Lecture 31 Flashcards
List the characteristics of cancer cells
Cells growing out of control
The become self sustaining (dont need signals to grow bc they secrete their own via autocrine secretion of growth factors)
ignore anti-growth signals and apoptosis signals
angiogenesis in order to feed the rapidly dividing cells that make up the tumor
gets help from stromal cells
do not show replicative-senescence (immortal)
Compare benign tumors to malignant tumors
Benign tumors: a group of cells that exhibits abnormal growth, yet is NOT invasive
Malignant tumors: a group of cells that exhibits abnormal growth but IS invasive (usually bloodstream invasion)
Describe Metastases
metastases exhibit the “invasiveness” characteristic of cancer by traveling to new areas of the body and forming secondary tumors
this is the major reason people die from cancer (not easy for the cells to do however)
Describe tumor development and progression
All tumors come from a single ancestor cell that became abnormal due to a mutation
tumors begin as benign, and then slowly develop the ability to successfully metastasize
List and describe the environmental causes of cancers
Tobacco: leads to lung, kidney, and bladder cancer
Diet high in fat and low in fiber: leads to bowel, pancreatic, prostate, and breast cancer
Chemicals/UV light/X-Rays: cause a variety of cancers
List and describe an example of viral cause of cancer
AIDs, which causes Kaposi’s sarcoma
Compare oncogenes and tumor suppressor genes
oncogenes: are “gain of function” genes formed by a single mutation event that occurs to a proto-oncogene
oncogenes cause exaggerated proliferation, and is a dominant allele
Tumor suppressor genes: are “loss of function” genes formed by 2 mutation events
Tumor suppressor genes only lead to cancer when both alleles are mutated (recessive) and tumors can no longer be suppressed
describe the process by which oncogenes are activated by a virus
Retroviruses inject their RNA information into the host where it is reverse transcribed into the host DNA
viral oncogenes (v-src) are very similar to normal cellular genes (c-src) which code for proto-oncogenes
v-src hijack the c-src and activate proto-oncogenes into oncogenes by either over expression or mutation
oncogenes then drive cell over-proliferation
What is the difference between oncogenes vs. tumor suppressor genes
oncogenes are “gain of function genes”
tumor suppressor genes are “loss of function genes”
both can lead to cancer via a different method
Name and describe the 4 mechanisms in which proto-oncogenes are activated into oncogenes
Deletion/point mutation: creates a hyperactive protein
Regulatory mutation: a promoter mutation that causes an abnormally excessive expression/production of the normal protein
Gene amplification: several copies of genes are created instead of one. This causes an overproduction of normal protein
Chromosomal rearrangement: brings in a new regulatory sequence that causes over production OR creates overactive fusion protein
Give an example of the deletion/point mutation mechanism for oncogene activation
Ras codon 12 Gly to Val
this keeps the Ras protein in the active state bc it can no longer be hydrolyzed from it’s GTP form to it’s GDP form (which would normally inactivate it)
List the 3 stages (omit normal epithelium) of cervical cancer) and state the most effect weapon against cervical cancer
low-grade intraepithelial neoplasia
high-grade intraepithelial neoplasia
invasive carcinoma
early detection (via pap smear) is the best weapon
List the 3 stages (omit normal epithelium) of cervical cancer) and state the most effect weapon against cervical cancer
low-grade intraepithelial neoplasia
high-grade intraepithelial neoplasia
invasive carcinoma
early detection (via pap smear) is the best weapon
Compare neovascularization and angiogenesis. which of these is more associated with cancer?
neovascularization: the formation of new blood vessels from scratch
angiogenesis: sprouting new/more blood vessel branches from pre-existing blood vessels
angiogenesis is more associated with cancer
Compare neovascularization and angiogenesis. which of these is more associated with cancer?
neovascularization: the formation of new blood vessels from scratch
angiogenesis: sprouting new/more blood vessel branches from pre-existing blood vessels
angiogenesis is more associated with cancer
What is the Ames test, and how is it conducted?
it tests a cell sample for DNA-mutation (cause of cancer)
histidine dependent salmonella, the sample, and liver extract are all mixed into the same agar
after culturing this mix, the higher the colony count of salmonella, the more mutagens were present in the sample
(this is bc mutagens produce histidine, which salmonella feeds off of)
What is the Philadelphia chromosome? what does it cause?
Philadelphia chromosomes are formed from a translocation even between Chr 9 and 22
this yields a small, mutate version of the 22nd chromosome that causes chronic myelogenous leukemia
DNA maintenance genes are a subset of ____ ____ ____, and involve the inactivation of caretaker genes that promote genomic stability. list 2 examples of these type of genes
tumor suppressor genes
DNA repair genes
Checkpoint genes
define “transformed cells”
small colonies of abnormally proliferating cells caused by an oncogene
(related to oncogenes formed by viral infections)
What occurs in a “truncated EGF receptor” as opposed to a normal EGF receptor? what is this issue associated with?
Truncated EGF receptors lose their extracellular domain and become active without the binding of it’s ligand
this signals for a constant signal for the cell to divide and is associated with glioblastoma (brain tumor)
What occurs in a “truncated EGF receptor” as opposed to a normal EGF receptor? what is this issue associated with?
Truncated EGF receptors lose their extracellular domain and become active without the binding of it’s ligand
this signals for a constant signal for the cell to divide and is associated with glioblastoma (brain tumor)
In B cell lymphoma, Bcl2 genes on chromosome 18 undergo a ____ translocation with chromosome ____. This causes the _____ of Bcl2 in B cells and prevents ____ of damaged cells
reciprocal
14
over-expression
apoptosis
In B cell lymphoma, Bcl2 genes on chromosome 18 undergo a ____ translocation with chromosome ____. This causes the _____ of Bcl2 in B cells and prevents ____ of damaged cells
reciprocal
14
over-expression
apoptosis
Describe methods that oncogenes can manipulate/over stimulate cell growth pathways that require a ligand to signal for cell proliferation
the can produce ligands constitutively (ligand-autocrine signaling)
RTKs (receptor tyrosine kinases) can be constitutively produced in such a way that they no longer require a ligand to signal for cell proliferation
