Copyright (c) by W. H. Freeman and Company Chapter 24 Cancer

Copyright (c) by W. H. Freeman and Company 24.1 Benign tumors arise with great frequency but pose little risk because they are localized and small Figure 24-1

Copyright (c) by W. H. Freeman and Company 24.1 Malignant tumors generally invade surrounding tissue and spread throughout the body Figure 24-2 Alterations in cell-cell interactions and the formation of new blood vessels are associated with malignancy

Copyright (c) by W. H. Freeman and Company 24.1 DNA from tumor cells can transform normal cultured cells Figure 24-3 Cells that continue to grow when normal cells have become quiescent are said to be transformed Transformed cells may exhibit many of the properties of malignant tumor cells normaltransformed

Copyright (c) by W. H. Freeman and Company 24.1 The identification and molecular cloning of a specific DNA sequence that causes transformation Figure 24-4

Copyright (c) by W. H. Freeman and Company 24.1 Epidemiology of human cancers indicates that development of cancer requires several mutations Figure 24-5

Copyright (c) by W. H. Freeman and Company 24.1 The development of colon cancer is characterized by a well-ordered series of mutations Figure 24-6 Inherited mutations in tumor-suppressor genes increase cancer risk

Copyright (c) by W. H. Freeman and Company 24.1 Overexpression of multiple oncogenes increases tumor formation Figure 24-7

Copyright (c) by W. H. Freeman and Company 24.1 Cancers originate in proliferating cells Figure 24-8 Formation of differentiated blood cells from hematopoietic stem cells in the bone marrow

Copyright (c) by W. H. Freeman and Company 24.2 Proto-oncogenes and tumor-suppressor genes: the seven types of proteins that participate in controlling cell growth Figure 24-9

Copyright (c) by W. H. Freeman and Company 24.2 Gain-of-function mutations convert proto-oncogenes into oncogenes  Oncogenes were first identified in cancer-causing retroviruses  The Rous sarcoma virus (RSV) contains a gene (src) that is required for cancer-induction but is not required for viral function  Normal cells contain a related gene that codes for a protein-tyrosine kinase  The normal gene (c-src) is the proto-oncogene, while the viral gene (v-src) is an oncogene that codes for a constitutively active mutant protein-tyrosine kinase  Many DNA viruses also contain oncogenes but these have integral functions in viral replication

Copyright (c) by W. H. Freeman and Company 24.2 Slow-acting carcinogenic retroviruses can activate cellular proto-oncogenes Figure 24-10

Copyright (c) by W. H. Freeman and Company 24.2 Loss-of-function mutations in tumor- suppressor genes are oncogenic Figure The first tumor-suppressor gene was identified in patients with inherited retinoblastoma

Copyright (c) by W. H. Freeman and Company 24.2 Loss of heterozygosity of tumor-suppressor genes occurs by chromosome mis-segregation or mitotic recombination Figure 24-13

Copyright (c) by W. H. Freeman and Company 24.3 Virus-encoded activators of growth- factor receptors act as oncoproteins Figure 24-14

Copyright (c) by W. H. Freeman and Company 24.3 Activating mutations or overexpression of growth-factor receptors can transform cells Figure 24-15

Copyright (c) by W. H. Freeman and Company 24.3 A chimeric oncoprotein resulting from chromosomal translocation Figure 24-16

Copyright (c) by W. H. Freeman and Company 24.3 Constitutively active signal-transduction proteins are encoded by many oncogenes Figure 24-17

Copyright (c) by W. H. Freeman and Company 24.3 Inappropriate expression of nuclear transcription factors can induce transformation Figure 24-18

Copyright (c) by W. H. Freeman and Company 24.4 Passage from G 1 to S phase is controlled by proto-oncogenes and tumor-suppressor genes Figure 24-19

Copyright (c) by W. H. Freeman and Company 24.4 Loss of TGF  signaling contributes to abnormal cell proliferation and malignancy Figure 24-20

Copyright (c) by W. H. Freeman and Company 24.5 Mutations in p53 abolish G 1 checkpoint control Figure Some human carcinogens cause inactivating mutations in the p53 gene and p53 activity is also inhibited by certain proteins encoded by DNA tumor viruses

Copyright (c) by W. H. Freeman and Company 24.5 Defects in DNA-repair systems perpetuate mutations and are associated with certain cancers

Copyright (c) by W. H. Freeman and Company 24.5 Chromosomal abnormalities are common in human tumors Figure 24-22

Copyright (c) by W. H. Freeman and Company 24.5 Cancer cells may contain localized regions containing multiple copies of a given DNA sequence Figure 24-23