Exam 3 pt 4 Flashcards
contact inhibition
normal cells stop moving when reach contact each other, cancer cells dont do this and keep growing
* cancer cells dont need survival factors/signals
* selective advantage because proliferate when normal cells would stop
cancer cells alterred sugar metabolism
- tumor cells have increased rate of glucose uptake
- small amount of oxidative phosphorylation
- cancer cells instead form lactate at high levels, promoting cell growth
tumors grow within
a framework of supporting connective tissue stroma
metastasis
- EMT for carcinomas allows decreased adhesion and escape from parent tissue
- enter blood through aid of angiogenesis
metastasis
- EMT for carcinomas allows decreased adhesion and escape from parent tissue
- enter blood through aid of angiogenesis
cancer critical gene
genes whose alteration frequenctly contributes to the causation of cancer
oncogenes
- gain of function mutations
- dominant
- non mutated forms are called proto oncogenes
tumor supressor genes
- loss of function mutations
- often recessive
- cant add to tester strain to find
_ can act as vectors for oncogenes
retroviruses
Ras oncogene
First identified and one of the most important cancer critical genes, it codes for a monomeric GTPase involved in control of cell proliferation
chromosomal rearrangements
The breaking and rejoining of DNA segments which can lead to the expression of a hyperactive or overexpressed fusion protein
EGF receptor in cancer
deltion that deletes extracellular domain of EGF receptor, causing it to always stay active and promote growth
excessive quantities of myc protein
causes cells to proliferate when they usually would not
Burkitt’s lymphoma
Type of lymphoma in which a translocation brings the Myc gene under the control of regulatory sequences which normally control the production of antibodies in B lymphocytes
individuals with heriditary form of retinoblastoma
have a deletion in one copy of the Rb gene in every somatic cell
* retinal cells become transformed when an event eliminates the good copy of a gene
loss of Rb gene
allows cells to enter the cell cycle when they otherwise would not
Rb gene
A universal regulator of the cell cycle in almost all cells in the body, its loss allows cells to enter the cell cycle when they otherwise would not
_ of tumor supressor genes causes cancer
inactivation
ways to see tumor supressor genes
- sequencing of cancer cell genomes
- analysis of methylation patterns
- karyotype analysis
drivers of cancer
Group of mutations present in a tumor that play a role in the development of the cancer
drivers of cancer
Group of mutations present in a tumor that play a role in the development of the cancer
passenger mutations
Group of mutations present in a tumor that arise due to the genetic instability of the cancer, but are irrelevant to the development of the disease
mutations found at _ are candidates for drivers
high frequencies
uncontrolled proliferation of cancer cells requires the loss of restraints on
cell cycle progression and also regulate cell growth
Warburg effect
The excessive rate of glycolysis that is observed in tumor cells
* result of PI3/AKt/mTOR pathway being activated abnormally
loss of p53 promotes cancer in four ways
- allows DNA damage to continue throughout cell cycle
- allows damaged cells to escape apoptosis
- allows continues division of damages cells
- cells become relatively resistant to anticancer drugs
_ copy/s of p53 has to be mutated
one copy only
cancer stem cells
Small subset of tumor cells which maintain the tumor cell population and are less sensitive to many types of anti-cancer therapies; they undergo self-renew without limit and give rise to transit amplifying cancer cells
carcinogens
Any agent (i.e. chemicals or radiation) that causes increased cancer rates
Ames test
A quick and accurate test for mutagenicity using bacteria defective in histidine synthesis and DNA repair
* if colony grow, then mutation has corrected his synthe
* means it is a mutagen
the most potent carcinogens are intially
initally chemically inert and only become damaging when altered by ctochrome p-450 oxidases in the liver
Hep A and B causes
liver cancer
HPV
Virus which causes warts, and is implicated in most cases of cervical cancer
products of viral oncogenes bind
Rb and p53
binding of Rb by _ allows _
E7 and E3 allows incontrolled entry into S phase
binding of p53 by _ allows _
E6 allows continued proliferation of abnormal cells
Brca 1 and 2 are
needed for homologous recombination, repair double stranded breaks
PARP
repairs single stranded breaks
Brac1 and 2 tumor supressor genes
Mutations in these tumor suppressor genes predispose humans to breast and ovarian cancers
drugs that block PARP
kill cells that dnt have Brac but spare normal cells
* good treatment
philadelphia translocation results in
formation of a hyperactive tyrosine kinase
imatinib (gleeve)
- binds and inhibits the activity of Bcr-Abl protein
- cells with philadelphia chromosome are yeeted
- relapse when cancer cells develop resistance to the drug
The process by which an initial mildly disordered cell behavior gradually accumulates more mutations and evolves into a full-blown cancer.
tumor progression
Human cancer cells display _____________________ which causes them to accumulate genetic changes at an abnormally rapid rate.
genetic instability
Loss-of-function mutations in these genes can promote the formation of cancer
tumor suppressor genes
A cancer arising from connective tissue or muscle cells.
sarcoma
Tumors whose cells have acquired the ability to invade other tissues are referred to as ______________________
malignant
Hepatitis-B and C cause
chronic inflammation of the liver (hepatitis) and are implicated in the development of liver cancer.
T or F: Oncogenes directly promote cancer by causing unregulated cell proliferation, while tumor suppressor mutations only promote cancer indirectly by causing genetic instability.
False
Most carcinogens are also .
mutagens
The activity of cytochrome P-450 oxidases in the liver may
sometimes convert chemically inert substances into potent carcinogens.
