Part 4 Flashcards
(18 cards)
Look at the ribosome assembly and know which ribosomal subunits make up the 40S and 60S
40S = 18S
60S = 28S, 5.8S, 5S
Understand the limitations of treating cells that lack p53 with radiation and chemotherapy
p35 regulates cell survival as well as cell cycle progression
Cells lacking p35 fail to undergo apoptosis in response to agents that damage DNA including radiation and other chemotherapy drugs
Failure to undergo apoptosis contributes to resistance of many tumors to chemotherapy
Induced with apoptosis induced by growth factor and oxygen deprivation
What is the basic definition of a tumor?
Any abnormal proliferation of cells which may be either benign or malignant
What are proto-oncogenes? What’s their association with oncogenes?
Proto-oncogenes: normal cell genes from which the retroviral oncogenes originated from
Important cell regulatory genes, encoding proteins that function in signal transduction pathway controlling cell proliferation
Oncogenes are abnormally expressed or mutated forms of the corresponding proto oncogenes, oncogenes induced abnormal cell proliferation
Look at density-dependent inhibition and contact inhibition in cancer cell proliferation
Normal cells proliferate until they reach a certain density and then stop but cancer cells continue to proliferate
Contact inhibition is where tumor cells are not inhibited by cell contact so they migrate over one another and grow in disorder multilayered pattern
What type of carcinogen is asbestos and what role does it have in cancer cell development?
Chemical carcinogen that is a tumor promoter (Stimulate cell proliferation instead of inducing mutations)
Facilitates the outgrowth of the cell population
Look at the impact of recombination of viral DNA with raf, and how it effects raf function
Normal Raf consists of an N terminal and C terminus (regulatory domains) that is inactive normally until Ras activated it
Oncogene Raf doesn’t have a regulatory domain by the N terminus instead has viral GAG sequence which activates Raf without Ras causing cell transformations
Look over slide 16 from the cancer powerpoint – what are tumor suppressor genes? What is loss-of-function and gain-of-function?
Tumor repressor Genes: loss of function mutations, recessive, heritable, first mutation even inactivates first gene
Second mutation event functionally eliminate tumor repressor gene promoting cell proliferation
Oncogenes: gain function mutations, dominant, not inherited, a single mutation event, can enable oncogenes to promte cell trans formations
- Oncogenes: gain of function, dominant, not inherited
- tumor suppressor: loss of function, recessive, inheritable
Read the section on Rb tumor suppressor genes and understand the impact on a single Rb gene mutation and when both copies of the Rb gene were mutated
Rb is a recessive tumor suppressor gene so one mutation will have no effect but two mutations will eliminate the tumor repressor gene Rb
Leaving unregulated E3F means uncontrolled transcription and growth
Uncontrolled trnascription leads to multiple tumors in eyes
Understand the role of oncogenic Ras molecules in the ERK signaling pathway
A mutation in Ras that always had GTP means there would be a continuous activated response of Ras meaning Raf, MEK, and ERK would all be overactive (Functions as transcription factors that stimulate cell growth.
Look at telomere stability – compare normal and metastatic cells
- metastatic: have less telomerase activity, loss of DNA
Look at the role of the DNA tumor virus SV40 and it’s role in disrupting cell cycle regulation
Disrupts cell cycle regulation. Induces tumors and SV40 disrupts normal cell cycle regulation by integrating’s its genome into host cell chromosomes leading to genomic instability affecting signaling pathways- results in cancer development
Look at the role of p53 in response to DNA damage (both low to severe damage)
Detects DNA damage and if the damage cannot be fixed it will initiate apoptosis
- ATM recognizes DNA damage
- Chk phosphorylates p53 = increased levels
- transcription site PUMA Noxa leads to apoptosis
What is angiogenesis?
Process by which the body forms new blood cells
What are the two main types of tumor and how are they different?
Benign = remains confined to its location and doesn’t invade the surrounding normal tissue or other parts of the body
Malignant - can invade surrounding normal tissue and move to other parts of the body
Look at the role of Solar ultraviolet radiation in cancer cell development
Damage DNA and induce mutations
Radiation and most chemical carcinogens act by inducing mutations in genes and cause skin cancer on epithelial cells
What is autocrine growth stimulation?
abnormal production of growth factors by a responsive cell leads to continuous autostimulation of cell division
What is metastasis?
The spread of malignant tumors - spread of cancer cells
