Molecular Oncology

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Molecular Oncology by Mind Map: Molecular Oncology

1. Transforming Genes

1.1. Oncogenes

1.1.1. protooncotype

1.1.1.1. precursor then ACT

1.1.2. promote cell proliferation

1.1.3. gatekeeper genes

1.1.3.1. apoptosis

1.1.4. Activation

1.1.4.1. Mutation

1.1.4.1.1. Point mutation

1.1.4.1.2. deletion

1.1.4.1.3. somatic > germ line

1.1.4.2. Chromosomal Translocations

1.1.4.3. Gene Amplification

1.1.5. MOA

1.1.5.1. classified as biochemical roles

1.1.5.1.1. Growth factors

1.1.5.1.2. Cell surface receptors

1.1.5.1.3. IC signal transduction

1.1.5.1.4. Transcription Fx

1.1.5.1.5. Cell cycle proteins

1.1.5.1.6. inhibitors of Apoptosis

1.1.6. 1/2 alleles must be altered

1.2. Tumor Suppresor Genes

1.2.1. Mutation

1.2.1.1. negative regulatory control of cell growth

1.2.1.2. suprressing cell proilferation

1.2.1.3. both alleles must be altered

1.2.1.3.1. heterozygous alleles

1.2.1.3.2. loss of heterzygosity

1.2.1.4. Example

1.2.1.4.1. Retinoblastoma Gene (13)

1.2.1.4.2. P53 (17)

1.2.1.4.3. WT01

1.2.1.4.4. NF-1

1.2.1.4.5. VHL

1.2.1.4.6. BRCA 1/2

1.2.1.4.7. PTEN

1.2.1.4.8. APC

1.3. Mutator Genes

1.3.1. DNA repair genes

1.3.2. caretaker genes

1.3.3. DNA mismatch repair

1.3.4. mutation

1.3.4.1. DNA susceptible

1.3.4.2. accumulation of mutations

2. Hereditary Forms

2.1. Germ line mutations

2.2. 1% of cancer

2.3. involve

2.3.1. Tumor suppressor genes

2.3.2. DNA repair genes

2.3.3. Examples

2.3.3.1. Retinoblastoma

2.3.3.2. endocrine tumors

2.3.3.3. colo-rectal tumors

2.3.3.3.1. non-polyposis colon cancer

2.3.3.4. xeroderma pigmentosum

2.3.3.5. breast cancer

2.3.3.5.1. BRCA 1/2

3. Viruses & Human Cancer

3.1. 14% due to secondaru mfectopm

3.2. HTLV I

3.2.1. T cell Leukemia

3.3. HPV

3.3.1. Uterine cancer

3.3.2. cervical cancer

3.4. Hepatitis B virus

3.4.1. hepatocellular carcinoma

3.5. EBV

3.5.1. burkitt lymphoma

3.5.2. nasopharyngeal carcinoma

3.6. Human Herpes Virus

3.6.1. kaposi sarcoma

3.6.2. body cavity based lymphoma

4. Epigenetics

4.1. Methlylation

4.1.1. promoter gene

4.1.1.1. supresss transcription

4.1.1.2. maintains gene silencing

4.1.2. hypermethylation

4.1.2.1. enhanced transcription

4.2. Telomeres

4.2.1. shorten w age

4.2.1.1. lose replication act

4.2.2. telomerase

4.2.2.1. prevents shortening

4.2.2.1.1. not active in somatic cells

4.2.2.1.2. 90% tumors

5. Tumor Progression

5.1. > 1 genetic alteration needed

5.2. Colon Cancer

5.2.1. Deletion of tumor suppressor gene (APC)

5.2.1.1. benign neoplasm

5.2.1.1.1. genetic alterations

5.2.1.2. colonic adenomatous polyp

5.3. Summary

6. Future Developments

6.1. oligonucleotide micro arrays

6.1.1. improve diagnosis

6.1.2. info on DNA, RNA, protein

6.2. pathologic exam + molecular data

6.2.1. diagnosis

6.2.2. pronosis

6.2.3. therapy

6.3. Recurrence

6.3.1. reexamine

6.3.1.1. molecular evolotion

6.3.1.2. targeted therapies

7. General Concepts

7.1. Stages

7.1.1. Clonal Process

7.1.2. Period of Silent Growth

7.1.3. Cell proliferation

7.1.3.1. Rapid

7.1.3.2. Slow

7.1.3.2.1. defective apoptosis

7.2. Factors

7.2.1. Cells produced > Die

7.2.1.1. secondary to mutations

7.2.1.1.1. control ceel growth

7.2.1.1.2. differntiation

7.2.1.1.3. apoptosis

7.2.1.1.4. defect in DNA replication

7.2.2. Mutations > 4-7 genes

7.2.2.1. multistep process

7.2.3. Transforming Genes