Cancer Genetics Flashcards
what two mutations do 100% and 90% of cancers have respectively?
p16Rb is 100
p53 is 90
viral oncogenes…how?
genes similar to human genes controlling cancer can insert themselves into human genome and cause cancer
what did we discover first, viral or cellular oncogenes?
viral actually led to cellular discovery because when we realized viral were similar to genes they inserted around we realized the cellular genes could cause cancer too if mutated
protooncogene definition
gene important for cell growth and development that can become an oncogene by mutation or over or under expression
two common tumor suppressor genes
p53 and p16ink4a
La Fraumeni Syndrome cause
one mutant allele of p53 which is in charge of killing bad cells…so only need one more muation on other allele to maybe have cancer
pathway affecting the G1 cycle and regulation of it
Rb blocks G1…inhibit growth
cyclins and cdk4 block Rb…promote growth
p16 blocks cyclins and cdk4…inhibit growth
p53 activated Rb so inhibits growth
how does Rb problems lead to cancer?
if Rb is low, then cell can proliferate since it is an inhibitor of growth
how does cdk4/cyclins lead to cancer?
if these are upregulated and have a lot of them then they turn more Rb off and not as much inhibition of growth
how does p16 lead to cancer?
since it blocks cdk4/cyclin from inhibiting the Rb…if no p16 can have free running cdk4/cyclins that inhibit Rb and lead to more growth
how does p53 lead to cancer?
p53 enhances Rb activity so without p53 may have less active Rb and more cell growth
it also leads to apoptosis so without will have less cell death
how do PTEN and Bcl2 lead to cancer?
both of these are blockers of apoptosis
examples of genomic instability in cancer
mismatch repair, nucleotide excision repair, chromsome segregation, telomere structure
how do we usually get to cancer?
normally a multistep process with many genetic events
is hyperplasia physiologic or pathologic?
can be both…increase in normal cells number
is hypertrophy physiologic or pathologic?
can be both, growth in cell size
is metaplasia physiologic or pathologic?
can be both…change in cell type
is metaplasia reversible?
usually yes
two examples of metaplasia
smoking and change epithelia in lungs…
acid reflux and change to get more goblet cells in esophagus epithelium
dysplasia characteristics
atypical proliferation of cells with variation in size/shape, nuclear enlargement and irregularity
also has disorderly arrangement…lack of polarity and odd mitotic location
type of neoplasia
can be well differentiated or poorly differentiated
anaplastic neoplasia
no cellular differentiation
what defines neoplasia
excessive growth of tissue that is uncoordinated and autonomous
characterstics of benign neoplasm
slow growing localized growth… that resembles surrounding tissue and is well differentiated
common name ending for a benign neoplasm
-oma
paraneoplastic syndrome mechanism and what it is associated with?
symptoms not due to neoplastic cell localization…rather due to tumor cells secreting humoral factors
associated with malignant neoplasms
differences in dysplasia, carcinoma in situ and carcinoma
dysplasia is abnormal appearing cells in epithelium
carcinoma in situ is dysplastic changes involving all layers of epithelium down to basement membrane
carcinoma is when dysplastic changes have now become malignant and are growing through the basement membrane
mesenchymal neoplasm name
sarcoma
epithelium neoplasm name
carcinoma
what is the histologic grade of neoplasms based on?
how well differentiated the cells are…well to moderate to poor differentiation
anatomic stage grading with TNM
tumor-0-4
nodes involved- 0-4
metastasis-0/+
