Cancer Flashcards
common hallmarks of cancer growth:
- altered homeostasis
- bypass of limits to cell proliferation
- evasion of cell death signals
- altered cellular metabolism
- ??? of tissue environment
- metastasis
manipulation of tissue environment e.g. angiogenesis
what are the two fundamental properties shared by cancer cells?
uncontrolled proliferation
metastasis
when is a tumour considered malignant?
when its cells break loose and travel to other tissues and organs (metastasis)
nomenclature of cancer is dependant on site of origin e.g sarcoma for ???
connective tissue
TRUE or FALSE: viruses such as DNA and RNA tumour viruses introduce foreign genetic material that can cause cancer E.g. human papilloma virus (cervical cancer)
TRUE
what are two examples of inherited mutations?
- colon cancer (tumour suppressor gene)
- Retinoblastoma (deletion of 13q gene)
What is the largest risk factor of cancer?
age
tumour progression: Mutant cells are ??? over their neighbouring, normal cells
selectively favoured
most commonly affected organs include: liver, lung, bone, ???
brain
Key phenotypic features are shared by benign and malignant tumour cells
- Nuclear alterations
- Altered morphology & disorganised growth
patterns
- ??? cells
Immortal
Nuclear alterations: aneuploidy due to defect in ??? checkpoint
mitotic spindle
altered morphology and disorganised growth: cancer cell proliferation is ??? and insensitive to population density
anchorage-independent
TRUE or FALSE: Normal cells do not grow well in culture without a solid
surface to attach to and stop dividing when they become confluent
True
Only those tumours containing cells that maintain their ??? length will be capable of unlimited growth i.e immortality cells
telomere
Any cell appearing within tumours that expresses ??? will have a tremendous growth advantage over cells that lack it. Over time, ???-containing cells will flourish, while those lacking it will die off until all of the cells in the tumour contain telomerase
telomerase
progression factors are the cellular alterations that lead to a malignant tumour being able to ???
metastasise
progression factors: invasive capacity or angiogenesis describes the following:
- Enhanced expression of tissue degrading proteases
- Epithelial-Mesenchymal Transition (EMT)
- together = enhanced motility
invasive capacity
progression factors: invasive capacity or angiogenesis describes the following:
- formation of new blood vessels
angiogenesis
Enhanced expression of proteases allows invasive properties of tumours:
1. Cleavage of cell surface proteins
2. Allows ??? breakdown
3. Activates growth factors or cytokines
ECM
what represents an initial step in the metastatic cascade that is necassary for cells to move from primary organ of origin to other sites?
motility of tumours
the metastatic cascade:
1. Dysplasia
2. Formation of primary tumour
3. Epithelial Mesenchymal Transition
4. Intravasation
5. ???
6. Arrest at new site
7. Extravasation
8. Mesenchymal Epithelial Transition
9. Micrometastasis
10. Macrometastasis
Circulation
oncogenes are GAIN or LOSS of function genes?
gain of function: protein gains new/altered activity
oncogenes act dominantly or recessively?
dominantly
Proto-oncogenes encode ??? factors that stimulate expression of other genes – involved in cell division or cell cycle. Protooncogenes normally regulate cell growth. Mutated/cancer causing proto-oncogenes = oncogenes
transcription
Tumour suppressor genes – normal genes that slow down cell division, repair mistakes, and regulate ???
apoptosis
Tumour suppressor genes are generally loss or gain (?) of function mutations
loss
When ??? are mutated or inactivated, the cell is unable to respond to cell cycle checkpoint or unable to undergo programmed cell death
tumour suppressor genes
oncogenes or tumour suppressor genes are a recessive cancer phenotype = both alleles of tumour suppressor gene affected to cause cancer
tumour suppressor genes
Bcl2/Bax genes control ???
apoptosis
single point mutation: a hyperactive ??? gene (a product of an oncogene) issues signals of its own = increased cell proliferation
ras gene
~25% of breast and ovarian cancers have amplified copies of the ERBB2 gene (HER2) Extra copies of this growth factor receptor causes ???
excessive cell proliferation
In Burkitt lymphoma, protooncogene MYC is moved from chr 8 next to a highly active region of ??? = enhanced transcription of MYC. c-MYC leads to increased expression of genes involved in cell proliferation
chr 14
When all or part of a chromosome
containing the normal allele of the
gene is deleted, chances of cancer
are increased. Known as ???
loss of heterozygosity
Alteration of RB which iS AN ONCOGENE OR TUMOUR SUPPRESSOR GENE (?) affects the
control of cell growth- Normally mediates transcription of enzymes and proteins required for S phase
TUMOUR SUPPRESSOR GENE
p53 tumour suppressor is the most
frequently mutated gene in human
cancers. DNA damage stimulates the p53 pathway, which triggers cell cycle ??? and ???. p53 gene disruption leads to a failure in these responses following DNA
damage = survival and reproduction of mutated cells
arrest and apoptosis
A mutation/deletion in both alleles of p53 allows damaged DNA to
enter the cell cycle. Consequence is either ??? & death or survival potentially leading to a tumour
mitotic failure
Epigenetic changes in gene expression refers to changes in ???
gene expression not related to changes in base sequence
