Cancer Biology Flashcards
define neoplasm
new growth, proliferation of cells
define neoplasia
formation of a neoplasm
define metaplasia
an adaptive substitution of one type of adult tissue to another type of adult tissue
define metastasis
spreading of neoplasm to distant sites
define adenoma
a benign epithelial neoplasm which produces a gland-like pattern or derives from glands
define papilloma
benign tumor of surface epithelium
define polyp
benign growth from mucosal surface of intestine or nose
what are the T,N,M staging associated with the stage of cancer?
T= size and extent of invasion
N= presence and number of lymph nodes involved
M= presence of distant metastasis
define stage 0 cancer
carcinoma that has not invaded into other tissue
define stage 1 and 2 cancer
variable, depends on tumor type and location
define stage 3/4 cancer
cancer has spread throughout the body
the epidermis of the skin consists of what cell type?
keratinocytes
the dermis of the skin consists of what cell type?
fibroblast
the hypodermis of the skin consists of what cell type?
adipocytes
which type of cancer cell is responsible for the bulk of tumor cell proliferation and is susceptible to cancer therapy?
TA cells
what are the cancer stem cell markers in the breast?
CD44, CD24
what is the cancer stem cell marker in melanoma?
CD20
what are the cancer stem cell markers in the prostate?
CD44, a2b1, CD133
what are the cancer stem cell markers in pancreatic cells?
CD44, EpCam, CD24
what are the different methods of how our body repairs DNA?
base-excision repair
nucleotide-excision repair
transcription-coupled repair
mismatch repair
double-strand-break repair
what is required to allow accumulation of sufficient mutations to generate cancer?
chromosomal instability
what is xeroderma pigmentosum?
an autosomal recessive disorder causing severe light sensitivity, severe pigmentation irregularities, and early onset of skin cancer
why are patients with xeroderma pigmentosum so vulnerable to skin cancer?
they cannot repair damage caused by UV rays
which factors are associated with familial melanoma?
p16/INK4a
CDKN2A
CDK4
12q14
which chromosomes are associated with burkitt’s lymphoma?
8q24, 14q, 22q, and 2p
how do epigenetic alterations affect gene epxression?
alters without changing DNA sequences, thereby turning gene expression on or off
also causes histone methylation, de-acetylation and phosphorylation
what are 2 main causes of human cancer?
loss of histone acetylation by histone deacetylase
or
induction of histone methylation by histone methyltransferase
what are epigenetic factors that cause tumorigenesis?
DNA methylation
histone methylation
histone deacetylation
how can we reverse DNA methylation?
inhibitors of DNA methyltransferase
how do we reverse histone methylation?
inhibitors of histone methyltransferase (HMAT)
how do we reverse deacetylation?
inhibitors of histone deacetylase (HDAC)
list the examples of genetic lesions that usually affect only one gene during tumorigenesis
Point Mutations
Frame Shift Mutations
Insertions/Deletions
Amplification
list the examples of Major Chromosome Abnormalities during tumorigenesis
Translocations
Chromosomal Loss
how is the C-Myc gene associated with Burkitt’s lymphoma?
C-Myc gene is normally off, but is kept on by immunoglobulin gene enhancer due to chromosomal translocation in B-cell tumors
chromosomal translocation is found in most cases of?
what forms as a result and causes said formation to not be under normal control?
chronic myelogenous leukemia (cancers of bone marrow and white blood cells)
BCR-ABL gene
what does the ABL1 gene do?
encodes tyrosine kinase ABL. it is activated in response to negative factors like growth factors and DNA damage to stimulate cell proliferation or differentiation, or survival or death
cancer is caused by alterations in? (these are our targets for therapeutic interventions)
tumor-suppressor genes, oncogenes, and tumor modifier genes (microRNAs)
what do tumor-suppressor genes do?
they encode proteins to inhibit cell proliferation and stabilize the genome
genetic alterations of tumor suppressor genes during tumorigenesis are classified as what kind of mutation? are they dominant or recessive?
loss of function
recessive
what is retinoblastoma?
cancer caused by alterations of tumor-suppressor genes. it forms retinoblastoma protein which is a substrate for cyclin-dependent kinase
what is the function of a transcription factor?
to help transcribe genes by converting DNA to RNA
what is E2F?
an important transcription factor that helps cells enter S phase
what is p53?`
a transcription factor that binds with DNA to activate or repress the expression of genes involved in growth arrest, apoptosis, DNA repair, and angiogenesis
what are oncogenes?
what type of mutation are they? is it dominant or recessive?
how do they progress?
altered proteins deriving from proto-oncogenes (normal genes) with increased expression
gain of function
dominant
by viral infections or exposure to carcinogens
proto-oncogenes encode for what signaling proteins?
receptors associated binding proteins, serine/threonine kinases, and non-receptor tyrosine kinases
how are oncogenes activated?
Point mutation
Amplification
Chromosome translocation
Overexpression due to DNA demethylation
why is the Ras gene important and what does it do?
it’s the most commonly mutated gene. it stimulates cell growth
what are tumor modifier genes (MicroRNAs)?
how do the interact with oncogenes?
genes which don’t encode proteins. they produce RNA to block gene expression by causing mRNA degradation or block protein translation
they suppress their expression
what is the deterministic pathway to cancer?
different tumors of same cancer type occur via mutation of each gene
what is the plastic pathway to cancer?
different tumors evolve along variable pathways via mutation of many possible sites
how does telomere erosion work?
a slow process of telomere shortening, leading to decreased proliferation of tumor cells
how does telomere uncapping work?
a rapid pathway to increase apoptosis and DNA damage response to decrease proliferation of tumor cells
what is GRN163L?
an anti-telomerase agent which targets the telomerase RNA template to affect telomere erosion and induce telomere uncapping
what are examples of direct vessel signaling inhibition of tumor angiogenesis?
VEGF ligand inhibitors
VEGFR receptor inhibitors
growth factor inhibitors
what drug class used for tumor angiogenesis inhibition blocks endothelial and pericyte cell activation to block proliferation?
tyrosine kinase inhibitors
what is paget’s theory of metastasis?
Cells are dispersed randomly but only grow in organs
that provide the correct factors necessary for growth
what is ewing’s theory of metastasis?
The first site to which a cancer metastasizes is the
closest one in which there are small blood vessels.
An aberrant proliferation of cells is _______, and discontinuous spread of a neoplasm to distant sites through lymphatic channels, blood vessels
etc. is ________.
A. Adenoma and Papilloma
B. Hepatoma and melanoma
C. Neoplasm and metastasis
D. Papilloma and Polyp
E. Neoplasm and metaplasia
C
Skin cancer progression is a multi-stage process that involves
I. Initiation stage by mutation of the K-Ras gene
II. Activation of the Ras-Raf-MAPK pathway
III. Promotion and progression stage to invasive carcinoma
A. I only
B. III only
C. I and II only
D. II and III only
E. I, II and III
D
What is “false” about Tumor suppressor genes ?
A. Encode proteins that inhibit cell-proliferation and
ensure stability of the genome.
B. “gain of function” genetic alterations occur in this
class of genes.
C. Usually recessive in nature.
D. Includes RB and p53 proteins.
E. RB is controlled through phosphorylation
B
An adenocarcinoma of the colon diagnosed at Stage
I is a:
A. Benign neoplasm that can be treated by surgical
removal and no further treatment.
B. Malignant neoplasm that has spread widely
throughout the body showing distant metastasis
C. Malignant neoplasm of glandular origin which is
restricted at the site of origin in colon (carcinoma in situ)
D. Epithelial cancer that has invaded into the
underlying connective tissue.
E. Aggressive colon cancer containing a combination of
epithelial and stromal cells
C
Which of the following is true for p53?
I. Is a transcription factor that binds to DNA in a sequence specific manner.
II. Activation and stabilization of p53 occurs by
phosphorylation and acetylation.
III. Cellular responses to activated p53 include growth
arrest, DNA repair and apoptosis.
IV.A downstream target of p53 is p16.
A. II, III
B. I, II, III
C. I, III, IV
D. II, III, IV
E. I, II, III, IV
B
define carcinoma
Arise from epithelial precursor cells
define sarcoma
Arise from stromal or mesenchymal components of organs
define carcinosarcomas and malignant teratomas
mixture of epithelial and mesenchymal cells
list tumors that are undifferentiated and highly metastatic
Squamous cell carcinoma
Adenocarcinoma
Fibrosarcoma
