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{{infobox biodatabase
{{infobox biodatabase|title=Network of Cancer Genes|logo=[[File:NCG6.0 logo.png|300px|Logo of the Network of Cancer Genes database version 6.0]]|description=A web resource on systems-level properties of cancer genes|scope=|organism=''[[Homo sapiens]]''|center=[[King's College London]]|laboratory=|author=|pmid=|released=August 2018|standard=|format=|url=http://ncg.kcl.ac.uk|download=|webservice=|sql=|sparql=|webapp=|standalone=|license=|versioning=|frequency=|curation=|bookmark=|version=6.0}}The '''Network of Cancer Genes''' (NCG) is a freely accessible web resource of [[cancer]] [[gene]]s and their associated properties.<ref name=":0">{{Cite journal|last1=Repana|first1=Dimitra|last2=Nulsen|first2=Joel|last3=Dressler|first3=Lisa|last4=Bortolomeazzi|first4=Michele|last5=Venkata|first5=Santhilata Kuppili|last6=Tourma|first6=Aikaterini|last7=Yakoleva|first7=Anna|last8=Palmieri|first8=Tommaso|last9=Ciccarelli|first9=Francesca D.|date=2018-12-01|title=The Network of Cancer Genes (NCG): a comprehensive catalogue of known and candidate cancer genes from cancer sequencing screens.|url=https://www.biorxiv.org/content/early/2018/12/01/389858|journal=bioRxiv|language=en|pages=389858|doi=10.1101/389858|doi-access=free}}</ref> The project started in 2010 and in August 2018 has reached its 6th release: NCG6.0. NCG6.0 reports information on 2,372 [[protein]]-coding cancer genes, including 711 known cancer genes from the Cancer Gene Census and the Vogelstein, Science 2013 list.<ref>{{Cite journal|last1=Kinzler|first1=Kenneth W.|last2=Diaz|first2=Luis A.|last3=Zhou|first3=Shibin|last4=Velculescu|first4=Victor E.|last5=Papadopoulos|first5=Nickolas|last6=Vogelstein|first6=Bert|date=2013-03-29|title=Cancer Genome Landscapes|journal=Science|language=en|volume=339|issue=6127|pages=1546–1558|doi=10.1126/science.1235122|issn=1095-9203|pmc=3749880|pmid=23539594|bibcode=2013Sci...339.1546V}}</ref> The remaining 1,661 cancer genes are candidate cancer genes annotated from the manual curation of 273 original publications. For each cancer gene NCG6.0 reports its system-level properties, the publications reporting it as a known or candidate cancer gene and information on the design of their cancer sequencing screens. In addition, the database provides annotations on 250 possible false positive genes, defined as candidate cancer genes whose association with cancer is likely to be spurious.<ref>{{cite journal|last1=Lawrence|first1=Michael S.|date=11 July 2013|title=Mutational heterogeneity in cancer and the search for new cancer-associated genes|journal=Nature|volume=499|issue=7457|pages=214–218|doi=10.1038/nature12213|pmc=3919509|pmid=23770567|bibcode=2013Natur.499..214L}}</ref><ref>{{Cite journal|last1=Bailey|first1=Matthew H.|last2=Tokheim|first2=Collin|last3=Porta-Pardo|first3=Eduard|last4=Sengupta|first4=Sohini|last5=Bertrand|first5=Denis|last6=Weerasinghe|first6=Amila|last7=Colaprico|first7=Antonio|last8=Wendl|first8=Michael C.|last9=Kim|first9=Jaegil|date=2018|title=Comprehensive Characterization of Cancer Driver Genes and Mutations|journal=Cell|volume=174|issue=4|pages=1034–1035|doi=10.1016/j.cell.2018.07.034|pmid=30096302|pmc=8045146|issn=0092-8674|doi-access=free}}</ref>
| title = Network of Cancer Genes
| logo =
| description = A web resource on systems-level properties of cancer genes
| scope =
| organism = ''[[Homo sapiens]]''
| center = [[The Francis Crick Institute]]
| laboratory = [[Cancer Systems Biology Lab - Ciccarelli Lab]]
| author =
| pmid =
| released = May 2023
| standard =
| format =
| url = http://http://www.network-cancer-genes.org/
| download =
| webservice =
| sql =
| sparql =
| webapp =
| standalone =
| license =
| versioning =
| frequency =
| curation =
| bookmark =
| version = 7.1
}}


The '''Network of Cancer Genes''' (NCG) is a freely accessible web resource of genes that, when altered in their sequence, drive clonal expansion of normal tissues (healthy drivers) or cancer (cancer drivers). The project was launched in 2010 and has reached its 7th release in 2022. In 2023 the additional annotation of cancer drivers that interact with the tumour immune microenvironment (TIME drivers) was added. NCG7.1 reports information on 3,347 cancer drivers and 95 healthy drivers <ref>{{Cite journal |last=Dressler |first=Lisa |last2=Bortolomeazzi |first2=Michele |last3=Keddar |first3=Mohamed Reda |last4=Misetic |first4=Hrvoje |last5=Sartini |first5=Giulia |last6=Acha-Sagredo |first6=Amelia |last7=Montorsi |first7=Lucia |last8=Wijewardhane |first8=Neshika |last9=Repana |first9=Dimitra |last10=Nulsen |first10=Joel |last11=Goldman |first11=Jacki |last12=Pollitt |first12=Marc |last13=Davis |first13=Patrick |last14=Strange |first14=Amy |last15=Ambrose |first15=Karen |date=2022 |title=Comparative assessment of genes driving cancer and somatic evolution in non-cancer tissues: an update of the Network of Cancer Genes (NCG) resource |url=https://genomebiology.biomedcentral.com/articles/10.1186/s13059-022-02607-z |journal=Genome Biology |language=en |volume=23 |issue=1 |doi=10.1186/s13059-022-02607-z |issn=1474-760X |pmc=PMC8790917 |pmid=35078504}}</ref>. Of these, 596 are also TIME drivers <ref name=":1">{{Cite journal |last=Misetic |first=Hrvoje |last2=Keddar |first2=Mohamed Reda |last3=Jeannon |first3=Jean-Pierre |last4=Ciccarelli |first4=Francesca D. |date=2023 |title=Mechanistic insights into the interactions between cancer drivers and the tumour immune microenvironment |url=http://biorxiv.org/lookup/doi/10.1101/2023.01.24.525325 |journal=Biorxiv |language=en |doi=10.1101/2023.01.24.525325}}</ref>. NCG7.1 also reports the system-level properties and the associated publications of each driver, as well as a list possible false positives. NCG7.1 enables advanced searches on the primary anatomical site, cancer type, type of sequencing screens and literature supports.
== Cancer sequencing screens ==

The 273 manually annotated publications in NCG6.0 describe a total 278 [[Whole genome sequencing|whole genome]] or [[Exome sequencing|whole exome]] cancer sequencing screens. These screenings included a total of 34,905 patients from 119 different [[List of cancer types|cancer types]]. These include cancer sequencing screens of samples from 31 different anatomical sites, as well as 4 adult and 2 paediatric pan-cancer sequencing screens. NCG6.0 allows to perform advanced searches and retrieve information on cancer genes by: primary anatomical site, cancer type, and by sequencing screens or publication.
== Cancer drivers ==
{| class="wikitable sortable mw-collapsible"
A main feature of cancer cells is to acquire an unstable genome leading to genetic alterations that are major drivers of cancer evolution. NCG7.1 collects 591 well-known (canonical) and 2,756 candidate cancer drivers. These lists derive from the manual curation of 313 original publications, including 3 sources of canonical drivers <ref>{{Cite journal |last=Vogelstein |first=B. |last2=Papadopoulos |first2=N. |last3=Velculescu |first3=V. E. |last4=Zhou |first4=S. |last5=Diaz |first5=L. A. |last6=Kinzler |first6=K. W. |date=2013 |title=Cancer Genome Landscapes |url=https://www.sciencemag.org/lookup/doi/10.1126/science.1235122 |journal=Science |language=en |volume=339 |issue=6127 |pages=1546–1558 |doi=10.1126/science.1235122 |issn=0036-8075}}</ref><ref>{{Cite journal |last=Saito |first=Yuki |last2=Koya |first2=Junji |last3=Araki |first3=Mitsugu |last4=Kogure |first4=Yasunori |last5=Shingaki |first5=Sumito |last6=Tabata |first6=Mariko |last7=McClure |first7=Marni B. |last8=Yoshifuji |first8=Kota |last9=Matsumoto |first9=Shigeyuki |last10=Isaka |first10=Yuta |last11=Tanaka |first11=Hiroko |last12=Kanai |first12=Takanori |last13=Miyano |first13=Satoru |last14=Shiraishi |first14=Yuichi |last15=Okuno |first15=Yasushi |date=2020 |title=Landscape and function of multiple mutations within individual oncogenes |url=http://www.nature.com/articles/s41586-020-2175-2 |journal=Nature |language=en |volume=582 |issue=7810 |pages=95–99 |doi=10.1038/s41586-020-2175-2 |issn=0028-0836}}</ref><ref>{{Cite journal |last=Sondka |first=Zbyslaw |last2=Bamford |first2=Sally |last3=Cole |first3=Charlotte G. |last4=Ward |first4=Sari A. |last5=Dunham |first5=Ian |last6=Forbes |first6=Simon A. |date=2018 |title=The COSMIC Cancer Gene Census: describing genetic dysfunction across all human cancers |url=http://www.nature.com/articles/s41568-018-0060-1 |journal=Nature Reviews Cancer |language=en |volume=18 |issue=11 |pages=696–705 |doi=10.1038/s41568-018-0060-1 |issn=1474-175X}}</ref> and 310 cancer sequencing screens. The latter describe [[Whole genome sequencing|whole genome]] or [[Exome sequencing|whole exome]] sequencing of cancer samples from a total of 41,780 patients from 122 different [[List of cancer types|cancer types]].
|+

Tumour primary sites and corresponding cancer types in NCG
== Healthy drivers ==
!Primary site
Recent technological advances have enabled detection of genomic instability also in healthy (non cancer) cells driving in situ formation of phenotypically normal clones <ref>{{Cite journal |last=Wijewardhane |first=Neshika |last2=Dressler |first2=Lisa |last3=Ciccarelli |first3=Francesca D. |date=2021 |title=Normal Somatic Mutations in Cancer Transformation |url=https://linkinghub.elsevier.com/retrieve/pii/S1535610820305948 |journal=Cancer Cell |language=en |volume=39 |issue=2 |pages=125–129 |doi=10.1016/j.ccell.2020.11.002}}</ref><ref>{{Cite journal |last=Kakiuchi |first=Nobuyuki |last2=Ogawa |first2=Seishi |date=2021 |title=Clonal expansion in non-cancer tissues |url=http://www.nature.com/articles/s41568-021-00335-3 |journal=Nature Reviews Cancer |language=en |volume=21 |issue=4 |pages=239–256 |doi=10.1038/s41568-021-00335-3 |issn=1474-175X}}</ref>. NCG7.1 collects 95 healthy drivers from 18 sequencing screens of healthy or diseased (non-cancer) tissues from 32,895 donors. Only 8 of these genes are not cancer drivers, suggesting a high overlap between genetic drivers of cancer and non-cancer evolution <ref>{{Cite journal |last=Acha-Sagredo |first=A. |last2=Ganguli |first2=P. |last3=Ciccarelli |first3=F.D. |date=2022 |title=Somatic variation in normal tissues: friend or foe of cancer early detection? |url=https://linkinghub.elsevier.com/retrieve/pii/S0923753422041485 |journal=Annals of Oncology |language=en |volume=33 |issue=12 |pages=1239–1249 |doi=10.1016/j.annonc.2022.09.156}}</ref>.
!Cancer types

|-
== TIME drivers ==
|Blood
Cancer evolution occurs in a complex ecosystem formed of cancer and non-cancer cells that compose the tumour microenvironment (TME). An important component of the TME are immune cells, which may hamper or help tumour growth. Cancer cells engage in a dynamic crosstalk with the TIME that often involves cancer drivers. NCG7.1 annotates 596 that may impact on and be impacted by the TIME. Of these, 205 derive from the manual curation of the literature <ref>{{Cite journal |last=Wellenstein |first=Max D. |last2=de Visser |first2=Karin E. |date=2018 |title=Cancer-Cell-Intrinsic Mechanisms Shaping the Tumor Immune Landscape |url=https://linkinghub.elsevier.com/retrieve/pii/S1074761318300803 |journal=Immunity |language=en |volume=48 |issue=3 |pages=399–416 |doi=10.1016/j.immuni.2018.03.004}}</ref><ref>{{Cite journal |last=Martin |first=Timothy D. |last2=Patel |first2=Rupesh S. |last3=Cook |first3=Danielle R. |last4=Choi |first4=Mei Yuk |last5=Patil |first5=Ajinkya |last6=Liang |first6=Anthony C. |last7=Li |first7=Mamie Z. |last8=Haigis |first8=Kevin M. |last9=Elledge |first9=Stephen J. |date=2021-09-17 |title=The adaptive immune system is a major driver of selection for tumor suppressor gene inactivation |url=http://dx.doi.org/10.1126/science.abg5784 |journal=Science |volume=373 |issue=6561 |pages=1327–1335 |doi=10.1126/science.abg5784 |issn=0036-8075}}</ref><ref>{{Cite journal |last=Mantovani |first=Alberto |last2=Allavena |first2=Paola |last3=Sica |first3=Antonio |last4=Balkwill |first4=Frances |date=2008-07-24 |title=Cancer-related inflammation |url=https://www.nature.com/articles/nature07205 |journal=Nature |language=en |volume=454 |issue=7203 |pages=436–444 |doi=10.1038/nature07205 |issn=0028-0836}}</ref><ref>{{Cite journal |last=Lawson |first=Keith A. |last2=Sousa |first2=Cristovão M. |last3=Zhang |first3=Xiaoyu |last4=Kim |first4=Eiru |last5=Akthar |first5=Rummy |last6=Caumanns |first6=Joseph J. |last7=Yao |first7=Yuxi |last8=Mikolajewicz |first8=Nicholas |last9=Ross |first9=Catherine |last10=Brown |first10=Kevin R. |last11=Zid |first11=Abdelrahman Abou |last12=Fan |first12=Zi Peng |last13=Hui |first13=Shirley |last14=Krall |first14=Jordan A. |last15=Simons |first15=Donald M. |date=2020-10-01 |title=Functional genomic landscape of cancer-intrinsic evasion of killing by T cells |url=https://www.nature.com/articles/s41586-020-2746-2 |journal=Nature |language=en |volume=586 |issue=7827 |pages=120–126 |doi=10.1038/s41586-020-2746-2 |issn=0028-0836 |pmc=PMC9014559 |pmid=32968282}}</ref><ref>{{Cite journal |last=Dhainaut |first=Maxime |last2=Rose |first2=Samuel A. |last3=Akturk |first3=Guray |last4=Wroblewska |first4=Aleksandra |last5=Nielsen |first5=Sebastian R. |last6=Park |first6=Eun Sook |last7=Buckup |first7=Mark |last8=Roudko |first8=Vladimir |last9=Pia |first9=Luisanna |last10=Sweeney |first10=Robert |last11=Le Berichel |first11=Jessica |last12=Wilk |first12=C. Matthias |last13=Bektesevic |first13=Anela |last14=Lee |first14=Brian H. |last15=Bhardwaj |first15=Nina |date=2022 |title=Spatial CRISPR genomics identifies regulators of the tumor microenvironment |url=https://doi.org/10.1016/j.cell.2022.02.015 |journal=Cell |volume=185 |issue=7 |pages=1223–1239.e20 |doi=10.1016/j.cell.2022.02.015 |issn=0092-8674 |pmc=PMC8992964 |pmid=35290801}}</ref>and 391 are instead computationally predicted <ref name=":1" />.
|Diffuse large B-cell lymphoma, acute lymphocytic leukemia, chronic myeloid leukemia, [[multiple myeloma]], [[chronic lymphocytic leukemia]], cutaneous T cell lymphoma, T-cell leukemia/lymphoma, [[non-Hodgkin lymphoma]], peripheral T-cell lymphoma, [[Burkitt's lymphoma]], angioimmunoblastic T-cell lymphoma, [[acute myeloid leukemia]], cutaneous DLBCL, acute monocytic leukemia, follicular lymphoma, chronic myelomonocytic leukemia, acute lymphoblastic leukemia, myeloproliferative neoplasm, acute promyelocytic leukemia, juvenile myelomonocytic leukemia, myelodysplasia, natural killer/T cell lymphoma, splenic marginal zone lymphoma, mediastinal B-cell lymphoma
|-
|Bladder
|[[Bladder cancer]]
|-
|Breast
|[[Breast cancer]], triple negative breast cancer, breast fibroepithelial tumours, male breast cancer, [[breast fibroadenoma]]
|-
|Brain
|Diffuse intrinsic pontine glioma, [[astrocytoma]], paediatric high-grade glioma, [[glioblastoma]], pan-glioma, [[meningioma]], [[neuroblastoma]], low grade glioma, paediatric low grade glioma, glioma, [[craniopharyngioma]], intracranial germ cell, [[medulloblastoma]], [[oligodendroglioma]]
|-
|Pancreas
|[[Pancreatic cancer]] (all histologies), pancreatic ductal adenocarcinoma, pancreatic neuroendocrine tumours, pancreatic neoplastic cysts
|-
|Colon and Rectum
|[[colorectal adenocarcinoma]]
|-
|Small Intestine
|[[Ampullary adenocarcinoma]], duodenal adenocarcinoma, [[neuroendocrine tumour]]
|-
|Hepatobiliary
|Pan-liver, hepatocellular carcinoma, [[cholangiocarcinoma]], biliary tract cancer, [[gallbladder carcinoma]]
|-
|Stomach
|[[Gastric adenocarcinoma]], diffuse gastric adenocarcinoma, mucinous gastric cancer
|-
|Lung
|Small cell lung cancer, [[lung cancer]] (all histologies), lung adenocarcinoma, lung squamous cell carcinoma, non-small cell lung cancer
|-
|Head and Neck
|Squamous head and neck cancer, nasopharyngeal carcinoma, ameloblastoma, oral squamous cell carcinoma, salivary gland adenocarcinoma
|-
|Prostate
|[[Prostate cancer]]
|-
|Soft tissue
|[[Angiosarcoma]], soft tissue sarcoma, [rhabdomyosarcoma]]
|-
|Uterus
|[[Endometrial cancer]], [[uterine carcinosarcoma]], serous endometrial cancer, leiomyoma, clear cell endometrial cancer
|-
|Peripheral Nervous System
|[[Neuroblastoma]], malignant peripheral nerve sheath tumour
|-
|Thymus
|[[Thymic carcinoma]]
|-
|Skin
|[[Melanoma]], mucosal melanoma, desmoplastic melanoma, skin basal cell carcinoma
|-
|Kidney
|[[Clear cell renal cancer]], renal cancer (all histologies), non-clear cell renal cancer, papillary renal cell carcinoma, rhabdoid tumour, chromophobe renal cell carcinoma, renal angiomyolipoma
|-
|Adrenal gland
|[[Adrenocortical adenoma]], adrenocortical carcinoma, pheochromocytoma, paraganglioma
|-
|Esophagus
|[[Esophageal squamous carcinoma]], [[esophageal adenocarcinoma]], esophageal (squamous and adenocarcinoma)
|-
|Bone
|[[Osteosarcoma]], [[Ewing sarcoma]], chondrosarcoma, chondromyxoid fibroma, chondroblastoma, bone giant cell tumour
|-
|Parathyroid gland
|[[Parathyroid carcinoma]]
|-
|Ovary
|[[Ovarian cancer]], [[ovarian serous carcinoma]], ovarian clear-cell carcinoma, ovarian small-cell carcinoma
|-
|Penis
|[[Penile squamous cancer]]
|-
|Thyroid
|[[Papillary thyroid cancer]], anaplastic thyroid carcinoma
|-
|Cervix
|[[Cervical cancer]] (all histologies)
|-
|Testis
|[[Testicular germ cell cancer]]
|-
|Retina
|[[Retinoblastoma]]
|-
|Pleura
|[[Malignant pleural mesothelioma]]
|-
|Uvea
|Melanoma
|-
|Vascular system
|[[Vascular cancer]]
|}


== Systems level properties ==
== Systems level properties ==


Systems-level properties are properties of genes independent on an individual's gene function.<ref>{{Cite journal|last=Ciccarelli|first=Francesca D.|date=2010-06-11|title=The (r)evolution of cancer genetics|journal=BMC Biology|volume=8|issue=1|pages=74|doi=10.1186/1741-7007-8-74|issn=1741-7007|pmc=2883958|pmid=20594288}}</ref> Some of these properties can be used to distinguish cancer genes from the rest of human genes.<ref name=":0" /><ref>{{Cite journal|last1=D'Antonio|first1=Matteo|last2=Ciccarelli|first2=Francesca D.|date=2013-05-29|title=Integrated analysis of recurrent properties of cancer genes to identify novel drivers|journal=Genome Biology|volume=14|issue=5|pages=R52|doi=10.1186/gb-2013-14-5-r52|issn=1474-760X|pmc=4054099|pmid=23718799}}</ref> The systems-level properties reported by NCG are:
Systems-level properties are properties of genes independent on an individual's gene function<ref>{{Cite journal|last=Ciccarelli|first=Francesca D.|date=2010-06-11|title=The (r)evolution of cancer genetics|journal=BMC Biology|volume=8|issue=1|pages=74|doi=10.1186/1741-7007-8-74|issn=1741-7007|pmc=2883958|pmid=20594288}}</ref> Some of these properties can be used to distinguish cancer and healthy drivers from the rest of human genes<ref name=":0">{{Cite journal |last1=Repana |first1=Dimitra |last2=Nulsen |first2=Joel |last3=Dressler |first3=Lisa |last4=Bortolomeazzi |first4=Michele |last5=Venkata |first5=Santhilata Kuppili |last6=Tourma |first6=Aikaterini |last7=Yakoleva |first7=Anna |last8=Palmieri |first8=Tommaso |last9=Ciccarelli |first9=Francesca D. |date=2018-12-01 |title=The Network of Cancer Genes (NCG): a comprehensive catalogue of known and candidate cancer genes from cancer sequencing screens. |url=https://www.biorxiv.org/content/early/2018/12/01/389858 |journal=bioRxiv |language=en |pages=389858 |doi=10.1101/389858 |doi-access=free}}</ref><ref>{{Cite journal|last1=D'Antonio|first1=Matteo|last2=Ciccarelli|first2=Francesca D.|date=2013-05-29|title=Integrated analysis of recurrent properties of cancer genes to identify novel drivers|journal=Genome Biology|volume=14|issue=5|pages=R52|doi=10.1186/gb-2013-14-5-r52|issn=1474-760X|pmc=4054099|pmid=23718799}}</ref>. The systems-level properties reported in NCG are:


* '''Duplicability''': i.e. the presence of additional genomic sequences matching at least 60% of the gene sequence.<ref>{{Cite journal|last1=Rambaldi|first1=Davide|last2=Giorgi|first2=Federico M.|last3=Capuani|first3=Fabrizio|last4=Ciliberto|first4=Andrea|last5=Ciccarelli|first5=Francesca D.|date=2008|title=Low duplicability and network fragility of cancer genes|journal=Trends in Genetics|volume=24|issue=9|pages=427–430|doi=10.1016/j.tig.2008.06.003|pmid=18675489|issn=0168-9525}}</ref>
* '''Duplicability''': i.e. the presence of additional genomic sequences matching at least 60% of the gene sequence.<ref>{{Cite journal|last1=Rambaldi|first1=Davide|last2=Giorgi|first2=Federico M.|last3=Capuani|first3=Fabrizio|last4=Ciliberto|first4=Andrea|last5=Ciccarelli|first5=Francesca D.|date=2008|title=Low duplicability and network fragility of cancer genes|journal=Trends in Genetics|volume=24|issue=9|pages=427–430|doi=10.1016/j.tig.2008.06.003|pmid=18675489|issn=0168-9525}}</ref>
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== Previous versions ==
== Previous versions ==


* NCG6.0<ref>{{Cite journal |last=Repana |first=Dimitra |last2=Nulsen |first2=Joel |last3=Dressler |first3=Lisa |last4=Bortolomeazzi |first4=Michele |last5=Venkata |first5=Santhilata Kuppili |last6=Tourna |first6=Aikaterini |last7=Yakovleva |first7=Anna |last8=Palmieri |first8=Tommaso |last9=Ciccarelli |first9=Francesca D. |date=2019 |title=The Network of Cancer Genes (NCG): a comprehensive catalogue of known and candidate cancer genes from cancer sequencing screens |url=https://genomebiology.biomedcentral.com/articles/10.1186/s13059-018-1612-0 |journal=Genome Biology |language=en |volume=20 |issue=1 |doi=10.1186/s13059-018-1612-0 |issn=1474-760X |pmc=PMC6317252 |pmid=30606230}}</ref>
* NCG5.0<ref>{{Cite journal|last1=An|first1=Omer|last2=Dall'Olio|first2=Giovanni M.|last3=Mourikis|first3=Thanos P.|last4=Ciccarelli|first4=Francesca D.|date=2016-01-04|title=NCG 5.0: updates of a manually curated repository of cancer genes and associated properties from cancer mutational screenings|url= |journal=Nucleic Acids Research|language=en|volume=44|issue=D1|pages=D992–D999|doi=10.1093/nar/gkv1123|pmid=26516186|pmc=4702816|issn=0305-1048}}</ref>
* NCG5.0<ref>{{Cite journal|last1=An|first1=Omer|last2=Dall'Olio|first2=Giovanni M.|last3=Mourikis|first3=Thanos P.|last4=Ciccarelli|first4=Francesca D.|date=2016-01-04|title=NCG 5.0: updates of a manually curated repository of cancer genes and associated properties from cancer mutational screenings|url= |journal=Nucleic Acids Research|language=en|volume=44|issue=D1|pages=D992–D999|doi=10.1093/nar/gkv1123|pmid=26516186|pmc=4702816|issn=0305-1048}}</ref>
* NCG4.0<ref>{{Cite journal|last1=An|first1=Omer|last2=Pendino|first2=Vera|last3=D'Antonio|first3=Matteo|last4=Ratti|first4=Emanuele|last5=Gentilini|first5=Marco|last6=Ciccarelli|first6=Francesca D.|date=2014-01-01|title=NCG 4.0: the network of cancer genes in the era of massive mutational screenings of cancer genomes|journal=Database|language=en|volume=2014|pages=bau015|doi=10.1093/database/bau015|pmc=3948431|pmid=24608173}}</ref>
* NCG4.0<ref>{{Cite journal|last1=An|first1=Omer|last2=Pendino|first2=Vera|last3=D'Antonio|first3=Matteo|last4=Ratti|first4=Emanuele|last5=Gentilini|first5=Marco|last6=Ciccarelli|first6=Francesca D.|date=2014-01-01|title=NCG 4.0: the network of cancer genes in the era of massive mutational screenings of cancer genomes|journal=Database|language=en|volume=2014|pages=bau015|doi=10.1093/database/bau015|pmc=3948431|pmid=24608173}}</ref>
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== External links ==
== External links ==


* NCG6.0: http://ncg.kcl.ac.uk
* NCG7.1: http://www.network-cancer-genes.org/
* NCG6.0: http://ncg.kcl.ac.uk/ncg6/
* NCG5.0: http://ncg.kcl.ac.uk/ncg5/
* NCG5.0: http://ncg.kcl.ac.uk/ncg5/
* NCG4.0: http://ncg.kcl.ac.uk/ncg4/
* NCG4.0: http://ncg.kcl.ac.uk/ncg4/

Revision as of 09:46, 20 May 2023

Network of Cancer Genes
Content
DescriptionA web resource on systems-level properties of cancer genes
OrganismsHomo sapiens
Contact
Research centerThe Francis Crick Institute
LaboratoryCancer Systems Biology Lab - Ciccarelli Lab
Release dateMay 2023
Access
Websitehttp://http://www.network-cancer-genes.org/
Miscellaneous
Version7.1

The Network of Cancer Genes (NCG) is a freely accessible web resource of genes that, when altered in their sequence, drive clonal expansion of normal tissues (healthy drivers) or cancer (cancer drivers). The project was launched in 2010 and has reached its 7th release in 2022. In 2023 the additional annotation of cancer drivers that interact with the tumour immune microenvironment (TIME drivers) was added. NCG7.1 reports information on 3,347 cancer drivers and 95 healthy drivers [1]. Of these, 596 are also TIME drivers [2]. NCG7.1 also reports the system-level properties and the associated publications of each driver, as well as a list possible false positives. NCG7.1 enables advanced searches on the primary anatomical site, cancer type, type of sequencing screens and literature supports.

Cancer drivers

A main feature of cancer cells is to acquire an unstable genome leading to genetic alterations that are major drivers of cancer evolution. NCG7.1 collects 591 well-known (canonical) and 2,756 candidate cancer drivers. These lists derive from the manual curation of 313 original publications, including 3 sources of canonical drivers [3][4][5] and 310 cancer sequencing screens. The latter describe whole genome or whole exome sequencing of cancer samples from a total of 41,780 patients from 122 different cancer types.

Healthy drivers

Recent technological advances have enabled detection of genomic instability also in healthy (non cancer) cells driving in situ formation of phenotypically normal clones [6][7]. NCG7.1 collects 95 healthy drivers from 18 sequencing screens of healthy or diseased (non-cancer) tissues from 32,895 donors. Only 8 of these genes are not cancer drivers, suggesting a high overlap between genetic drivers of cancer and non-cancer evolution [8].

TIME drivers

Cancer evolution occurs in a complex ecosystem formed of cancer and non-cancer cells that compose the tumour microenvironment (TME). An important component of the TME are immune cells, which may hamper or help tumour growth. Cancer cells engage in a dynamic crosstalk with the TIME that often involves cancer drivers. NCG7.1 annotates 596 that may impact on and be impacted by the TIME. Of these, 205 derive from the manual curation of the literature [9][10][11][12][13]and 391 are instead computationally predicted [2].

Systems level properties

Systems-level properties are properties of genes independent on an individual's gene function[14] Some of these properties can be used to distinguish cancer and healthy drivers from the rest of human genes[15][16]. The systems-level properties reported in NCG are:

Previous versions

References

  1. ^ Dressler, Lisa; Bortolomeazzi, Michele; Keddar, Mohamed Reda; Misetic, Hrvoje; Sartini, Giulia; Acha-Sagredo, Amelia; Montorsi, Lucia; Wijewardhane, Neshika; Repana, Dimitra; Nulsen, Joel; Goldman, Jacki; Pollitt, Marc; Davis, Patrick; Strange, Amy; Ambrose, Karen (2022). "Comparative assessment of genes driving cancer and somatic evolution in non-cancer tissues: an update of the Network of Cancer Genes (NCG) resource". Genome Biology. 23 (1). doi:10.1186/s13059-022-02607-z. ISSN 1474-760X. PMC 8790917. PMID 35078504.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  2. ^ a b Misetic, Hrvoje; Keddar, Mohamed Reda; Jeannon, Jean-Pierre; Ciccarelli, Francesca D. (2023). "Mechanistic insights into the interactions between cancer drivers and the tumour immune microenvironment". Biorxiv. doi:10.1101/2023.01.24.525325.
  3. ^ Vogelstein, B.; Papadopoulos, N.; Velculescu, V. E.; Zhou, S.; Diaz, L. A.; Kinzler, K. W. (2013). "Cancer Genome Landscapes". Science. 339 (6127): 1546–1558. doi:10.1126/science.1235122. ISSN 0036-8075.
  4. ^ Saito, Yuki; Koya, Junji; Araki, Mitsugu; Kogure, Yasunori; Shingaki, Sumito; Tabata, Mariko; McClure, Marni B.; Yoshifuji, Kota; Matsumoto, Shigeyuki; Isaka, Yuta; Tanaka, Hiroko; Kanai, Takanori; Miyano, Satoru; Shiraishi, Yuichi; Okuno, Yasushi (2020). "Landscape and function of multiple mutations within individual oncogenes". Nature. 582 (7810): 95–99. doi:10.1038/s41586-020-2175-2. ISSN 0028-0836.
  5. ^ Sondka, Zbyslaw; Bamford, Sally; Cole, Charlotte G.; Ward, Sari A.; Dunham, Ian; Forbes, Simon A. (2018). "The COSMIC Cancer Gene Census: describing genetic dysfunction across all human cancers". Nature Reviews Cancer. 18 (11): 696–705. doi:10.1038/s41568-018-0060-1. ISSN 1474-175X.
  6. ^ Wijewardhane, Neshika; Dressler, Lisa; Ciccarelli, Francesca D. (2021). "Normal Somatic Mutations in Cancer Transformation". Cancer Cell. 39 (2): 125–129. doi:10.1016/j.ccell.2020.11.002.
  7. ^ Kakiuchi, Nobuyuki; Ogawa, Seishi (2021). "Clonal expansion in non-cancer tissues". Nature Reviews Cancer. 21 (4): 239–256. doi:10.1038/s41568-021-00335-3. ISSN 1474-175X.
  8. ^ Acha-Sagredo, A.; Ganguli, P.; Ciccarelli, F.D. (2022). "Somatic variation in normal tissues: friend or foe of cancer early detection?". Annals of Oncology. 33 (12): 1239–1249. doi:10.1016/j.annonc.2022.09.156.
  9. ^ Wellenstein, Max D.; de Visser, Karin E. (2018). "Cancer-Cell-Intrinsic Mechanisms Shaping the Tumor Immune Landscape". Immunity. 48 (3): 399–416. doi:10.1016/j.immuni.2018.03.004.
  10. ^ Martin, Timothy D.; Patel, Rupesh S.; Cook, Danielle R.; Choi, Mei Yuk; Patil, Ajinkya; Liang, Anthony C.; Li, Mamie Z.; Haigis, Kevin M.; Elledge, Stephen J. (2021-09-17). "The adaptive immune system is a major driver of selection for tumor suppressor gene inactivation". Science. 373 (6561): 1327–1335. doi:10.1126/science.abg5784. ISSN 0036-8075.
  11. ^ Mantovani, Alberto; Allavena, Paola; Sica, Antonio; Balkwill, Frances (2008-07-24). "Cancer-related inflammation". Nature. 454 (7203): 436–444. doi:10.1038/nature07205. ISSN 0028-0836.
  12. ^ Lawson, Keith A.; Sousa, Cristovão M.; Zhang, Xiaoyu; Kim, Eiru; Akthar, Rummy; Caumanns, Joseph J.; Yao, Yuxi; Mikolajewicz, Nicholas; Ross, Catherine; Brown, Kevin R.; Zid, Abdelrahman Abou; Fan, Zi Peng; Hui, Shirley; Krall, Jordan A.; Simons, Donald M. (2020-10-01). "Functional genomic landscape of cancer-intrinsic evasion of killing by T cells". Nature. 586 (7827): 120–126. doi:10.1038/s41586-020-2746-2. ISSN 0028-0836. PMC 9014559. PMID 32968282.{{cite journal}}: CS1 maint: PMC format (link)
  13. ^ Dhainaut, Maxime; Rose, Samuel A.; Akturk, Guray; Wroblewska, Aleksandra; Nielsen, Sebastian R.; Park, Eun Sook; Buckup, Mark; Roudko, Vladimir; Pia, Luisanna; Sweeney, Robert; Le Berichel, Jessica; Wilk, C. Matthias; Bektesevic, Anela; Lee, Brian H.; Bhardwaj, Nina (2022). "Spatial CRISPR genomics identifies regulators of the tumor microenvironment". Cell. 185 (7): 1223–1239.e20. doi:10.1016/j.cell.2022.02.015. ISSN 0092-8674. PMC 8992964. PMID 35290801.{{cite journal}}: CS1 maint: PMC format (link)
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  15. ^ Repana, Dimitra; Nulsen, Joel; Dressler, Lisa; Bortolomeazzi, Michele; Venkata, Santhilata Kuppili; Tourma, Aikaterini; Yakoleva, Anna; Palmieri, Tommaso; Ciccarelli, Francesca D. (2018-12-01). "The Network of Cancer Genes (NCG): a comprehensive catalogue of known and candidate cancer genes from cancer sequencing screens". bioRxiv: 389858. doi:10.1101/389858.
  16. ^ D'Antonio, Matteo; Ciccarelli, Francesca D. (2013-05-29). "Integrated analysis of recurrent properties of cancer genes to identify novel drivers". Genome Biology. 14 (5): R52. doi:10.1186/gb-2013-14-5-r52. ISSN 1474-760X. PMC 4054099. PMID 23718799.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  17. ^ Rambaldi, Davide; Giorgi, Federico M.; Capuani, Fabrizio; Ciliberto, Andrea; Ciccarelli, Francesca D. (2008). "Low duplicability and network fragility of cancer genes". Trends in Genetics. 24 (9): 427–430. doi:10.1016/j.tig.2008.06.003. ISSN 0168-9525. PMID 18675489.
  18. ^ Repana, Dimitra; Nulsen, Joel; Dressler, Lisa; Bortolomeazzi, Michele; Venkata, Santhilata Kuppili; Tourna, Aikaterini; Yakovleva, Anna; Palmieri, Tommaso; Ciccarelli, Francesca D. (2019). "The Network of Cancer Genes (NCG): a comprehensive catalogue of known and candidate cancer genes from cancer sequencing screens". Genome Biology. 20 (1). doi:10.1186/s13059-018-1612-0. ISSN 1474-760X. PMC 6317252. PMID 30606230.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  19. ^ An, Omer; Dall'Olio, Giovanni M.; Mourikis, Thanos P.; Ciccarelli, Francesca D. (2016-01-04). "NCG 5.0: updates of a manually curated repository of cancer genes and associated properties from cancer mutational screenings". Nucleic Acids Research. 44 (D1): D992–D999. doi:10.1093/nar/gkv1123. ISSN 0305-1048. PMC 4702816. PMID 26516186.
  20. ^ An, Omer; Pendino, Vera; D'Antonio, Matteo; Ratti, Emanuele; Gentilini, Marco; Ciccarelli, Francesca D. (2014-01-01). "NCG 4.0: the network of cancer genes in the era of massive mutational screenings of cancer genomes". Database. 2014: bau015. doi:10.1093/database/bau015. PMC 3948431. PMID 24608173.
  21. ^ D'Antonio, Matteo; Pendino, Vera; Sinha, Shruti; Ciccarelli, Francesca D. (2012). "Network of Cancer Genes (NCG 3.0): integration and analysis of genetic and network properties of cancer genes". Nucleic Acids Res. 40 (Database issue): D978–83. doi:10.1093/nar/gkr952. PMC 3245144. PMID 22080562.
  22. ^ Syed, Adnan S.; D'Antonio, Matteo; Ciccarelli, Francesca D. (2010). "Network of Cancer Genes: a web resource to analyze duplicability, orthology and network properties of cancer genes". Nucleic Acids Res. 38 (Database issue): D670–5. doi:10.1093/nar/gkp957. PMC 2808873. PMID 19906700.

External links

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