. Have you actually read the new paragraph I've written to address your points? JFW | T@lk 02:33, 28 October 2005 (UTC)

Peer review

This page looks great. I'm putting it up for peer review here. JFW | T@lk 21:20, 3 December 2005 (UTC)

Diagnosis Section

The page is looking great now, but it seems odd to me that the diagnosis section is before the sections detailing what the cancer disease process is. Wouldn't it be better for the diagnosis bit to be with the rest of the clinical information, before the treatment section? I don't want to make this change without support, because it would be a lot of effort to get everything working well. --Mike C | talk 14:11, 4 December 2005 (UTC)

All medical pages on Wikipedia follow the outline mentioned on Wikipedia:WikiProject Clinical medicine. This outline suggests that the clinical syndrome needs to be discussed before pathophysiology. There are things to say for both approaches, but I'll say that the intro already explains what cancer is (in a nutshell). Long rambles about pathophysiology make the average reader fall asleep. JFW | T@lk 15:23, 4 December 2005 (UTC)

Jfdwolff - I do not agree

I do not agree Jfdwolff's revert. GRID.org needs hundres of new members. People does not join, if they do not know about the project. How many people uses the keyword "Cancer research"? Not many. How many people uses the keyword "Cancer"? Very many. So, it would be sensible to put the link on the Cancer-page, so that many people would find it. Henri Tapani Heinonen 06:44, 9 December 2005 (UTC)

Yes, but Wikipedia is to provide information, not to recruit new participants. JFW | T@lk 07:32, 9 December 2005 (UTC)