cellular cancer Flashcards

1
Q

what are the 4 stages of cancer

A

stage 1: localised small tumour
stage 2: localised large tumour
stage 3: large tumour with potential to spread to lymph nodes and other organs
stage 4: cancer has spread to lymph nodes and other organs

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2
Q

what are the checkpoints in the cell cycle and what are they checking

A

G1-S checkpoint: checks if the conditions for DNA replication are favourable
G2-M checkpoint: checks if DNA was synthesised correctly and if ant damage has been repaired
Spindle Fibre Assembly: checks if all chromatids are attached to the mitotic spindle

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3
Q

what is a proto-oncogene

A

a regular gene that when altered by a mutation may become an oncogene and contribute to cancer

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4
Q

what are some examples of photo oncogenes

A

Src, Ras, Myc and BCR-ABL

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5
Q

what are tumour suppressor genes

A

genes that act in normal cells to stop uncontrolled proliferation. If these genes lose their function due to mutation then they will contribute to cancer

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6
Q

what are examples of tumour suppressor genes

A

p53, BRCA, Rb and APC

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7
Q

what are the different ways in which a oncogene can gain its function

A

-the gene itself could mutate creating a hyperactive version of the protein
-the gene could duplicate creating the normal protein in greater amounts
-the locus could change and the protein would be under different controls, creating the same protein but in excess

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8
Q

what is Src

A

proto oncogene
Src is a pro mitotic tyrosine protein kinase
mutations in Src can cause constitutional activation where mitosis is triggered even in the absence of pro mitotic factors

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9
Q

what is constitutional activation

A

when cell proliferation is promoted even in the absence of pro mitotic stimuli

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10
Q

what is Ras

A

proto oncogene
G protein that promotes cell division and proliferation
the mutant version of Ras is always bound to GTP and so is always on
this triggers constitutional activation

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11
Q

what is BCR-ABL

A

chimeric oncogene
causes leukaemia in white blood cells
occurs when the gene ABL on chromosome 9 joins to BCR on Chromosome 22
the altered BCR-ABL protein causes unregulated kinase activity and phosphorylates lots of downstream molecules
this causes uncontrolled proliferation and suppresses apoptosis

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12
Q

what is p53

A

tumour supressor gene
activates lots of protection and repair functions within the cell
causes apoptosis, cell cycle arrest and DNA repair
p53 loss of function is seen in almost all cancer types

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13
Q

what is Rb

A

tumour supressor gene
repressor protein that binds to transcription factor E2F and stops transcription before the S phase
if it is bound then the S phase can not start so mitosis does not occur
The Ras pathway triggers the phosphorylation of Rb causing it to leave.

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14
Q

how is the Rb repressor protein effected by Knudsons two hit hypothesis

A

in healthy people the Rb gene may be deleted on occasion, but there are two copies so the DNA is able to repair itself and the function is not lost
If the mutated chromosome is inherited then then any occasional deletions will result in both Rb genes being deleted.
This causes excessive cell proliferation

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15
Q

what is BCRA1

A

tumour repressor gene
involved in repairing DNA after damage by mutagens e.g. UV light
loss of function associated with breast cancer

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16
Q

what is beta catenin

A

proto oncogene
responds to pro mitotic stimuli from WNT signalling
activates transcription factors that causes cell proliferation
in absence of stimuli it is degraded by APC
if it gains function due to mutation then beta catenin activation is unregulated

17
Q

what is APC

A

tumour supressor gene
in the absence of mitotic stimuli it forms a protein degradation complex with beta catenin leading to its degradation
when mutation causes it to lose its function it causes unregulated beta catenin activation

18
Q

what is angiogenesis

A

angiogenesis is how the body grows new blood vessels to tissue that require it.
cancer cells often take advantage of this since the inner cell layers within cancer tumours are hypoxic and stimulate the production of new vessels

19
Q

what are HER2 blockers

A

HER2 is a cell receptor that is over expressed in many cancers, promoting cell proliferation
monoclonal antibodies inhibit its signal, reducing cell proliferation.

20
Q

what is imatinib

A

a targeted therapy for BCR-APC associated cancers
it stops inhibits the BCR-APC protein by occupying its ATP binding site
This makes BCR-APC dangerous, but easily treatable.

21
Q

what is T-vec

A

a modified herpese virus that infects both healthy and cancerous cells, but can only replicate in cancer cells, causing them to lyse and die