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Cancer > Oncogenes and tumour suppressors > Flashcards

Oncogenes and tumour suppressors Flashcards

1
Q

The hallmarks of cancer

A
  • Sustaining proliferative signalling
  • Evading growth suppressors
  • Activating invasion and metastasis
  • Enabling replicative immortality
  • Inducing angiogenesis
  • Resisting cell death
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2
Q

Added hallmarks of cancer

A 
EMERGING HALLMARKS
-Deregulating cellular energetics
-Avoiding immune destruction
ENABLING CHARACTERISTICS
-Genome instability and mutation 
-Tumour-promoting inflammation
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3
Q

The cell cycle

A
  • Cycle checkpoints (growth arrest ensure genetic fidelity)
  • Specific proteins accumulate/are destroyed during the cycle (cyclins, cycle dependent kinases, cycle dependent kinase inhibitors)
  • Permanent activation of a cyclin can drive a cell through a checkpoint
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4
Q

Proto-oncogenes

A
  • code for essential proteins involved in maintenance of cell growth, division and differentiation
  • mutation converts a proto-oncogene to an oncogene, whose protein product no longer responds to control influences (can be single mutation)
  • oncogenes can be abnormally expressed, over-expressed or abnormally active (eg: MYC, RAS, ERB, SIS)
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5
Q

Oncogene activation

A
  • Begin with normal proto-oncogene
  • Mutation in the coding sequence (point mutation of deletion)
  • Gene amplification (multiple gene copies)
  • Chromosomal translocation (chimaeric genes)
  • Insertional mutagenesis (eg: viral infection)
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6
Q

Philadelphia chromosome

A

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7
Q

Proteins involved in signal transduction are potential critical gene targets

A

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8
Q

Activation of proto-oncogenes to oncogenes disrupts normal activity

A

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9
Q

Mutant Ras has abnormal activity

A
  • Upon binding GTP, Ras becomes active

- Dephosphorylation of GTP to GDP switches Ras off=mutant Ras faills to dephosphorylate GTP and remains active

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10
Q

Ras signalling

A

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11
Q

Oncogenes and human tumours: SRC

A

Function: tyrosine kinase
Mechanism of activation: overexpression/C-terminal deletion
Location: cytoplasmic
Associated human cancers: breast, colon, lung

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12
Q

Oncogenes and human tumours: MYC

A

Function: transcription factor
Mechanism of activation: translocation
Location: nuclear
Associated human cancers: Burkitt’s lymphoma

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13
Q

Oncogenes and human tumours: JUN

A

Function: transcription factor
Mechanism of activation: overexpression/deletion
Location: nuclear
Associated human cancers: lung

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14
Q

Oncogenes and human tumours: Ha-RAS

A

Function: G protein
Mechanism of activation: point mutation
Location: cytoplasmic
Associated human cancers: bladder

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15
Q

Oncogenes and human tumours: Ki-RAS

A

Function: G protein
Mechanism of activation: point mutation
Location: cytoplasmic
Associated human cancers: colon, lung

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16
Q

Tumour suppressor genes

A
  • typically proteins whose function is to regulate cellular proliferation and maintain cell integrity (eg: RB)
  • each cell has 2 copies of each tumour suppressor gene
  • mutation or deletion of 1 gene copy is usually insufficient to promote cancer=mutation or loss of both copies means loss of control
17
Q

Knudson’s two hit hypothesis

A

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18
Q

Inherited cancer susceptibility features

A
  • family history of related cancers
  • unusually early age of onset
  • bilateral tumours in paired organs
  • synchronous or successive tumours
  • tumours in different organ systems in same individual
  • mutation inherited through the germline
19
Q

Retinoblastoma

A
  • malignant cancer of developing retinal cells
  • sporadic disease usually involving one eye
  • hereditary cases can be unilateral or bilateral and multifocal
  • due to mutation of RB1 tumour suppressor gene on chromosome 13q14
  • RB1 encodes nuclear protein involved in cell cycle regulation
20
Q

Functional classes of tumour suppressor genes

A

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21
Q

Tumour suppressor genes and human tumours: p53

A

Function: cell cycle regulator
Location: nuclear
Associated human cancers: many (colon, breast, bladder, lung etc)

22
Q

Tumour suppressor genes and human tumours: BRCA1

A

Function: cell cycle regulator
Location: nuclear
Associated human cancers: breast, ovarian, prostate

23
Q

Tumour suppressor genes and human tumours: PTEN

A

Function: tyrosine and lipid phosphatase
Location: cytoplasmic
Associated human cancers: prostate, glioblastoma

24
Q

Tumour suppressor genes and human tumours: APC

A

Function: cell signalling
Location: cytoplasmic
Associated human cancers: colon

25
Q

Tumour suppressor genes and human tumours: p16^-INK4A

A

Function: cell cycle regulator
Location: nuclear
Associated human cancers: colon and others

26
Q

Tumour suppressor genes and human tumours: MLH1

A

Function: mismatch repair
Location: nuclear
Associated human cancers: colon, gastric

27
Q

p53

A
  • ‘the guardian of the genome’
  • tumour suppressor gene
  • mutants of p53 act in a dominant manner and mutation of a single copy is sufficient to give activity dysregulation
28
Q

APC tumour suppressor gene

A
  • familial adenomatous polyposis coli
  • due to deletion in 5q21 resulting in loss of APC gene (a tumour suppressor gene)
  • APC gene involved in cell adhesion and signalling
  • sufferers develop multiple benign adenomatous polyps of the colon
  • 90% risk of developing colorectal carcinoma=APC gene mutation is a frequent event in colon cancer
  • APC gene participates in WNT signalling pathway
  • APC protein is a negative regulator of beta-catenin (preventing uncontrolled cell division)
29
Q

The route to cancer

A

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30
Q

The development of colorectal cancer

A
  • Normal epithelium
  • Hyperproliferative epithelium
  • Adenoma
  • Carcinoma
  • Metastasis
31
Q

Oncogenes

A
  • gene active in tumour
  • specific translocations/point mutations
  • mutations rarely hereditary
  • dominant at cell level
  • broad tissue specificity
  • leukaemia and lymphoma
32
Q

Tumour suppressor gene

A
  • gene inactive in tumour
  • deletions or mutations
  • mutations can be inherited
  • recessive at cell level
  • considerable tumour specificity
  • solid tumours
33
Q

COSMIC

A

-Catalogue Of Somatic Mutations In Cancer

Cancer (15 decks)

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