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    Biologi Kanker

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    Norsarida Aryani
    This document discusses the biology of cancer. It begins by defining cancer as abnormal cell growth or neoplasia that can be malignant and involve rapid growth, invasion, and metastasis. It then lists some of the hallmarks of cancer, including mutated oncogenes that promote cell growth and mutated tumor suppressor genes that normally control cell growth. Examples provided are the retinoblastoma gene RB1 and the p53 gene, both of which are tumor suppressors. The document also discusses mutagens like viruses and chemicals that can cause mutations, as well as oncogenes and their role in cancer development.

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    Biologi Kanker

    Uploaded by

    Norsarida Aryani
    25 views45 pages
    This document discusses the biology of cancer. It begins by defining cancer as abnormal cell growth or neoplasia that can be malignant and involve rapid growth, invasion, and metastasis. It then lists some of the hallmarks of cancer, including mutated oncogenes that promote cell growth and mutated tumor suppressor genes that normally control cell growth. Examples provided are the retinoblastoma gene RB1 and the p53 gene, both of which are tumor suppressors. The document also discusses mutagens like viruses and chemicals that can cause mutations, as well as oncogenes and their role in cancer development.

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    This document discusses the biology of cancer. It begins by defining cancer as abnormal cell growth or neoplasia that can be malignant and involve rapid growth, invasion, and metastasis. It then lists some of the hallmarks of cancer, including mutated oncogenes that promote cell growth and mutated tumor suppressor genes that normally control cell growth. Examples provided are the retinoblastoma gene RB1 and the p53 gene, both of which are tumor suppressors. The document also discusses mutagens like viruses and chemicals that can cause mutations, as well as oncogenes and their role in cancer development.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    25 views45 pages

    Biologi Kanker

    Uploaded by

    Norsarida Aryani
    This document discusses the biology of cancer. It begins by defining cancer as abnormal cell growth or neoplasia that can be malignant and involve rapid growth, invasion, and metastasis. It then lists some of the hallmarks of cancer, including mutated oncogenes that promote cell growth and mutated tumor suppressor genes that normally control cell growth. Examples provided are the retinoblastoma gene RB1 and the p53 gene, both of which are tumor suppressors. The document also discusses mutagens like viruses and chemicals that can cause mutations, as well as oncogenes and their role in cancer development.

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    Biology of Cancer

    A.M. FORENTIN., M.SI., APT.


    What is cancer?
    Abnormal cell growth (neoplasia)
    Malignant as opposed to benign
    ◦ Benign: slow growth, non-invasive, no metastasis
    ◦ Malignant: rapid growth, invasive, potential for metastasis
    Hallmarks of cancer
    What types of genes get mutated in cancer?

    Oncogenes are activated


    ◦ Normal function: cell growth, gene transcription
    Tumor suppressor genes are inactivated
    ◦ Normal function: DNA repair, cell cycle control, cell death

    Mutator Genes
    ◦ Genes whose products ensure accurate DNA replication and DNA repair
    Mutagens
    Viruses: insertional mutagenesis

    Chemicals: DNA adducts

    UV and ionizing radiation: single and


    double strand DNA breaks
    Oncogenes
    All are involved in positive control of cell growth and division.
    ◦ About 100 different oncogenes have been identified

    Can be various kinds of proteins:


    ◦ Growth factors, regulatory genes involved in the control of cell multiplication.
    ◦ Protein kinases, add phosphate groups to target proteins, important in signal transduction
    pathways.

    “Proto-oncogenes”
    ◦ Normal form of the gene that is involved in positive regulation of the cell cycle
    Oncogenes
    A few cancer syndromes are caused by inherited mutations of proto-oncogenes that cause the
    oncogene to be turned on (activated). But most cancer-causing mutations involving oncogenes
    are acquired, not inherited.

    They generally activate oncogenes by:

    o Chromosome rearrangements: Changes in chromosomes that put one gene next to another,
    which allows one gene to activate the other

    o Gene duplication: Having extra copies of a gene, which can lead to it making too much of a
    certain protein
    Tumor suppressors

    • “Guardian(s) of the genome”


    • Often involved in maintaining genomic integrity (DNA repair,
    chromosome segregation)
    • Mutations in tumor suppressor genes lead to the “mutator
    phenotype”—mutation rates increase
    Tumor Suppressor Genes
    Normally inhibit cell growth
    Example: retinoblastoma
    ◦ RB protein normally blocks a
    transcription factor, E2F
    Rb—a classic tumor suppressor

    • Rb binds to a protein called E2F1


    • E2F1 initiates the G1/S cell cycle transition
    • When bound to Rb, E2F1 can't function
    • Thus, Rb is a crucial cell cycle checkpoint
    RB1
    • RB1 gene provides instructions for making a protein called pRB.
    • RB1 is a tumor suppressor gene, which means that it normally
    regulates cell growth and stops cells from dividing too rapidly or in an
    uncontrolled way.
    • Mutations in the RB1 gene are responsible for most cases
    of retinoblastoma

    https://ghr.nlm.nih.gov/condition/retinoblastoma
    A small percentage of retinoblastomas are caused by deletions in the region of
    chromosome 13 that contains the RB1 gene
    p53—a classic tumor suppressor

    • “The guardian angel of the genome”


    • Senses genomic damage
    • Halts the cell cycle and initiates DNA
    repair
    • If the DNA is irreparable, p53 will initiate
    the cell death process
    p53 Gene
    Detects DNA damage
    The “Last Gatekeeper”
    ◦ Involved in 50% of cancers
    ◦ Often not malignant despite other cancer-causing mutations until p53 is
    inactivated by mutation.
    Two possible responses to DNA damage:
    ◦ 1) Acts as a Transcription Factor to activate expression of p21, which inhibits
    CDK/G1 cyclin to halt the cell cycle; then activates DNA repair.
    ◦ 2) Triggers Apoptosis (programmed cell death) if damage can’t be repaied.
    Apoptosis pathways

    http://www.cell-research.com/20014/20014cover.htm

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