clinical presentation does not predict how an oral
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OMPR Exam 2 Latest Update
T/F Oral SCC has very unpredictable clinical behavior.
T/F Oral SCC can be exophytic, endophytic, white, red or white, subtle, can affect any
surface. - Answer BOTH TRUE
T/F Clinical presentation does NOT predict how an oral SCC will behave. - Answer TRUE
its totally unpredictable!
It is currently unknown which oral dysplasias will progress to SCC
What % of pts with SCC and metastasis to regional lymph nodes die within 5 years of
diagnosis? - Answer 50%!!
current management of pts is surgical tumor removal and prophylactic neck lymph node
dissection
What is the major prognostic factor in oral SCC? - Answer *metastasis to regional lymph
nodes*
What tx do oropharyngeal (HPV+) head and neck cancers respond well to? - Answer
radiation/surgery and excellent response to therapy
some don't need surgery because response to therapy is so great!
HPV+ oropharyngeal SCC show what with H&E?
p16?
DNA ISH?
RNA scope RISH? - Answer H&E: blue basoloid
p16: strongly positive
DNA ISH: positive
RNA scope RISH: positive
two most common strains are HPV 16 & 18
but there are discordant HPV+ oropharyngeal cancers i.e. strong p16 but negative for
DNA ISH
*so although the tumors might be HPV related, for some reason DNA ISH were negative*
so now the most confirmative test is RNA ISH
,T/F The most confirmative test for HPV+ oropharyngeal cancer is DNA ISH. - Answer
FALSE!!! Some are discordant
*use RNA RISH*
Oral SCC H&E: - Answer looks predominantly pink, that means producing a lot of
*keratin* there are *keratin pearls*
with blue inflammatory immune response
lots of keratin = well differentiated
How does moderately differentiated Oral SCC look on H&E:
poorly differentiated? - Answer cells are still clumping together can tell they're
epithelial, producing some keratin every now and then but distinction between tumor
and surrounding muscle is much less
note: poorly differentiated you can't even tell there's a cancer in there, loss of epithelial
characteristics, can even look like CT or mesenchymal phenotype
T/F HPV is very important in the context of oral SCC. - Answer FALSE!!! that's true of
oropharyngeal SCC
there is so much data we didn't know what to do with it, now bioinformatics helped with
volume of cancer data and research produced showed
*HEAD AND NECK CANCERS ARE VERY HETEROGENOUS* (mutations are all extremely
different there is no one magic bullet that will allow us to cure this)
What genetic mutations are prevalent in HNSCC: - Answer 22% CCND1 amplified
25% CDKN2A mut/del
22% NOTCH1,2,3 mut/del
24% SYNE1,2 mut
63% TP53 mut/del
there are others on a slide in this lecture (second cancer lecture)
What does the genomic era herald for the management of oral cancer? - Answer 70-80%
of oral SCCs and dysplasias are characterized by copy number aberrations in the
,cohort profiled but not all cancers are represented here aka LOTS OF HETEROGENEITY
Dysplasias show certain regions of genomic aberrations: gains and losses the cancers: -
Answer had those regions too
AND!! the Oral SCCs acquire *additional* recurrent gains and losses
T/F The genomic profile of a dysplasia and an oral SCC are pretty similar - Answer TRUE
(they share some gains/losses)
therefore if you profile a dysplasia it gives you an idea of what kind of cancer its going to
be
T/F The genomic profile can distinguish metastatic vs. non metastatic tumors - Answer
TRUE
+3q, -8p, +8q and +20 were frequent in N+ tumors but ABSENT in N0 tumors
T/F Methylation could be a significant biomarker in the diagnosis of oral cancer - Answer
TRUE, methylation plays a role in regulating multiple pathways involved in cancer
development (i.e. miRNA levels, focal adhesion expression etc)
T/F Oral cavity microbiome plays a very important role in Oral cavity SCC
What might be important in oral cancer? - Answer TRUE
oral cancer is associated with changes in 5 abundant phyla
Sri lanka has - Answer one of the highest rates of oral cancer in the world
Define oral potentially malignant disorder: - Answer any persistent and progressive
epithelial lesion for which a clinician can determine no clear cause should raise
suspicion and must be evaluated to rule out premalignant or malignant changes.
*its a clinical diagnosis*
OPMR lesions from white to red - Answer Leukoplakia
Homogenous
Non homogenous (speckled leukoplakia, leukoerythroplakia, erythroleukoplakia,
speckled erythroplakia)
Erythroplakia (<0.5% prevalence)
+/- ulceration, +/- exophytic
What's the MOST common OPM lesion we find? - Answer Leukoplakia (white patch that
cannot be wiped off and you cannot explain why it's there)
What is the prevalence of leukoplakias? - Answer 1-5% in general population
, What are the two phenotypes of leukoplakias? - Answer *Homogenous* (look the
essentially same from one side to the other, they're sharply demarcated, may have
shallow fissuring, same color white throughout lesion) very rarely they're nothing worse
than mild dysplasia can be early malignancy
and
*Non homogenous* (has white but could be mixture of red/white, or one part of the
lesion could be translucent and in another a thicker white, surface topography,
verrucous etc)
T/F Erythroplakias are all red with some white
T/F Erythroplakias are extremely rare
T/F Erythriplakias are usually high grade dysplasia or early carcinomas - Answer
FALSE, they're all red
TRUE VERY RARE
TRUE
What shows greater degree of severity red or white? - Answer red
What's something that's like a leukoplakia but caused by sun damage? - Answer Actinic
keratosis
What is proliferative verrucous leukoplakia? Who does it affect? - Answer another OPMD
affects Women, 6th/7th decade
multifocal leukoplakia
*extremely high potential for malignant transformation
OPM includes lichen planus which - Answer in a small subset are at higher risk of
malignant transformation (cause unknown, inflammation related? medications?)
Graft versus host disease most common malignancy to occur? - Answer Oral squamous
cell carcinoma
What two diseases have genetic mutations that put them at very high risk for developing
malignancy? - Answer Dyskeratosis congenita (telomerase defect, early senescence)
Fanconi anemia (myeloproliferative disease)
T/F Leukoplakias are more than 3x more prevalent in women. - Answer FALSE *3x more
in men*
T/F The global prevalence of leukoplakias is approx 1-5% - Answer TRUE
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