HPV-positive oropharyngeal cancer: Difference between revisions

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Radiation dose recommendations are largely based on older clinical trials with few HPV+OPC patients, making it difficult to determine the optimum dose for this group. For lateralized tonsil cancer unilateral neck radiation is usually prescribed, but for tongue base primaries bilateral neck radiation is more common, but unilateral radiation may be used where tongue base lesions are lateralised.{{sfn|Beitler et al|2014}}{{sfn|Nguyen-Tan et al|2014}}
Radiation dose recommendations are largely based on older clinical trials with few HPV+OPC patients, making it difficult to determine the optimum dose for this group. For lateralized tonsil cancer unilateral neck radiation is usually prescribed, but for tongue base primaries bilateral neck radiation is more common, but unilateral radiation may be used where tongue base lesions are lateralised.{{sfn|Beitler et al|2014}}{{sfn|Nguyen-Tan et al|2014}}


It is thought that HPV+ OPC patients benefit better from radiotherapy and concurrent [[cetuximab]] treatment than HPV- OPC patients receiving the same treatment,<ref>{{Cite journal| doi = 10.1016/S1470-2045(10)70035-8| title = Do all patients with head and neck cancer benefit from radiotherapy and concurrent cetuximab?| year = 2010| last1 = Eriksen | first1 = J. G.| last2 = Lassen | first2 = P.| last3 = Overgaard | first3 = J.| journal = The Lancet Oncology| volume = 11| pages = 312–3| pmid = 20359659| issue = 4}}</ref> and that radiation and cisplatin induce an immune response against an [[antigenic]] tumour which enhances their effect on the cancer cells.{{sfn|Spanos et al|2009}}
It is thought that HPV+ OPC patients benefit better from radiotherapy and concurrent [[cetuximab]] treatment than HPV- OPC patients receiving the same treatment,{{sfn|Erikson et al|2010 }} and that radiation and cisplatin induce an immune response against an [[antigenic]] tumour which enhances their effect on the cancer cells.{{sfn|Spanos et al|2009}}


==Prognosis==
==Prognosis==
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* {{Cite journal|last1 = Elmofty| first1 = S.| last2 = Patil|first2 = S.|title = Human papillomavirus (HPV)-related oropharyngeal nonkeratinizing squamous cell carcinoma: Characterization of a distinct phenotype|journal = [[Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology]]| year = 2006|volume = 101|issue = 3|
* {{Cite journal|last1 = Elmofty| first1 = S.| last2 = Patil|first2 = S.|title = Human papillomavirus (HPV)-related oropharyngeal nonkeratinizing squamous cell carcinoma: Characterization of a distinct phenotype|journal = [[Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology]]| year = 2006|volume = 101|issue = 3|
pages = 339–345|pmid = 16504868 | doi = 10.1016/j.tripleo.2005.08.001|ref=harv }}
pages = 339–345|pmid = 16504868 | doi = 10.1016/j.tripleo.2005.08.001|ref=harv }}
* {{Cite journal|last1 = Eriksen | first1 = J. G.| last2 = Lassen | first2 = P.| last3 = Overgaard | first3 = J.|title = Do all patients with head and neck cancer benefit from radiotherapy and concurrent cetuximab?|journal = [[The Lancet Oncology]]|
volume = 11|issue = 4|pages = 312–313| year = 2010|doi = 10.1016/S1470-2045(10)70035-8| pmid = 20359659|ref={{harvid|Erikson et al|2010 }} }}
* {{cite journal|last1=Fakhry|first1=Carole|last2=Gillison|first2=Maura L.|title=Clinical Implications of Human Papillomavirus in Head and Neck Cancers|journal=[[Journal of Clinical Oncology]]|date=10 June 2006|volume=24|issue=17|pages=2606–2611|doi=10.1200/JCO.2006.06.1291|ref=harv}}
* {{cite journal|last1=Fakhry|first1=Carole|last2=Gillison|first2=Maura L.|title=Clinical Implications of Human Papillomavirus in Head and Neck Cancers|journal=[[Journal of Clinical Oncology]]|date=10 June 2006|volume=24|issue=17|pages=2606–2611|doi=10.1200/JCO.2006.06.1291|ref=harv}}
* {{Cite journal| last1 = Fakhry | first1 = C.| last2 = Westra | first2 = W.| last3 = Li | first3 = S.| last4 = Cmelak | first4 = A.| last5 = Ridge | first5 = J.| last6 = Pinto | first6 = H.| last7 = Forastiere | first7 = A.| last8 = Gillison | first8 = M.| title = Improved survival of patients with human papillomavirus-positive head and neck squamous cell carcinoma in a prospective clinical trial| url = http://jnci.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=18270337| journal = [[Journal of the National Cancer Institute]]| volume = 100| issue = 4| pages = 261–269| date=Feb 2008 | issn = 0027-8874| pmid = 18270337 | doi = 10.1093/jnci/djn011|ref={{harvid|Fakhry et al|2008}} }}
* {{Cite journal| last1 = Fakhry | first1 = C.| last2 = Westra | first2 = W.| last3 = Li | first3 = S.| last4 = Cmelak | first4 = A.| last5 = Ridge | first5 = J.| last6 = Pinto | first6 = H.| last7 = Forastiere | first7 = A.| last8 = Gillison | first8 = M.| title = Improved survival of patients with human papillomavirus-positive head and neck squamous cell carcinoma in a prospective clinical trial| url = http://jnci.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=18270337| journal = [[Journal of the National Cancer Institute]]| volume = 100| issue = 4| pages = 261–269| date=Feb 2008 | issn = 0027-8874| pmid = 18270337 | doi = 10.1093/jnci/djn011|ref={{harvid|Fakhry et al|2008}} }}
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* {{cite book|editor-last1=Cardesa|editor-first1=Antonio|editor-last2=Slootweg|editor-first2=Pieter J.|editor-last3=Gale|editor-first3=Nina|editor-last4=Franchi|editor-first4=Alessandro| |title=Pathology of the Head and Neck|url=https://books.google.com/books?id=ag4bDgAAQBAJ|date=2017|publisher=[[Springer Science+Business Media|Springer]]|isbn=978-3-662-49672-5|edition=2nd}}
* {{cite book|editor-last1=Cardesa|editor-first1=Antonio|editor-last2=Slootweg|editor-first2=Pieter J.|editor-last3=Gale|editor-first3=Nina|editor-last4=Franchi|editor-first4=Alessandro| |title=Pathology of the Head and Neck|url=https://books.google.com/books?id=ag4bDgAAQBAJ|date=2017|publisher=[[Springer Science+Business Media|Springer]]|isbn=978-3-662-49672-5|edition=2nd}}
* {{cite book|last=Chaturvedi|first=Anil|last2=Gillison|first2=Maura L.| title=Human Papillomavirus and Head and Neck Cancer|pages=87–116| url=https://books.google.com/books?id=EKIFGVDeDPEC&pg=PA87|isbn=978-1-4419-1471-2|ref={{harvid|Chaturvedi|Gillison|2010}}}}, in {{harvtxt|Olshan|2010}}
* {{cite book|last=Chaturvedi|first=Anil|last2=Gillison|first2=Maura L.| title=Human Papillomavirus and Head and Neck Cancer|pages=87–116| url=https://books.google.com/books?id=EKIFGVDeDPEC&pg=PA87|isbn=978-1-4419-1471-2|ref={{harvid|Chaturvedi|Gillison|2010}}}}, in {{harvtxt|Olshan|2010}}
* {{cite book|last1=Munck-Wikland|first1=Eva|last2=Hammarstedt|first2=Lalle |last3=Dahlstrand|first3=Hanna|editor=M. A. Hayat|title=Methods of Cancer Diagnosis, Therapy, and Prognosis|url=http://www.springerlink.com/content/tq615217r705nh53/|volume=7|year=2010|publisher=Springer|isbn=978-90-481-3185-3|pages=271–283|chapter=Role of Human Papillomavirus in Tonsillar Cancer |ref={{harvid|Munck-Wikland|2010}}}}
* {{cite book|editor-last=Hayat|editor-first=M. A.|title=Methods of Cancer Diagnosis, Therapy, and Prognosis: Volume 7 - General Overviews, Head and Neck Cancer and Thyroid Cancer|url=https://books.google.com/books?id=saE1RuGXbgYC|date= 2010|publisher=Springer Science & Business Media|isbn=978-90-481-3186-0|ref=harv}}
* {{cite book|last1=Munck-Wikland|first1=Eva|last2=Hammarstedt|first2=Lalle |last3=Dahlstrand|first3=Hanna|title=Role of Human Papillomavirus in Tonsillar Cancer|url=https://books.google.com/books?id=saE1RuGXbgYC&pg=PA272|pages=271–283||ref={{harvid|Munck-Wikland|2010}}}}, in {{harvtxt|Hayat|2010}} (''additional extract'' [http://www.springerlink.com/content/tq615217r705nh53/ here])
* {{cite book|editor-last1=Myers|editor-first1=Jeffrey N.|editor-last2=Sturgis|editor-first2=Erich M.|title=Oral Cavity and Oropharyngeal Cancer, An Issue of Otolaryngologic Clinics, E-Book|url=https://books.google.com/books?id=XYRRAAAAQBAJ|date= 2013|publisher=Elsevier Health Sciences|isbn=978-0-323-18632-2|ref=harv}}
* {{cite book|editor-last1=Myers|editor-first1=Jeffrey N.|editor-last2=Sturgis|editor-first2=Erich M.|title=Oral Cavity and Oropharyngeal Cancer, An Issue of Otolaryngologic Clinics, E-Book|url=https://books.google.com/books?id=XYRRAAAAQBAJ|date= 2013|publisher=Elsevier Health Sciences|isbn=978-0-323-18632-2|ref=harv}}
* {{cite book|editor-last=Olshan|editor-first=Andrew F.|title=Epidemiology, Pathogenesis, and Prevention of Head and Neck Cancer|url=https://books.google.com/books?id=EKIFGVDeDPEC|date= 2010|publisher=[[Springer Science & Business Media]]|isbn=978-1-4419-1471-2|ref=harv}}
* {{cite book|editor-last=Olshan|editor-first=Andrew F.|title=Epidemiology, Pathogenesis, and Prevention of Head and Neck Cancer|url=https://books.google.com/books?id=EKIFGVDeDPEC|date= 2010|publisher=[[Springer Science & Business Media]]|isbn=978-1-4419-1471-2|ref=harv}}

Revision as of 13:54, 1 June 2017

HPV-positive oropharyngeal cancer
SpecialtyOncology Edit this on Wikidata

Human papillomavirus (HPV)-positive oropharyngeal cancer (OPC) also known as HPV16+ oropharyngeal cancer or HPV+ OPC is a recognized subtype of oropharyngeal squamous cell carcinomas (OSCC), associated with the HPV type 16 virus.

Causation

Most mucosal head and neck cancers have historically been attributed to tobacco and alcohol use, and similarly with oropharyngeal cancer (OPC). However this has changed considerably since the 1980s. HPV has become a major driver of this disease since, with HPV-negative cancer declining alongside increasing HPV-positive cancer, with an estimated further increase in coming years.[1] Since there are marked differences in clinical presentation and treatment response relative to HPV status, HPV associated OPC (HPV+OPC) is now viewed as a distinct biologic and clinical entity.[2][3]

Human HPV has for long been implicated in the pathogenesis of several anogenital cancers including those of the anus, vilva, vagina, cervix, and penis. In 2007 it was also implicated by molecular and epidemiological evidence in cancers arising outside of the anogenital tract, namely oral cancer. HPV infection is common among healthy individuals, and is acquired largely through sexual contact. Although less data is available, prevalence of HPV infection is at least as common among men as among women, where 2004 estimates were about 27% among US women aged 14–59.[4]

HPV oral infection precedes the development of HPV+OPC.[4][5] Slight injuries in the mucous membrane serve as an entry gate for HPV, which thus works into the basal layer of the epithelium.[6][7] People testing positive for HPV16 oral infection have a 14 times increased risk of developing HPV+ OPC.[6] Immunosuppression seems to be an increased risk factor for HPV+ OPC.[5] Individuals with TGF-β1 genetic variations, specially T869C, are more likely to have HPV16+OPC.[8] TGF-β1 plays an important role in controlling the immune system. A 1993 study has found that patients with human papillomavirus (HPV)-associated anogenital cancers had a 4.3-fold increased risk of tonsillar squamous-cell carcinoma.[9] Although evidence suggests that HPV16 is the main cause of OPC between non-smokers and non-drinkers, the degree to which tobacco and/or alcohol use may contribute to increase the risk of HPV+ OPC is unclear.[5] Concomitant human herpesvirus-8 infection can potentiate the effects of HPV-16.[10]

Mechanism

A prospective study has found that increased HPV+ OPC risk was observed more than 15 years after HPV exposure,[4] pointing to a slow development of the disease, like in cervical cancer. HPV associated cancers are caused by the expression of HPV's E6 and E7 proteins that bind to and inactivate tumor suppressor proteins p53 and retinoblastoma protein (pRB), respectively, leading to malignant transformation of HPV infected cells.[4][11] The biology of HPV+ OPC is distinct of HPV- OPC with P53 degradation (inactivated by E6 instead of by genetic mutation), pRB pathway inactivation (by E7 instead of Cyclin D1 amplification), and P16 upregulation (over-expression of p16 instead of inactivation due to reduced negative feedback from pRB).[12][13] The tonsils epithelia (palatine and lingual) share similar nonkeratinization characteristics with the cervix, where HPV infection play the major role in cases of cervical cancer.[6][14]

Diagnosis

HPV+OPC is usually diagnosed at a more advanced stage than HPV-OPC.[4] Genetic signatures of HPV+ and HPV- OPC are different.[15][16][17][18][19] HPV+OPC is associated with expression level of the E6/E7 mRNAs and of p16.[20] Nonkeratinizing squamous cell carcinoma strongly predicts HPV-association.[21][22] HPV16 E6/E7-positive cases are histopathologically characterized by their verrucous or papillary structure and koilocytosis of the adjacent mucosa. Approximately 15% of HNSCCs are caused by HPV16 infection and the subsequent constitutive expression of E6 and E7, and some HPV-initiated tumors may lose their original characteristics during tumor progression. [23] High-risk HPV types may be associated with oral carcinoma, by cell-cycle control dysregulation, contributing to oral carcinogenesis and the overexpression of mdm2, p27 and cathepsin B. [24]

HPV+OPC is not merely characterized by the presence of HPV-16. Only the expression of viral oncogenes within the tumor cells plus the serum presence of E6 or E7 antibodies is unambiguously conclusive.[6] There is not a standard HPV testing method in head and neck cancers,[25] both in situ hybridization and PCR are commonly used.[12] [26] A 2010 study has concluded that both have comparable performance for HPV detection, however it is important to use appropriate sensitivity controls.[27] P16 staining is frequently used as a cost effective surrogate for HPV in OPC compared to in situ hybridization or PCR.[28][29]

Staging

Staging is generally by the TNM system.[29] HPV+OPC has been treated similarly to stage-matched and site-matched unrelated OPC, but its unique features, which contrast smoking-related HPV-OPC head and neck cancers, for which patients' demographics, comorbidities, risk factors, and carcinogenesis differ markedly, suggest that a distinct staging system be developed to more appropriately represent the severity of the disease and its prognosis.[30] Standard TNM staging while predictive for HPV-OPC has no prognostic value in HPV+OPC[28][30] The 8th edition of the AJCC TNM Staging Manual (2016) incorporates this specific staging for HPV+OPC.[31] Current treatment guidelines do not account for the different outcomes observed in HPV+OPC. Consequently less intensive (de-intensification) use of radiotherapy or chemotherapy, as well as specific therapy, is under investigation, enrolling HPV+OPC in clinical trials to preserve disease control and minimise morbidity in selected groups based on modified TNM staging and smoking status.[32][33][34][35][36]

Tumours of the oropharynx are staged as (AJCC 8th ed. 2016):[31]

  • T0 no primary identified
  • T1 2 cm or less in greatest dimension
  • T2 2–4 cm
  • T3 >4 cm, or extension to lingual surface of epiglottis
  • T4 moderately advanced local disease, invading larynx, extrinsic muscle of tongue, medial pterygoid, hard palate, or mandible or beyond


  • Nx regional lymph nodes cannot be assessed
  • N0 no regional lymph nodes involved
  • N1 1 or more ipsilateral nodes involved, less than 6 cm
  • N2 contralateral or bilateral lymph nodes, less than 6 cm
  • N3 lymph node(s) larger than 6 cm


  • Stage I: T0N1, T1–2N0–1
  • Stage II: T0–2N2, T3N–2
  • Stage III: T0–3N3, T4N0-3
  • Stage IV: any metastases

Treatment

There is no high quality Level I evidence from prospective clinical trials in HPV+OPC, therefore treatment guidelines must rely on data from treatment of OPC and from some subsetting of those studies.[29] Treatment for OPC has traditionally relied on radiotherapy, chemotherapy and/or other systemic treatments, and surgical resection. Depending on stage and other factors treatment may include a combination of modalities.[37] The mainstay has been radiotherapy in most cases.[28] a pooled analysis of published studies suggested comparable disease control between radiation and surgery, but higher complication rates for surgery +/- radiation.[37][38]

Radiotherapy

Intensity modulated radiation therapy (IMRT) can provide good control of primary tumours while preserving excellent control rates, with reduced toxicity to salivary and pharyngeal structures. IMRT has a two year disease free survival between 82 and 90 %, and a two year disease specific survival up to 97 % for stage I and II.[39][40]

Reported toxicities include dry mouth (xerostomia) 18 % (grade 2); difficulty swallowing (dysphagia) 15 % (grade 2); subclinical aspiration up to 50  % (reported incidence of aspiration pneumonia approximately 14  %); hypothyroidism 28–38 % at three years {may be up to 55 % depending on amount of the thyroid gland exposed to over 45 Gy radiation; esophageal stenosis 5 %; osteonecrosis of the mandible 2.5 %; and need for a gastrostomy tube to be placed at some point during or up to one year after treatment 4 % (up to 16 % with longer follow up).[40][41][42]

Radiation dose recommendations are largely based on older clinical trials with few HPV+OPC patients, making it difficult to determine the optimum dose for this group. For lateralized tonsil cancer unilateral neck radiation is usually prescribed, but for tongue base primaries bilateral neck radiation is more common, but unilateral radiation may be used where tongue base lesions are lateralised.[43][44]

It is thought that HPV+ OPC patients benefit better from radiotherapy and concurrent cetuximab treatment than HPV- OPC patients receiving the same treatment,[45] and that radiation and cisplatin induce an immune response against an antigenic tumour which enhances their effect on the cancer cells.[46]

Prognosis

The presence of HPV within the tumour has been realised to be an important factor for predicting survival since the 1990s.[47] Tumor HPV status is strongly associated with positive therapeutic response and survival compared with HPV-negative cancer, independent of the treatment modality chosen. Response rates of over 80% are reported in HPV+ cancer and three-year progression free survival has been reported as 75–82 % and 45–57 %, respectively, for HPV+ and HPV- cancer, and improving over increasing time.[3][48][49][50]

In RTOG clinical trial 0129, in which all patients with advance disease received radiation and chemotherapy, a retrospective analysis at thee years, three risk groups for survival were identified (low, intermediate, and high) based on HPV status, smoking, and stage. 64% were HPV+ and all were in the low and intermediate risk group, with all non-smoking HPV+ patients in the low risk group. 82% of the HPV+ patients were alive at three years compared to 57% of the HPV- patients, a 58% reduction in the risk of death.[51] Locoregional failure is also lower in HPV+, being 14% compared to 35% for HPV-.[52] HPV positivity confers a 50–60 % lower risk of disease progression and death, but the use of tobacco is an independently negative prognostic factor.[51] The majority of recurrences occur within the first year after treatment and are locoregional,[53] but HPV does not reduce the rate of metastases, which are predominantly to the lungs.[53] Even if recurrence or metastases occur, HPV positivity still confers an advantage.[3]

A possible explanation is "the lower probability of occurrence of 11q13 gene amplification, which is considered to be a factor underlying faster and more frequent recurrence of the disease"[6] Presence of TP53 mutations, a marker for HPV- OPC, is associated with worse prognosis.[4] High grade of p16 staining is thought to be better than HPV PCR analysis in predicting radiotherapy response.[26]

Epidemiology

The global incidence of pharyngeal cancer in 2013 was estimated at 136,000 cases.[3][54] In the United States the estimated number of cases was 13,930 in 2013[55] and 17,000 for 2017.[56] Of these cases, HPV-positive cancer (HPV+) has been increasing compared to HPV-negative cancer (HPV-).

HPV+ OPC patients tend to be younger than HPV- patients.[57]The clinical presentation is also changing from the “typical” head and neck cancer patient with advanced age and major substance usage.[3] By contrast patients with HPV+ cancer are younger (4th–6th decades), male (ratio 8:1) with no or only a minimum history of smoking, generally caucasian, reached higher education levels, are married, and have higher income.[58] The presenting features are also different between HPV+ and HPV- OPC. HPV+ tumours have smaller primary lesions (less than 4 cm) but more advanced nodal disease resulting in higher TNM staging. This in turn may overestimate the severity.[59][60]

Trends

A survey of 23 countries between 1983 and 2002 showed an increase in oropharyngeal squamous cell carcinoma that was particularly noticeable in young men in economically developed countries.[3] Currently in the US there is a growing incidence of HPV associated oropharyngeal cancers,[61]In the early 1980s HPV+ accounted for only 7.5% of cases in the US but by 2016 this was 70%.[3][62][63][64] perhaps as a result of changing sexual behaviors, decreased popularity of tonsillectomies, improved radiologic and pathologic evaluation, and changes in classification.[65][66][67] Tonsil and oropharyngeal cancers increased in male predominance between 1975 and 2004, despite reductions in smoking.[68] The decline in smoking may be linked to the decreasing proportion of HPV negative cancers, while changes in sexual activity may be reflected in increasing proportion of HPV positive cancers.[69] Recently, in the US, HPV associated OPC represent about 60% of OPC cases[52][70][71] compared with 40% in the previous decade.[71] By 2007, in the US, incidence of general OPC, including non-HPV associated, is 3.2 cases per 100,000 males/year and 1.9 per 100,000 all-sexes/year.[72]

The higher increase incidence of HPV associated OPC is also seen in other countries, like Sweden, with a 2007 incidence of over 80% for cancer in the tonsils,[73][74] Finland[75] and Czech Republic.[76] Partners of patients with HPV positive oropharyngeal cancer do not seem to have elevated oral HPV infection compared with the general population.[77] In Australia incidence of HPV associated OPC is 1.56 cases per 100,000 males/year.[78]

Prevention

Main article: HPV-associated oropharyngeal cancer awareness and prevention

Risk factors are high number of sexual partners,[79][80][81] (25% increase >= 6 partners)[82] history of oral-genital sex,[80][81] (125% >= 4 partners)[82] history of anal–oral sex,[80] female partner had a history of either an abnormal Pap smear or a cervical dysplasia,[80][83] chronic periodontitis,[84][85] and, among men, decreasing age at first intercourse[79] and history of genital warts.[79]

A 2010 study concluded that current tobacco users with advanced HPV+ OSCC are at higher risk of disease recurrence compared with never-tobacco users.[86]

HPV vaccines have a theoretical potential to prevent oral HPV infection.[4]

A 2010 review study has found that HPV16 oral infection was rare (1.3%) among the 3,977 healthy subjects analyzed.[87]

History

In 1983, it was first suggested[5] that HPV might be the agent involved in the development of at least certain special types of oral cancers.[88] In 2007 the World Health Organization stated HPV was a cause for oral cancers.[4][89]

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