Chapter 2 G enetics and Cancer. Figure 24.1 Estimated number of new cases and deaths from specific types of cancer in the United States in 1997. 2006 年台灣十大死因. 2006 年台灣主要癌症死亡率. 2006 年台灣地區主要癌症死亡原因. 男性. 女性. 資料來源 : 行政院衛生署.
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Figure 24.1 Estimated number of new cases and deaths from specific types of cancer in the United States in 1997.
Benign tumor: Tumor cells do not invade the surrounding tissues.
Malignant tumor: Cells detach from a tumor and invade the surrounding tissues, i.e. metastasis.
Carcinogens: Agents such as radiation, mutagenic chemicals, and certain types of viruses can transform normal cells into cancerous cells.
Checkpoint: A mechanism that halts progression through the cycle until a critical process such as DNA synthesis is completed, or until damaged DNA is repaired.
CDK: cyclin-dependent kinase
In tumor cells, checkpoints in the cell cycle are typically deregulated.
Figure 24.2 A schematic view of the START checkpoint in the mammalian cell cycle. Passage through the checkpoint depends on the activity of the cyclinD/CDK4 protein complex.
Oncogene:Gene that causes cancer is called oncogene
Cellular homologues of viral oncogenes: The proto-oncogenes (c-onc)
Figure 24.3 Structures of the v-src and c-src genes
- v-onc produces much more protein - v-onc genes express at inappropriate times
- v-onc genes express mutant forms of the proteins
Figure 24.4 The transfection test to identify DNA sequences capable of transforming normal cells into cancer cells.
Dr. Robert Weinberg
(b) Oncogenic Ras protein signaling
Figure 24.5 Ras protein signaling and cancer
bcr/c-abl fusion protein: constitutively activated c-abl tyrosine kinase function
Figure 24.6 The reciprocal translocation involved in the Philadelphia chromosome associated with chronic myelogenous leukemia (CML).
Figure 24.7 A reciprocal translocation involved in Burkitt’s lymphoma. Immunoglobulins in B cell: H (chromo. 14), l (chromo. 22), k (chromo. 2)
Figure 24.8 Knudson’s two-hit hypothesis to explain the occurrence of inherited and sporadic cases of retinoblastoma. Two inactivating mutations are required to eliminate the function of the RB gene.
Homozygous or hemizygous for the RB- alleles (recessive mutation)
Figure 24.9 Role of pRB in progression of the cell cycle.
Damage to the DNA induces an increase in the abundance of p53
Cell-cycle Arrest Pathway
Figure 24.10 (a) Principal domains within p53. (b) Role of p53 in cellular response to DNA damage.
TAD, transcription activation domain
DBD, DNA binding domain
OD, homo-oligomerization domain
Figure 24.11 (a) Principal domains within pAPC. (b) Role of pAPC in cell-cycle control.
Autosomal dominant disease, familial adenomatous polyposis (FAP)
APC adenomatous polyposis coli
Androgen- independent prostate cancer
Figure 24.12 Genetic pathways to cancer.