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Year 2 - Cancer > Cancer 10 > Flashcards

Cancer 10 Flashcards

1
Q

what are the first 6 hallmarks of cancer?

A
  • Disregard of signals to stop proliferating
  • Disregard of signals to differentiate
  • Capacity for sustained proliferation
  • Evasion of apoptosis
  • Ability to invade
  • Ability to promote angiogenesis
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2
Q

what 4 hallmarks of cancer were added?

A
  • degregulating cellular energetics
  • genome instability and mutation
  • avoiding immune destruction
  • tumor-promoting inflammation
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3
Q

what occurs briefly at each stage of the cell cycle?

A
  • G0 = the cell is in a quiescent phase = it is not replicating
  • G1 = the cell makes sure that it has enough nutrients, nucleotides etc. to replicate
  • At the end of G1, the cell has a checkpoint where you get growth arrest to ensure the genetic fidelity of the cell
  • Specific proteins accumulate/are destroyed during the cycle eg. cyclins
  • Permanent activation of a cyclin can drive a cell through a checkpoint
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4
Q

what is a proto-oncogene?

A
  • proto-oncogene is normal
  • it codes for essential proteins involved in maintenance of cell

growth, division and differentiation

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5
Q

what is an oncogene?

A
  • Mutation can convert a proto-oncogene into an oncogene, whose protein product no longer responds to control influences
  • oncogenes might be aberrantly expressed, over=expressed or aberrantly active
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6
Q

how might an proto-oncogene be converted into an oncogene?

A
  • A proto-oncogene can be converted to an oncogene by a single mutation
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7
Q

show the stages of oncogene activation?

A
  • normal proto-oncogene
  • mutation in the coding sequence
  • gene amplification
  • gene amplification is the production of multiple gene copies
  • it can occur due to problems with a polymerase protein
  • having multiple copies will lead to overproduction of the product
  • chromosomal translocation

​this produces chimeric genes, these are genes formed by combinations of portions of coding sequences to produce new genes

eg. if one of the pieces of translocated DNA is a promoter it will lead to the upregulation of the other gene portion eg. Burkitt’s lymphoma
* insertional mutagenesis

​can also be a problem if the fusion gene formed produces an abnormal protein (e.g. Philadelphia chromosomes in CML)

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8
Q

explain the example of chromosomal translocation in cancer :

eg. Philadelphia chromosome

A
  • philidelphia chromosome is formed by the translocation of chromosome segments from chromosomes 9 + 22
  • chromosome 9 = ABL
  • chromosome 22- BCR
  • the BCR - ABL fusion gene leads to development of cancer
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9
Q

show the signal transduction pathway:

A
  • blue spots are the proto-oncogenes
  • Activation of proto-oncogenes to oncogenes can disrupt normal activity
  • the oncogenes have the ability to
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10
Q

explain the activity of mutant RAS?

A
  • normally upon binding to GTP, RAS becomes active and activates the kinase cascade leading to the production of gene regulatory proteins
  • dephosphorylation of the GTP to GDP switches RAS off
  • Mutant Ras will fail to dephosphorylate GTP so it remains active
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11
Q

what more complicated pathway is Ras part of?

A

The Ras pathway is part of a much more complex signaling cascade called the mitogen-activated protein kinase cascade (MAPK)

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12
Q

what does Ras code for?

A

Ras codes for a family of proteins such as Ki-Ras and Ha-Ras, which are membrane-bound GTPases that are important in the stimulation of cell proliferation

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13
Q

what cancers are the following oncogenes associated with?

SRC

MYC

JUN

Ha - RAS

Ki- RAS

A

SRC = breast , colon lung

MYC = burkitts lymphoma

JUN = lung

Ha - RAS = bladder

Ki- RAS = colon lung

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14
Q

what is the function of tumor suppressor genes?

A
  • Typically proteins whose function is to regulate cellular proliferation and maintain cell integrity
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15
Q

how can cancer occur from mutation of tumour suppressor genes?

A
  • Each cell has two copies of each tumor suppressor gene
  • mutation or deletion of just one copy is not enough to promote the cancer
  • Mutation or loss of both copies means loss of control
  • (knudsons two hit hypothesis)
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16
Q

what are the features of inherited cancer susceptibility?

A
  • Family history of related cancers
  • Unusually early onset
  • Bilateral tumors in paired organs
  • Synchronous or successive tumors
  • Tumors in different organ systems in the same individual
  • Mutation inherited through the germline
17
Q

explain an example of inherited cancer - retinoblastoma?

what tumor suppressor gene does it mutate?

A
  • It is a malignant cancer of developing retinal cells
  • Sporadic disease usually involves one eye
  • Hereditary causes can be unilateral or bilateral and multifocal
  • It is caused by mutation of the RB1 tumour suppressor gene on the chromosome 13q1
  • RB1 encodes a nuclear protein that is involved in regulation of the cell cycle
18
Q

what are the functional classes of tumor suppressor genes?

A
  • Regulate cell proliferation

Maintain cellular integrity

Regulate cell growth

Regulate the cell cycle

Nuclear transcription factors

DNA repair proteins

Cell adhesion molecules

Cell death regulators

  • overall they suppress they stop cancer developing
19
Q

what are the common human tumor suppressor genes?

what are their functions?

what cancers are they associated with?

A
20
Q

what are some of the examples of the purposes of P53?

A
  • they have many different functions (very broad)
  • some include
  • metabolic homeostasis
  • antioxidant defense
  • DNA repair
  • growth arrest
  • senescence
  • apoptosis
21
Q

when is P53 active and inactive?

A
  • When p53 is bound to MDM2 it is inactive
  • when p53 is NOT bound to MDM2 it is active
22
Q

how can P53 get mutated to cause cancer?

A
  • mutants of p53 act in a DOMINANT manner and mutation of a single copy is sufficient to get dysregulation of activity
  • Phosphorylation of p53 destabilises it so that it isn’t degraded so quickly and can exert its effects
  • Phosphorylation is triggered by cellular stress
23
Q

what is the function of APC?

A
  • APC participates in the WNT signalling pathway
  • APC protein is a negative regulator of B catenin therefore preventing uncontrolled cell division
  • mutation of APC can result in colon cancer
24
Q

how does mutation of APC cause colon cancer?

A
  • deletion in 5q21 results in loss of the APC gene
  • sufferers develop thousands of multiple benign polyps
  • there is a 90% chance of developing a colorectal carcinoma
25
Q

what are the stages of development of colorectal cancer?

A
  • hyperplasia
  • metaplasia
  • dysplasia
  • carcinogenesis
26
Q

show a summary table of the functions of oncogenes and tumor suppressor genes?

A
27
Q
A

Year 2 - Cancer (15 decks)

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