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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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Chapter 2 G enetics and Cancer

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Chapter 2 g enetics and cancer

Chapter 2 Genetics and Cancer


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.


Chapter 2 g enetics and cancer

2006年台灣十大死因


Chapter 2 g enetics and cancer

2006年台灣主要癌症死亡率


Chapter 2 g enetics and cancer

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


Chapter 2 g enetics and cancer

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.


Chapter 2 g enetics and cancer

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.

Mid-G1 phase

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.


Chapter 2 g enetics and cancer

Cancer is caused by genetic malfunctions

  • The cancerous state is clonally inherited. The cancerous condition is transmitted from each cell to its daughters at the time of cell division.

  • Certain types of viruses can induce the formation of tumors in experimental animal, indicating that viral genes are involved in the transformation process.

  • Cancers can be induced by mutagenic agents that cause mutations of genes.

  • Certain types of cancer tend to run in families, e.g. retinoblastoma and colon cancers.

  • Certain type of leukemias and lymphomas are associated with particular chromosomal aberrations.


Chapter 2 g enetics and cancer

Tumor-Inducing Retroviruses and Viral Oncogenes

  • Rous sarcoma virus

  • The first tumor-Inducing retroviruses

  • Discovered in 1910 by Dr. Peyton Rous

  • Caused sarcoma in the connective tissue of chicken

  • Encode four gene, gag (capsid protein), pol (reverse transcriptase), env (envelope), and v-src (protein kinase)

  • V-src is a oncogene that responsible for the virus’s ability to form tumors

Oncogene:Gene that causes cancer is called oncogene


Chapter 2 g enetics and cancer

Viral oncogene (v-onc)


Chapter 2 g enetics and cancer

Single exon

Cellular homologues of viral oncogenes: The proto-oncogenes (c-onc)

Figure 24.3 Structures of the v-src and c-src genes


Chapter 2 g enetics and cancer

Why do v-oncs induce tumors, whereas normal c-oncs do not?

- v-onc produces much more protein - v-onc genes express at inappropriate times

p707

- v-onc genes express mutant forms of the proteins


Chapter 2 g enetics and cancer

Figure 24.4 The transfection test to identify DNA sequences capable of transforming normal cells into cancer cells.

Dr. Robert Weinberg

c-H-ras oncogene


Chapter 2 g enetics and cancer

(a) Normal Ras protein signaling

Dominant activator

(b) Oncogenic Ras protein signaling

Figure 24.5 Ras protein signaling and cancer


Chapter 2 g enetics 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).


Chapter 2 g enetics and cancer

Figure 24.7 A reciprocal translocation involved in Burkitt’s lymphoma. Immunoglobulins in B cell: H (chromo. 14), l (chromo. 22), k (chromo. 2)


Chapter 2 g enetics and cancer

Tumor Suppressor Genes


Chapter 2 g enetics and cancer

Knudson’s Two-Hit Hypothesis

Non-inherited

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.


Chapter 2 g enetics and cancer

The Retinoblastoma Tumor-Suppressor Gene

Dominant

inheritance

Somatic divisions

Homozygous or hemizygous for the RB- alleles (recessive mutation)


Chapter 2 g enetics and cancer

Inherited Cancer Syndromes


Chapter 2 g enetics and cancer

Early G1

Late G1

S

M

Figure 24.9 Role of pRB in progression of the cell cycle.


Chapter 2 g enetics and cancer

dominant

DBD

OD

TAD

recessive

Damage to the DNA induces an increase in the abundance of p53

Cell-cycle Arrest Pathway

Apoptotic Pathway

Cell death

Cell-cycle arrest

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


Chapter 2 g enetics and cancer

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


Chapter 2 g enetics and cancer

Metastatic colorectal cancer

Androgen- independent prostate cancer

Glioblastoma

Figure 24.12 Genetic pathways to cancer.


Chapter 2 g enetics and cancer

Six hallmarks of the pathways leading to malignant cancer

  • Cancer cells acquire self-sufficiency in the signaling processes that stimulate division and growth.

  • Cancer cells are abnormally insensitive to signals that inhibit growth.

  • 3. Cancer cells can evade programmed cell death.

  • 4. Cancer cells acquire limitless replicative potential.

  • 5. Cancer cells develop ways to nourish themselves.

  • 6. Cancer cells acquire the ability to invade other tissues and colonize them.

Pages 704-705


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