Scientific basis of cancer

Question 1

examples of tumour suppressor genes?

Answer 1

p53-cell cycle regulation
APC-cell adhesion
Rb-cell cycle regulation-retinoblastoma and osteosarcoma
BRCA 1 and 2-DNA repair and maintenance
MLH1, MSH2-DNA repair and maintenance, mutations cause HNPCC.

Question 2

which cancers can anti-HER2 drugs be used in the treatment of?

Answer 2

breast cancer

gastric cancer

Question 3

what alterations in growth control occur to allow cancer development?

Answer 3

increased cell proliferation-can grow indefinitely with telomerase activation allowing DNA to continue to be added to telomeres so prevents telomere shortening with each cell cycle that would eventually restrict number of cell cycles. cells can become resistant to anti-growth signals e.g. cyclin dependent kinase inhibitors.
reduced cell death-resistant to apoptosis e.g. gene translocation of bcl-2 gene that normally inhibits apoptosis.
altered GFs/hormones and receptors-VEGF-allow tumour blood supply, HER2 gene amplification-encodes for a growth factor receptor, allowing self-sufficient growth.
altered cell to cell interactions-malignant cell receptor loss causes disorganised cytoskeleton disrupting normal cell to cell interactions that inhibit motility so cells can spread e.g. lack E-cadherin.

Question 4

name for cells with no resemblance to any tissue?

Answer 4

anaplastic

Question 5

role of TSGs in cancer?

Answer 5

normally act as cell cycle brakes, slowing cell proliferation
germline mutations behave as autosomal dominant familial cancer predispositions, with requirement of loss of both functional alleles to support a cancer (need a 2nd hit)
unlike oncogenes where 1 mutant allele is sufficient.