Oral cancer and precancer Flashcards
International Classification of Disease (ICD)10 (4)
C00-C06, C12-C14
What does ‘oral’ cancer include? (2)
Includes oropharynx, but not salivary glands
How common is oral cancer? -what place -total cases -frequency incidence -deaths -death rate
16th most common 355,000 cases 2% frequency 5.8/100,000 128,000 deaths* 50% death rate (H&N is 6th most common worldwide)
Oral Cancer: England stats
Total cases: 7587 including pharynx, 4379 true oral cavity
Frequency: 3% of all cancers
Incidence: M 20.1/100,000, F 9.3/100,000
58% 5 year survival
Regional differences: h&N cancer (4)
NI < England < Wales < Scotland
Increasing incidence (3)
On the rise
Men: 32%increase over last 10 years, now 10th
33% increase in women over last 10 years, now 15th
Age group is changing
Still predominantly older men
Now more women, and younger age demographic
Older patients decreasingly affected
Survival rates of H&N cancer: the change over time
Not much change over 50 years at all
- 7% of pts present with late stage disease (stage III or stage IV)
- in some IO subsites (further back in the oral cavity), >60% of pts die
- -> survival goes down the further back the lesion as harder to be seen
Aetiology of oral cancer (2)
Multifactorial
-no single factor identified
-genetic predisposition in some (pretty rare)
-environmental
Factors vary in different geographical regions or ethnic groups
Inherited factors in oral cancer (2)
Polymorphisms in genes involved in the
metabolism of carcinogens have been linked
to individual susceptibility (e.g. in Japan and South Korea):
• tobacco - glutathione transferases
• alcohol - alcohol dehydrogenase (ALDH2)
An increased risk of oral cancer is associated with a number of inherited cancer syndromes (in skin lesions including the lip):
• Li-Fraumeni (abnormal P53)
• Fanconi anaemia (DNA damage repair abnormality - primarily related to bone marrow but if they survive that, 60% of them get oral cancer)
• Xeroderma pigmentosum (DNA damage repair abnormality)
Risk factors for oral cancer (5)
Tobacco -strongest risk factor Alcohol Sunlight Infections • Viruses • Fungi • Bacteria Diet and nutrition Age
Tobacco use: types of use (2)
Smoking -cigarettes -pipes -cigars -reverse smoking Smokeless -betel quid (pan) -snuff -chewing tobacco
Tobacco smoking risk (3)
• definite relationship with oral cancer • risk is greatest in heavy users (>20/day) • risk is greater if accompanied by alcohol use
Smokeless tobacco (3)
Definite relationship with oral cancer established by: • epidemiological studies • observation of lesions - area in contact with tobacco is the area that gets cancer Risk is greatest in heavy users Risk is greater if accompanied by smoking or alcohol
Alcohol as a risk factor (3)
Consumption of alcoholic drinks is a risk factor for oral cancer • ethanol alone is not carcinogenic • amount of ethanol more important than type Risk is greatest when accompanied by tobacco use Increasing importance in young patients
Sunlight and oral cancer (2)
• UV is an important cause of lip (skin) cancer (BCC, SCC, melanoma) • UV light cause solar keratosis and dysplasia of the skin -squamous cell carncinomas
Viruses and oral cancer (4)
HPV • Good evidence for a role in oropharynx -some evidence in oral lesions • HPV 6 & 18 have been implicated • HPV associated with about 60% of OPSCC cases in the UK
HPV-related Oropharyngeal SCC (4)
Younger patient demographic • less traditional risk factors Often present with LN metastases Prognosis is good (chemoradiotherapy) • “advantage” lost if also a smoker Effects of vaccination?? -stained with p16 in histology
Evidence about candida and oral cancer (4)
Candida infection has an association with oral cancer development
• candida often infects pre-malignant lesions
• candidal leukoplakia is often dysplastic
• candidal leukoplakias are often non-homogeneous
• candida can produce carcinogens from nicotine and alcohol
Oral cancer genetics (3)
Oncogenes • differing oncogenes activated • geographical variations • no clear relationship with disease Tumour suppressor genes • p53 mutation or inactivation • many other genes Viral component – what role does HPV play?
Social deprivation and oral cancer
Social deprivation has an impact Highest rates in most deprived males -smoking -access to good nutrition -access to healthcare and related behaviours
Multistage carcinogenesis (3)
Inititaion (normal cell) — multiple genetic effects –> induction (precancer) — multiple genetic events –> progression (cancer)
*genetic events due to inherited and environmental factors
Field change (3)
• All/most of the oral mucosa is abnormal – but not necessarily clinically or on histology
• Common genetic abnormalities
• Subsequent tumours may develop in the “field” of abnormal mucosa, or may be
completely different
“Field of cancerisation”
Need to treat the whole field rather than just the lesion
Stages of cancer development (3)
Keratosis –> dysplasia –> carcinoma
Precancerous lesion definition (2)
a morphologically altered tissue in which cancer is more likely to occur than in its apparently
normal counterpart
The preferred term is now
“potentially malignant oral lesion”
WHO definition of leukoplakia (2)
WHO definition:
A white patch that cannot be rubbed off and cannot be characterised clinically or
histologically as any other disease…
…and that is not associated with any physical or chemical causative agent except the use of tobacco
