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H2 Biology > Molecular Biology of Cancer > Flashcards

Molecular Biology of Cancer Flashcards

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1
Q

what does cancer result from?

A

uncontrolled cell division
- dysregulation of cellular checkpoints
- rate of cell division to far exceed the rate of cell death
- more altered daughter cells, passing on unstable genome and accumulating more mutations
- cancer develops via multi-step model, and metastasis

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2
Q

what do carcinoma, lymphoma, polyp, sarcoma (cancer terminology) mean?

A

carcinoma: cancer that starts in skin or tissues that line the inside or cover the outside of internal organs
lymphoma: cancer of lymphatic system
polyp: growth of normal tissue that usually sticks out from organ’s lining
sarcoma: cancer in tissues that support and connect body (eg. fat and muscle)

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3
Q

state the eight important characteristics of cancer cells

A
  1. high rate of cell division:
  2. genome instability and mutation
  3. replicative immortality
  4. loss of anchorage dependence
  5. loss of contact and density-dependent inhibition
  6. inducing angiogenesis / vascularisation
  7. metastasis
  8. avoiding immune destruction
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4
Q

what are benign and malignant tumours? (what are they a result of, and required treatment)

A

uncontrolled cell division

benign: few genetic mutations, completely removable by surgery (no metastasis)
malignant: invasive, individuals with them = CANCER, radiation / chemotherapy required

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5
Q

compare the features of benign and malignant tumours (nucleus shape, differentiation, nuclear : cytoplasmic volume ratio, rate of mitosis, tumour boundary, ability to metastasise)

A

BENIGN VS MALIGNANT
nucleus: small and regular VS large and irregular
differentiation: well VS poorly
nuclear to cytoplasmic volume ratio: low VS high (more nuclear division)
rate of mitosis: low VS high
tumour boundary: well-defined VS poorly-defined
ability to metastasis: cannot VS can

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6
Q

what are the three cell cycle checkpoints, when do they occur, and what do they check for?

A

G1 checkpoint (interphase):
- presence of growth factors
- DNA damage and cell size, - sufficient nutrients
G2 checkpoint (interphase):
- successful DNA replication sans damage
Metaphase checkpoint (during mitosis)
- successful formation of spindle fibres
- attachment of spindle fibres to chromosomes’ kinetochores

if there is irreparable damage, apoptosis occurs
if there is repairable damage, repaired and proceeds
if there is no damage, checkpoint is passed and proteins signal the cell to proceed

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7
Q

what are maturation-promoting factors in the cell cycle, and how do they become active?

A
  • cyclins (proteins with no enzymatic activity alone) bind to cyclin-dependent kinases (Cdks) - form cyclin-Cdk complexes called maturation-promoting factors (MPFs)
  • cyclins have a cyclically fluctuating cellular concentration according to stages of the cell cycle (eukaryotes have multiple cyclins)
    *Cdks are always there, just whether they are in active or inactive form
  • MPFs promote mitosis by phosphorylating activating stuff
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8
Q

what does uncontrolled cell division mean, and what controls the rate of cell division?

A

relationship between rate of cell division and rate of cell loss
in normal tissues, relationship balanced, no net accumulation of new cells

in cancer cells, rate of cell division far exceeds rate of cell loss, net uncontrolled proliferation of new cells

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9
Q

what are two classes of cancer-critical genes, and their normal functions?

A

tumour suppressor genes: inhibits uncontrolled cell division
proto-oncogene: stimulates normal cell division

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10
Q

what are the functions of tumour-suppressor proteins, coded for by tumour suppressor genes (a class of cancer-critical gene)?

A
  • take part in cell signalling pathways to inhibit cell cycle
  • halt cell division if DNA is damaged
  • trigger DNA repair mechanisms to prevent accumulation of DNA damage
  • initiate apoptosis
  • maintain cell anchorage
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11
Q

what happens when a loss of function mutation occurs in the tumour suppressor gene?

A
  • abolished protein function
  • diploid organism has two copies of every gene
  • both copies must be mutated for no functional gene product (one copy alone is okay)
  • mutated tumour suppressor genes act in a recessive manner
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12
Q

what is the p53 gene, and why is it known as the “Guardian of the Genome”?

A

tumour suppressor gene (mutated in ~half of all human cancers)
- cell cycle control
- apoptosis
- maintenance of genetic stability

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13
Q

what is the function of the p53 protein in the cell cycle?

A

transcription factor, binds to DNA to trigger transcription of cell cycle inhibition genes
- activate DNA repair proteins
- arrest growth: p53 protein binds to specific DNA control elements, promotes transcription for relevant genes, like p21, which stops cell cycle by binding to proteins involved in cell cycle progression such as Cdks
- initiate apoptosis (programmed cell death)

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14
Q

what are the functions of proto-oncogenes?

A
  • growth factors (GFs)
  • growth factor receptors
  • protein kinases
  • inhibitors of apoptosis
  • transcription factors
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15
Q

what occurs when proto-oncogenes undergo gain-of-function mutations?

A

encode a protein that promotes excessive cell division
oncogene is dominant,
- 1/2 copies mutated can cause abnormal cell proliferation
- genes gain function by: over-expressed OR code for hyperactive protein

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16
Q

what is the ras gene and protein?

A

the ras gene encodes the ras protein, which belongs to a super-family of proteins known as “low-molecular-weight G-proteins”
G-proteins are involved in signal transduction (transmitting chemical signals from outside the cell to cause changes inside the cell)

17
Q

what is the ras protein’s role in the cell cycle-stimulating pathway?

A

the activated ras protein relays signals from a growth factor receptor to a series of protein kinases known as the phosphorylation cascade
the last protein kinase of this signal transduction pathway activates transcription of genes encoding proteins that stimulate cell division
- activation of ras signalling causes cell division

18
Q

what happens when the ras gene undergoes a gain in function mutation?

A
  • changes specific 3D conf
  • GTP remains bonded to ras (G-protein) as a ras-GTP complex
  • ras constantly activated (even w/o growth factor)
  • transcription and consequently stimulates the cell cycle
  • hyperactive ras protein = excessive cell division
19
Q

state the 4 steps of the multi-step model of cancer progression

A
  1. accumulation of mutations (several independent mutations in cancer-critical genes in a single cell lineage)
  2. activation of telomerase
  3. angiogenesis
  4. metastasis
20
Q

what happens during accumulation of mutations and activation of telomerase in the progression of cancer?

A
  1. accumulation of mutations: gradual accumulation of several INDEPENDENT mutations in CANCER-CRITICAL genes in a SINGLE cell lineage
    - cancer-critical genes: proto-oncogenes, tumour suppressor genes, telomerase gene, angiogenesis-activating protein genes
21
Q

what happens during the activation of telomerase in the progression of cancer?

A
  1. activation of telomerase: ribonucleoprotein complex that adds telomere repeat sequences to 3’ ends of DNA through reverse transcription (RNA to DNA), maintaining telomere lengths so cancer cells divide infinitely
22
Q

what happens during angiogenesis of cancer progression?

A

angiogenesis / vascularisation: stimulating the formation of new blood vessels
- angiogenesis-activating proteins: vascular endothelial growth factor (VEGF) OR fibroblast growth factor (FGF)
- balance between concentration of angiogenesis-activating proteins and angiogenesis inhibitors determines whether angiogenesis occurs

angiogenic process:
1. tumour cell releases angiogenesis-activating proteins that attract endothelial cells and promote their proliferation
2. endothelial cells secrete protein-degrading enzyme called matrix metalloproteinases (MMPs)
3. endothelial cells’ enzymes break down the extracellular matrix (ECM), so endothelial cells can be organised into new networks of blood vessels.

23
Q

what happens during metastasis of cancer progression?

A

after angiogenesis, cancer cells can invade and metastasis.
invasion: direct migration and penetration into neighbouring tissues
metastasis: entering the circulatory system and travelling to distant sites, forming secondary tumours called metastases

  1. cancer cells invade surrounding tissues, penetrate through walls of lymphatic and blood vessels, accessing the bloodstream
  2. transported by circulatory system throughout the body
  3. establish new secondary tumours at distant sites from the primary tumour
24
Q

state the causative factors of cancer

A
  1. lifestyle and diet
    - cigarette and tobacco smoking
    - exposure to chemical carcinogens
  2. radiation exposure
    - ionising radiation
    - ultraviolet radiation
  3. age
  4. genetic predisposition
  5. loss of immunity
  6. viral infections
25
Q

how do lifestyle and diet factors contribute to cancer?

A

smoking: PAH (polycyclic aromatic hydrocarbons) bind to DNA and form adducts at several sides of p53 gene, preventing production of functional p53 protein, loss of normal growth control mechanisms, uncontrollable cell division

chemical carcinogens:
- nitrates contribute to cancer
- HCA (heterocyclic amines) + polycyclic aromatic hydrocarbons formed, they bind to DNA and cause mistakes in DNA synthesis

26
Q

how does radiation exposure contribute to cancer?

A

ionising radiation: produce free radicals of water (OH), produce double stranded breaks leading to chromosomal rearrangements and deletions
ultraviolet radiation: DNA-damaging (thymine dimers, base pair substitutions, insertions, deletions)

27
Q

how does age, genetic predisposition, and loss of immunity contribute to cancer?

A

age: accumulation of mutations
genetic predisposition: inheritance of an oncogene or mutant allele of tumor-suppressor gene (predisposition inherited, to cancer itself)
loss of immunity: suppressed immune system cannot detect and destroy cancerous cells

28
Q

how do viral infections contribute to cancer

A

15% of human cancers involve viruses: tumour viruses
- inactivating tumour suppressor genes / converting proto-oncogene to oncogene
- directing expression of viral proteins that inactivate p53 and other tumour suppressor proteins
- introducing oncogene into normal cell

29
Q

name the four genes mutated in colorectal cancer (sequentially)

A
  • APC (tumor suppressor)
  • ras (proto-oncogene)
  • DCC (tumor suppressor)
  • p53 (tumor suppressor)

H2 Biology (24 decks)

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