8 Malignant Epithelial Lesions Flashcards
- high-risk premalignant condition
- chronic, progressive, scarring
oral submucous fibrosis
prevalent in India, Southeast Asia, Taiwan, China, Papua New Guinea, results from habitual use of betel quid (betel quid/betel “nut” or paan
oral submucous fibrosis
Contents of betel quid:
A) betel leaf from piper betel pepper plant
B) slacked lime (calcium hydroxide) stimulates release of alkaloids from areca nut to produce feeling of euphoria and well-being
C) areca nut from the areca palm tree
D) tobacco
E) sweeteners and condiments
Signs and symptoms:
- brown/red colored mucosa with rigidity
- irregular surface tends to desquamate
- may be painful when eating spicy foods
- submucosal fibrous bands (buccal mucosa, soft palate, labial mucosa, may extend beyond oral cavity to oropharynx and upper esophagus)
- leukoplakia of the surface mucosa
- development of SCC (high risk)
- does not regress with habit cessation
oral submucous fibrosis
tx for oral submucous fibrosis
- monitor for premalignant/malignant change
- mild cases = intralesional corticosteroids to attempt to reduce the scarring/fibrous bands
- later stages = surgical splitting or excision of the fibrous bands may improve mouth opening and mobility
Head and neck cancer is the ____th most common type of cancer. Men? Women?
7th
5th
12th
Percentage of new cases of cancers that are oral and pharynx?
How many of these die?
Percentage of patients that live 5 years?
Median age at dx
Median age at death
3%
2%
67%
64/68
lowest % of dx but highest % of death from oral and pharyngeal cancers
black males
cancer staging
Stage 1: primary tumor < 2 cm, no nodal metastasis
Stage 2: primary tumor >2 but < 4 cm
Stage 3: metastasis to regional lymph node, primary tumor > 4 cm
Stage 4: distant metastasis
What percentage of cases or cancer are diagnosed at stages III or IV?
65-70%
About ___% of cancers in the oral cavity are SCC.
SCC is the ____th most common type of cancer in the world.
90%
11th
SCC is seen most often in men who…
have been aware of an alteration in an oral cancer site for 4-8 months.
men:women for SCC
2.5:1
types of genes affected that cause SCC
- oncogenes, proto-oncogenes
- tumor suppressor genes
- replication error repair genes
Head and neck cancers in NONSMOKERS are more likely to be?
- female
- oral (especially tongue)
- younger
- demonstrate mutations of the p53 and other tumor suppressor genes
extrinsic vs intrinsic risk factors for oral and oropharyngeal SCC
Extrinsic
- smoked tobacco
- smokeless tobacco
- alcohol
- betel quid
- HPV (oropharynx primarily)
- sunlight (lip and skin lesions only)
- radiation therapy
Intrinsic
- age
- reduced cellular immunity
- immunodeficiency
- general malnutrition
- severe irone deficiency
risk vs relative risk of tobacco smoking
Risk is dose and time dependent
Relative risk is dose dependent for cigarette smokers
- 5x greater = smoke 40 cigs
- 17x greater = smoke 80 or more cigs daily
- 10-100x in people who drink and smoke
*Risk increases as # of years smoking increases (packs/day x # of years)
Most likely to be smokers:
- men ages 25-44
- non-Hispanic Indians/Alaksa natives and people of multiple races
- disability/limitation
- US midwest
- persons living below the poverty level
- those with a GED
of carcinogens in tobacco smoke
70+
% of patients with head and neck cancers who are smokers
65-86%
major risk factor for ocal cavity SCC
smoking with a synergistic association with alcohol consumption
When it comes to alcohol, is dose or time put you at a greater risk for pharyngeal/oral cancer?
of years heavy drinking is more important (not the # of drinks/day)
Effects of alcohol (local vs systemic):
Local
- solvent action increases the permeability of oral mucosa to carcinogens in tobacco smoke
- contaminates in the alcohol
- alters epithelial metabolism
- ethanol by oral flora to acetaldehyde (known carcinogen)
Systemic
- nutritional deficiencies
- decreases liver’s ability to detoxify carcinogens
% of oral cavity proper SCC are HPV associated
2.2% (HPV 16 is highly prevalent –> 90%)
What makes up the oropharynx?
- posterior third/base of tongue
- soft palate
- tonsillar pillars
- pharyngeal walls
others types of cancers that have HPV DNA
cervical, anal, vaginal, vulvar, penile
possible causes for an increase in HPV-associated cancers
Focuses on changes in sexual patterns- increased oral sex partners, increased numbers of sex partners
prevalence of oncogenic oral HPV (who is at risk?)
- higher in men than women
- increased risk with increasing # of lifetime oral sex partners
- increased with tobacco use
- men who currently smoked and has greater than 5 or more lifetime oral sexual partners has elevated risk
characteristics of patients with HPV-positive OpSCC
- younger compared to oral cavity SCC patients
- majority of patients have little to no history of tobacco and/or high alcohol consumption
How does HPV infect cells?
Virus is epitheliotropic –> enters through wound/abrasions –> infects basal cells (only actively dividing cells in the epithelium)
How does HPV 16 cause cancer?
HPV genome eventually becomes incorporated into the host DNA. Integration can involve disruption of the E2 gene and its regulatory function. E2 gene product is a transcriptional repressor that inhibits transcription of oncogenic E6 and E7 proteins.
E6 and E7 account for the carcinogenic potential for HPV. The HPV 16 E6 and E7 proteins are highly expressed in differentiated keratinocytes. They inactive p53 and retinoblastoma pRb proteins (important transcriptional regulators/tumor suppressor genes).
E6 inactivates p53.
E7 inactivates pRb.
Clinical features:
- small primary tumor
- large, often cystic nodal involvement
- tumors are usually endophytic and can be difficult to detect clinically
- 90% are found in tonsillar tissue or base of tongue
OpSCC
Clinical features:
- leukoplakia, erythroplakia, erythroleukoplakia
- ulceration
- mass lesion that is fixed and indurated (exophytic and/or endophytic)
- may see destruction of underlying bone
oral SCC
What to do if you see a lesion suspicious of SCC?
- Take a pic
- Measure the lesion
- Examine neck for possible nodal involvement
- Discuss with patient and be honest about your concern
- Refer for biopsy ASAP
- Document your findings
Histo of malignant neoplasms (well differentiated vs poorly differentiated)
Well differentiated = closely resemble tissue of origin,
Poorly differentiated = does not resemble tissue of origin
*Cancers that are less differentiated tend to exhibit: more aggressive and rapid growth, more aggressive invasion, more likely to metastasize
Histo: malignant cells break through the basement membrane and invade into the adjacent tissue (islands and cords of tumor cells invade the underlying CT), increased numbers of mitotic figures, abnormal mitotic figures, larger nuclei, prominent nucleoli, hyperchromatic cells, pleomorphism of cells and nuclei, keratin pearl formation
SCC
1-10% of all oral cancers, a “low grade” variant of oral SCC
verrucous carcinoma
Verrucous carcinoma is more commonly seen in:
- men
- ages 65-70
- use smokless tobacco
common sites for verrucous carcinoma
mandibular vestibule, buccal mucosa, hard palate
Clinical presentation:
- diffuse
- usually painless thick white plaque (may have erythematous areas)
- numerous papillary or verruciform projections
- exophytic mass with a warty surface texture
- “frozen doormat” or “shag carpet” appearance
- adjacent leukoplakia or tobacco pouch keratosis
verrucous carcinoma
tx for verrucous carcinoma
- surgical excision
- radiation
- chemo
- combination of all of the above dependent on TNM staging and if its HPV +/-
Which is better? HPV +/- OpSCC
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