exam 3 - cancer 1 Flashcards

1
Q

What are the characteristics of cancers cells?

A
  • Two heirtable properties
    • 1 .) Reproduce in defience of normal retriants on cell divisions and cell growth
    • 2.) invade areas normally reserved for other cells
  • Cancer cells (decontrolled proliferation)
    • more selfsufficent
      • dont need signals to grow
        • grow via little autocrine growth factor signals
      • ignore anti-growth signals and apoptosis signals
        • defective in cell cycle control mechanisms
    • gets help form stromal cells
    • induces angiogenesis
    • invasive to other tissues
    • Does NOT show Replicative sensece (stops dividing after a # of divisons ) but ARE IMMORTAL
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2
Q

How do benig tumors relate to malignate tumors

A
  • Tumors
    • when an abnormal cell grows and proliferates out of control and fibes rise to a neoplastic growth called a tumor
  • Benign Tumors
    • When a tumor has not become invasive and can be surgically removed
    • Benign tumor presence DOES NOT mean cancer
  • Malignant tumors
    • Tumor is considered cancer when it is malignant (if cells have the ability to invade surround tissues
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3
Q

WHat is Metastases ?

A
  • Invasiveness of cancer
  • cancer cells can break loose, enter into blood orlymph , travel to new areas and formed secondary tumors
  • Cant be eradicated by surgery or irradiation
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4
Q

how do tumors develope?

A
  • Involves multiple mutational events
  • all tumors from single ancestor
  • confer a proliferative advantage
  • mutations allow cells to grow more rapidly than normal
  • Tumors evolve form benign growth o invasive cancers and ultimately metastatic
  • represents tumor progression
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5
Q

How does tumor development occur in colon cancer?

A
  • cells with APC mutation gain advantage in growth
    • Tumor suppressor
  • form polyps
    • at this point still benign
  • Mutation in RAS which becomes a cancer gene
  • Loss of other tumor suppressor - lose p53
    • carcinoma (epithelial cells)
  • Rumor moves out into blood stream
  • gains capacity to invade
  • becomes malignant tumor
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6
Q

What is the Philadelphia Chromosome?

A
  • It is mutation that results form the translocation between Chr 9 + 22
  • Responsible for chronic myeogenous leukemia
  • all cancers cells have the same chromosomal aberration
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7
Q

What are the causes of cancers?

A
  • Carcinogenesis is linked to mutagenesis (mutant change of DNA)
    • two types carcinogens: Chemical carcinogens and radiation (xrays, UV)
    • carcinogens can be detected via ames test and look for bacteria dependent histadine growth
    • Tobacco is most important environmental factor to cause cancer
  • Virsus and infections are linked to cancer
    • AIDS: HIV - human immunodeficiency virus causes kaposi sarcoma
    • Ulcers and Helicobacter pylori can cause stomach cancer
    • Virus that hijacks c-src ( gene for cellgrowth and prloferation) will cause over expression froma storng viral promoter or cause protooncogene into an oncogene
  • Can be cause by either increased in cell divison or a decrease in apoptois
    • a loss of programmed cell death or DNA repair causes a build up of mutations then leads to cancer
  • Diets high fat/low fiber: accounts for 37% of bowel,pacreas, prostate, and breast cancer
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8
Q

How does tumor progression occur in the cervix?

A
  • cervical cancer occurs in the cervix which is made out of stratified epithelia
  • cell proliferation begins in basal epithelia
  • Low grade and high grade intraepithelial neoplasia
    • Can be removed at this stage
  • It can develope into a cacinoma when the cells move through basal lamina and invade surrounding tissues and can enter blood
  • BEst weapon we have agains cancer is early detection
    • in this case a pap smear (scaping cells off of cervix)
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9
Q

What is the difference between Angiogenesis and Neovascularization?

A
  • Angiogensis
    • is the formtion of new blood vessels that are sprouted from old vessels
      • tumors mmust get oxygen and nutrients like normal cells
      • relase factor to induce new blood vessel formation
  • NEovascularization
    • is the formation of new blood vesels basically from scratch or on the spot
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10
Q

What are Oncogenes

A
  • Overactivity mutation that causes a gain in function = ONCOGENES
  • onvolves a snigle mutation event and activation of gene proliferation (dominant)

Remember ONCO genes = GAIN of FUNCTION

A single copy of a mutation in the proto-oncogene converts and has a dominant effect

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11
Q

What are Tumor Supressor Genes?

A
  • Underativity mutations: Loss of function - tumor repressor genes involve genes that inhibit growth. Mutation event: one gene - no effect ; second mutation causes probelms (recessive)

TUMOR REPRESSORS GENES = LOSS OF FUNCTION

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12
Q

What is the difference between oncogenes and tumor repressor genes?

A
  • Oncogenes
    • overactivity mutations
    • gain of function
    • invovles single mutation event and activation of gene causing proliferation
  • Tumor Supression genes
    • underactivity mutations
    • loss of function
    • involves geens that inhibit growth
    • mutattionevnet
      • one gene = no affect
      • two genes = 2 affects
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13
Q

How do mutations in DNA maintenance genes work?

A
  • Subset of tumor supressors genes
  • mutations invovle inactivation of caretaker genes that create geneomic stability
  • include DNA repair genes, Checkpoint genes
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14
Q

What are two ways inwhich protoonco genes are converted into oncogenes?

A
  • Deletion or point mutation in coding sequence
    • hyperactive protein made in normal amounts
  • Regulatory mutation (promotor mutation)
    • normal protein greatly overproduced
  • gene amplification
    • normal protein greatly overprodice
      • ( several copies instead on 1 )
  • chromsome rearrangement
    • Nearby regulatory DNA sequences cayses normal protein to be overproduced
    • Fusion to actively transcribed gene produces hyperactive fusion protein

Fun fact: first oncogene found was RAS. Ras is monomeric GTPase for signal transduction. Ras oncogenes cant shut off by hydrolyzing GTP and GDP

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15
Q

What are the cellular functions of oncogenes (essential other situations that it causing cancer)

A
  • Ligands:
    • If ligands produced constitutively they cause proliferation and grow all the time (cancer cells produce own ligand autocrone signaling)
  • Receptors:
    • Tyrosine Kinase receptors - when RTKs constitutively produced dont even need a ligand
  • transcription factors :
    • in nucles, these proteins constantly induce trasncription
    • activatie gene expression including those important for cell cycle progression - over production can lead these to act as oncogenes
  • cell cycle proteins
    • anything that can cause cell proliferation - overproduction of these leads to cancer
  • Proteins that inhibit apoptosis
    • Promotes cell survival despite DNA damage
    • overproduction allow cancerous cells to survive and grow
    • Ex: Bcl2
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16
Q

What is the Bcl2 oncogene?

A
  • Results in over expression Bcl2 in B cells
  • Instead of expression of AB, makes lots of Bcl2
  • So prevents apoptosis of damaged cells - get DNA damage and cell proliferation and development of B cell lymphoma