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

Copyright (c) by W. H. Freeman and Company

Chapter 24

Cancer


24.1 Benign tumors arise with great frequency but pose little risk because they are localized and small

Figure 24-1


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


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 transformedTransformed cells may exhibit many of the properties of malignant tumor cells

normal transformed


24.1 The identification and molecular cloning of a specific DNA sequence that causes transformation

Figure 24-4


24.1 Epidemiology of human cancers indicates that development of cancer requires several mutations

Figure 24-5


24.1 The development of colon cancer is characterized by a well-ordered series of mutations

Figure 24-6

Inherited mutations intumor-suppressor genesincrease cancer risk


24.1 Overexpression of multiple oncogenes increases tumor formation

Figure 24-7


24.1 Cancers originate in proliferating cells

Figure 24-8

Formation of differentiated blood cells from hematopoieticstem cells in the bone marrow


24.2 Proto-oncogenes and tumor-suppressor genes: the seven types of proteins that participate in controlling cell growth

Figure 24-9


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


24.2 Slow-acting carcinogenic retroviruses can activate cellular proto-oncogenes

Figure 24-10


24.2 Loss-of-function mutations in tumor-suppressor genes are oncogenic

Figure 24-12

The first tumor-suppressor gene was identified in patients with inherited retinoblastoma


24.2 Loss of heterozygosity of tumor-suppressor genes occurs by chromosome mis-segregation or mitotic recombination

Figure 24-13


24.3 Virus-encoded activators of growth-factor receptors act as oncoproteins

Figure 24-14


24.3 Activating mutations or overexpression of growth-factor receptors can transform cells

Figure 24-15


24.3 A chimeric oncoprotein resulting from chromosomal translocation

Figure 24-16


24.3 Constitutively active signal-transduction proteins are encoded by many oncogenes

Figure 24-17


24.3 Inappropriate expression of nuclear transcription factors can induce transformation

Figure 24-18


24.4 Passage from G1 to S phase is controlled by proto-oncogenes and tumor-suppressor genes

Figure 24-19


24.4 Loss of TGF signaling contributes to abnormal cell proliferation and malignancy

Figure 24-20


24.5 Mutations in p53 abolish G1 checkpoint control

Figure 24-21

Some human carcinogens cause inactivating mutations in the p53 gene andp53 activity is also inhibited by certain proteins encoded by DNA tumor viruses


24.5 Defects in DNA-repair systems perpetuate mutations and are associated with certain cancers


24.5 Chromosomal abnormalities are common in human tumors

Figure 24-22


24.5 Cancer cells may contain localized regions containing multiple copies of a given DNA sequence

Figure 24-23

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

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