Cancer Flashcards
(19 cards)
What is the basic definition of a tumor?
Any abnormal proliferation of cells
What is metastasis?
The spread of malignant tumors (cancer cells)
What are the two main types of tumor, and how are they different?
Benign: confined to original location, doesn’t spread so limited in size, and closely resembles and functions like normal cells.
Malignant: capable of invading normal tissues and spreading throughout the entire body.
What are the groups of cancers?
Carcinomas: epithelial cells (90%).
Sarcomas: connective tissues (muscle, bone, cartilage, super rare <2%).
Leukemias: blood-forming cells and immune system cells (8%)
Explain density-dependent inhibition and contact inhibition in cancer cell proliferation.
Normal cells proliferate until they reach a certain density and then stop and enter G0, 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 a disordered, multilayer pattern.
What is autocrine growth stimulation?
Many cancer cells produce growth factors that stimulate their own proliferation, leading to continuous autostimulation of cell division (autocrine growth stimulation), making cancer cells less dependent on growth factors from normal sources.
What type of carcinogen is asbestos, and what role does it have in cancer cell development?
It is a chemical carcinogen that is a tumor promoter (stimulates cell proliferation instead of inducing mutation) that facilitates outgrowth of cell population.
What is the role of solar UV radiation in cancer cell development?
Radiation and most chemical carcinogens act by inducing mutations in genes and causes skin cancer on epithelial cells.
What are proto-oncogenes? What’s their association with oncogenes?
Proto-oncogenes are normal cell genes that help cells grow and divide and stay alive.
Oncogenes are the mutated form of a proto-oncogene, where it becomes more active or more abundant than normal.
What is the impact of recombination of viral RNA with Raf, and how does it affect Raf function?
Normal Raf consists of an N (regulatory domain) and C terminus, and is inactive normally until Ras activates it. Oncogene Raf does not have a regulatory domain by the N terminus and instead has a viral Gag sequence, which activates Raf without Ras, causing cell transformations.
What is the role of oncogenic Ras molecules in the ERK signaling pathway?
A mutation in Ras means there would be a continuous activated response of Raf, meaning Raf, MEK, and ERK would all be overactive.
What is the impact of a single Rb gene mutation, and when both copies of the Rb gene are mutated?
Rb is a recessive tumor suppressor gene, so one mutation will have no effect, but two mutations will eliminate the tumor suppressor gene Rb, leaving an unregulated E2F transcription factor, which means uncontrolled transcription and growth of the cell. This uncontrolled transcription of E2F leads to multiple tumors in both eyes (retinoblastoma).
What are the limitations of treating cells that lack p53 with radiation and chemotherapy?
Radiation and chemotherapy disrupt the DNA structure, and p53 should promote cellular apoptosis induced by radiation, but without p53, there will be no cell death.
What is the role of the DNA tumor virus SV40, and its role in disrupting cell cycle regulation?
SV40 disrupts the Rb/E2F complex by binding to Rb and not allowing Rb to bind to E2F (which would repress transcription), leading to an insensitivity to anti-growth signals and over transcription.
What is the role of p53 in response to DNA damage? What happens with the MDM2 oncogene?
p53 regulates cell survival and cell cycle progression by inducing cell cycle arrest and apoptosis for damaged DNA. When the MDM2 oncogene protein (ubiquitin ligase) targets p53, its overexpression enhances cell proliferation and survival by degrading and lowering p53 levels
What is angiogenesis and the two properties of cancer cells?
1) cancer cells secrete proteases that facilitate invasion of adjacent tissues
2) cancer cells secrete growth factors that promote the formation of new blood vessels
What is gene instability?
The driving force allowing cells to acquire the characteristics of cancer cells
What are hallmarks of cancer cells and examples?
Sustaining proliferative signaling; evading growth suppressors - alteration of intracellular signaling pathways like Ras, insensitivity to anti growth signals like Rb; activating invasion and metastasis (cause of 90% of human cancers); enabling replicative immortality - progressive loss of telomeres, lacking telomerase, and low telomerase induces chromosomal instability; inducing angiogenesis; resisting programmed cell death
What are anti cancer therapies?
- dNTP synthesis blockers
- DNA-damaging agents
- mitotic spindle disruptors
- HER2: epidermal growth factor receptor family tyrosine kinase
