1. Chapter 17: Regulation of cell number
[omit material on cell cycle regulation, apoptosis, cell signalling
(pp ) – covered in BIO 315]
Cell number is regulated by two primary systems:
Cell cycle control
Apoptosis control
Fig. 17-1

3. Cancer: malignant tumor; clone of cells that have
lost normal cell growth regulation
- result from sequential mutations in
genes that regulate cell growth
Oncogene: dominant, gain-of-function mutation
causes cancer
- originally identified in tumor viruses which
transduce the gene into cells (e.g., v-ras)
- correspond to normal genes that regulate
cell growth in cells (e.g., c-ras)

5. Ras oncogene is a mutant form of the normal Ras gene
Fig
(regulated cell proliferation)

6. Ras oncogene is a mutant form of the normal Ras gene
mutation
Fig
Fig
(regulated cell proliferation)
(constitutive cell proliferation→tumor)

7. Ras oncogene is a mutant form of the normal Ras gene
mutation
Fig
Fig
(regulated cell proliferation)
(constitutive cell proliferation→tumor)

8. The v-erB oncogene is a truncated EGF receptor gene
Fig

9. The v-erB oncogene is a truncated EGF receptor gene
Fig

10. Chronic myelogenous leukemia is caused by reciprocal translocation
known as the “Philadelphia chromosome
(regulated protein tyrosine kinase)
Fig

11. Chronic myelogenous leukemia is caused by reciprocal translocation
known as the “Philadelphia chromosome
(unregulated protein tyrosine kinase → unregulated cell proliferation)
Why is this translocation
not inherited?
Why is proliferation limited
to leukocytes?
Fig

12. Tumor-suppressor genes: wild-type alleles
negatively regulate cell growth or
positively regulate cell death
- cancer-causing alleles are usually
recessive, loss-of-function mutations
- cell must be homozygous for the
mutation to exhibit a tumor phenotype
- alleles can be inherited; homozygosity
arises by somatic mutation or mitotic
crossingover

13. The Rb protein is an E2F tethering protein
required for cell cycle regulation
Loss of Rb results in constitutive E2F activation → unregulated cell proliferation
Fig. 17-4

14. Fig

15. Fig

16. Recommended problems in Chapter 17: 8, 9, 11, 12, 22

17. Fig. 17-