Oncogenic Viruses

Question 1

features of human cancer cells

Answer 1

make tumors if transplanted to animals, undifferentiated, immortal, not contact inhibited, resistant to apoptosis, abnormal chromosomes. all of these features can be induced experimentally by viruses

Question 2

myc

Answer 2

transcription factor

Question 3

src

Answer 3

membrane signalling of growth factor binding

Question 4

ras

Answer 4

signal transduction from surface receptors

Question 5

sis

Answer 5

platelet-derived growth factor

Question 6

erb B and fms

Answer 6

growth factor receptor

Question 7

LMO2

Answer 7

hematopoiesis

Question 8

what does inactivation of P53 or Rb allow cells to do?

Answer 8

proliferate and accumulate other mutations

Question 9

how are oncogenes overexpressed in some human cancers?

Answer 9

amplification, mutation, or translocation

Question 10

P53 is often mutated in what cancers?

Answer 10

breast, bladder, prostate, liver, lung, skin, colon

Question 11

cell transformation by RNA and DNA viruses

Answer 11

RNA viruses carry activated oncogenes, or insert their promoter and activate an oncogene. DNA oncogenic viruses degrade cell cycle genes

Question 12

what does T antigen do?

Answer 12

allows cells to proliferate without control. it has to be expressed continually for tumors to grow

Question 13

E1A and E1B

Answer 13

analogous to T antigen and are always expressed in transformed cells

Question 14

only example of non-species specificity

Answer 14

gene therapy viruses can have side effects. mouse leukemia virus modified to transduce stem cells. cured cases, but 4/9 developed T cell leukemia due to insertion of virus adjacent to LMO2 oncogene.

Question 15

oncogenes may have which function in normal cells?

Answer 15

surface receptors for growth factors

Question 16

human papilloma viruses

Answer 16

related to the SV40 virus. over 100 types. Low risk: 4,6,8 give warts. Intermediate: 11 gives laryngeal papillomas. High risk: 16,18 give cervical and pharyngeal cancer

Question 17

E6 and E7 in HPV

Answer 17

E6 binds p53 and leads to degradation through the ubiquitination pathway. E7 binds non-phosphorylated Rb, and prevents its interaction with E2F. transfection of cells with E6 and E7 leads to immortalization. co-transfection with mutated ras leads to transformation.

Question 18

E2 in HPV

Answer 18

E2 normally suppresses E6 and E7. loss of E2 function due to integration allows overexpression of E6 and E7

Question 19

Epstein-Barr virus

Answer 19

in western world this causes mononucleosis. in-vitro can transform human B cells. prevalent in africa and asia

Question 20

Burkitt’s lymphoma

Answer 20

endemic in african malaria belt. affects pre-pubertal boys. maxilla most common site. contains EBV and expresses genes continually

Question 21

naso-pharyngeal cancer

Answer 21

endemic in south china, vietnam, arctic eskimos. contains EBV and expresses genes continually. environmental co-factors involved. IgA antibodies to EBV capsid antigen predicts tumors or recurrences

Question 22

pathogenesis of EBV-related lymphomas

Answer 22

translocation allows for overexpression of Myc gene, causing cancer

Question 23

B-cell lymphomas in the western world

Answer 23

most b cell lymphomas are EBV negative. in rare cases, EBV is present and some genes expressed. seen in patients with AIDs or long term immunosupporession (SCID or graft recopients. may regress if immune function is restored

Question 24

hepatitis B virus

Answer 24

liver cancer incidence is higher in countries with endemic HBV infection. HBV is a risk factor for cancer. prospective studies show greater risk with cirrhosis of liver, or high level expression of viral genes.

Question 25

pathogenesis of HBV liver cancer association

Answer 25

tumor cells contain integrated HBV but no consistent expression of any viral protein in cancer cells. no activation of cellular oncogene.

Question 26

effect of Hep B virus vaccine

Answer 26

universal immunization of babies in taiwan has led to 50% reduction in incidence of hepatocellular carcinoma in adolescents. eliminated in alaska!

Question 27

human T cell leukemia virus prevalence

Answer 27

africa and south america

Question 28

HTLV-1 pathogenesis

Answer 28

1/20 people get T cell leukemia after many years. HTLV-1 is integrated into genome of all leukemic cells. tax experssion declines, but HBZ persists. genetic changes accumulate

Question 29

kaposi’s sarcoma herpes virus prevalence

Answer 29

africa