Cancer genetics Flashcards
What is cancer?
(aka tumour/neoplasia) is a genetic disease => accumulation of mutations => Uncontrolled growth abnormal cells
What is the difference between a benign and malignant tumor?
Benign: non-invasive & localised
Malignant: invasive & can metastasis
What does cancer metastasis mean?
Cancer (tumour) which can move/spread away from 1º site and invade another (2º) site
What is a tumor suppressor gene? How does it work?
Are genes which inhibit cells w/ mutations from becoming cancerous by:
- stopping proliferation to allow DNA repair mechanisms to fix mutated DNA (if damage is small)
- inducing apoptosis if damage is large
Which part/s of the cell cycle are critical checkpoints for cancer? (3)
- G1/S checkpoint: allow time to repair damage
- S-phase: delay replication to “ “ “ “ “
- G2/M: (same as G1/S)
What are the internal and external factors that can cause cancer?
- Int.: Faults in DNA repair mechan.; inherited mutation; epigenetic factors
- Ext.: Chem. mutagens; radiation; Infection (e.g. viral)
Differentiate between a proto-oncogene and an oncogene?
- Proto-: genes which are responsible for normal cellular functions (e.g. produce a protein/hormone)
- Oncogene: mutated genes => overexpress proteins = loss of growth control => development of cancer (e.g. upregulation of protein/hormone)
What is a c-onc? What is a v-onc?
C-onc: cellular oncogene- means the mutated gene remains in cell’s DNA
V-onc: refers to the mutated gene being incorporated in the virus
How did scientists discover what caused cancer?
(Peyton) Rous injected cell-free extracts of tumour to healthy chicken -> developed cancer
=> cancer transmitted by virus (carried cancer gene)
- Three ways an RNA tumor virus can cause cancer.
- virus integrates RNA (tumour) in host cell’s chromo. (provirus) & replicates
- 3.
*Differentiate between a DNA tumor virus and an RNA tumor virus.
DNA: DNA (genome) in virus
RNA: RNA (genome) in virus
directly causing cancer
*How do DNA viruses cause cancer?
- Replication of viral genome in the host’s nucleus
- Transcribe genes
- cell down-regulates apoptosis & proliferate = cancer
*Which point mutation causes a proto-oncogene to become an oncogene for KRAS? What affect does this mutation have?
Substitution (missense mutation) => change AA = change structure & function of protein
How p53 is activated, and the effect this has.
- defects in repair
- damage in DNA-damage checkpoint
=> p53 protein activated => introduce apoptosis
How p53 is inactivated, and the effect this has.
Both copies in the segments of 2 chromo. are missing (homozygous) => cancer cells proliferate
How does retinoblastoma (RB) protein regulate the cell cycle? At which part of the cell cycle does this occur?
“regulates cell proliferation by restricting cell cycle progression at… G1” *(cite)
What causes sporadic retinoblastomas?
2 separate mutations need to be introduced in the same gene of 2 chromo. (homozygous)
*What is apoptosis? Which cellular processes are involved?
is programmed cell death. Cellular processes involved*
Which enzymes cause apoptosis?
RB & p53 proteins
What are the 2 tumour-associated antigens?
- Tumour-specific: only tumour cells have antigen bc overexpressed (silenced in normal cells)
- Tiss. differentiation: both normal & tumour tissue have it but it’s over exbressed in tumour cells
What does p53 do?
translation factor > activates expression of proteins for cell regulation & apoptosis
