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Cancer Flashcards

(52 cards)

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1
Q

What enzymes are needed in DNA repair and in what order

A

Helicase unwinding the helix
Endonucleases cut the strand
Gap is filled by DNA polymerase
Sealed by ligase

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2
Q

what does lack of ability to remove TT diners mean for repair

A

During replication DNA polymerase does not know how to proceed so leaves gaps in new DNA. Induces SOS

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3
Q

What is the problem with SOS

A

It makes many mistakes itself and may leave errors in TSG or Oncogenes= cancer initiation

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4
Q

What is xeroderma pigmentosuim

A 
Autosomal recessive disease
Unusual response to sunlight 
Pigmentation abnormalities
Skin cancer 
-lack endonuclease activity needed for DNA repair
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5
Q

What are PAHs

A

Polycyclic aromatic hydrocarbons. Eg benzo(a)pyrene benzanthracene formed by incomplete combustion of organic matter, burnt food, coal tar, cigarette smoke.

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6
Q

What is AHH

A

Aryl hydrocarbon hydroxylase. Enzyme that is activated by benzos, acts to remove them from our body by making more water soluble (add O2) but makes ultimate carcinogenic (benzapyrenediol epoxide) in the process
A) detoxified and excreted
B) attacked by electron rich atoms eg guanine in DNA causing mutations

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7
Q

How does bp diol epoxide cause mutations

A

A)causes incorrect bases pairing when DNA replicates, may cause a point mutation in an oncogene/TSG
B) can cause SOS repair, which has a high error rate- mutations in oncogene/TSG

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8
Q

What is the significance of AHH inducers

A

Genetically determined, high inducers are at higher risk of cancer

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9
Q

What gene mutation predisposes to breast cancer

A

BRCA1/2

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10
Q

What gene mutations predispose to colorectal cancer

A

APC

HNPCC

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11
Q

What is variable expression

A

Mutation in a single cancer gene can predispose to different rumours of the same individual

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12
Q

What is age related penetrance

A

Time needed for other outside hits to accumulate to cause a tumour

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13
Q

In what can inherited cancer predisposing genes occur

A

Protoncogenes
Tumour supressor genes
Mutator genes

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14
Q

Give two examples of mutations in protoncogenes

A 
RET- multiple endocrine neoplasia type 2 
Medullary thyroid cancer
Parathyroid tumours
Phaeochromocytoma 
MET-hereditary papillary renal carcinoma
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15
Q

Give four examples of mutations in tumour supressor genes

A

TP53 - li fraumeni syndrome
BRCA1/2
APC-familial adenomatous polposis coli
PTEN-breast cancer, particular skin tumours and thyroid cancer, together make Cowden syndrome

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16
Q

What is the difference between BRCA 1 and 2

A

1- cumulative risk of breast and ovarian cancer
Contra lateral tumour risk
Prostate cancer
2- cumulative risk of breast and ovarian cancer, also prostrate, pancreatic and male breast cancer

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17
Q

What is APC linked to p

A

Familial adenomatous polyposis coli -FAP
Greater than 100 colorectal adenomatous polyps or fewer than 100 polyps + fdr with FAP
7% of untreated develop CRC by 21
Extra colorectal cancers- thyroid, duodenum, pancreas, liver

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18
Q

What mutations are in mutator genes?

A

hMLH1 and hMLH2, problems with mismatch DNA repair
Causes colorectal, endometrial, ovarian, ureteric, or renal pelvis
And brain cancer

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19
Q

What is HNPCC

A

Hereditary non-polyposis colorectal cancer.
Ovarian
Endometrial
And bowel cancer

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20
Q

Name 6 key features when looking at familial cancer predisposition

A 
Early onset rumours
Multiple tumours in close relatives
Multiple tumours in an individual 
Clusters of different tumours in a pattern
Breast cancer in males
First degree relatives with cancer
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21
Q

Name and uncommon cancer predisposition syndrome

Study These Flashcards
A 
Von Hippel-Lindau syndrome
Cluster of:
Harmangioblastomas
Renal cell carcinoma/multiple renal cysts/ phaeochromocytoma
Multiple pancreatic cysts/tumours
22
Q

What options are there for reducing risk in familial predisposition

Study These Flashcards
A

Surveillance
Prophylactic surgery/chemo prevention
Diagnostic and predictive molecular genetic testing

23
Q

What mediators of growth control are there (5)

Study These Flashcards
A 
Secreted growth factors
Environmental growth inhibitors
Secreted growth inhibitors
Intrinsic programme of differentiation/apoptosis 
Tumour immune response
24
Q

For a tumour to become malignant what three things does it need

Study These Flashcards
A

Limitless replication
Angiogenesis
Invasion and metastasis

25
Name 6 factors that lead to tumourigenesis
``` Evading apoptosis Tissue invasion and metastasis Insensitivity to anti-growth signals Sustained angiogenesis Limitless replicating potential Self sufficiency in growth signals ```
26
How can mutations occur (4)
``` Sequence change Gene amplification Gene deletion Gene silencing (epigenetic) ```
27
How can a tumour gain self-sufficiency of growth signals
Mutations that cause: Increased secretion of GF's Up regulation of GF receptors Activation of GF Receptors
28
How might a mutation allow evasion of apoptosis
Up regulation of anti-apoptotic factors Down regulation of pro-apoptotic factors Loss of function of pro-apoptotic factors
29
What are PAHs
Polycyclic aromatic hydrocarbons. Eg benzo(a)pyrene benzanthracene formed by incomplete combustion of organic matter, burnt food, coal tar, cigarette smoke.
30
What is AHH
Aryl hydrocarbon hydroxylase. Enzyme that is activated by benzos, acts to remove them from our body by making more water soluble (add O2) but makes ultimate carcinogenic (benzapyrenediol epoxide) in the process A) detoxified and excreted B) attacked by electron rich atoms eg guanine in DNA causing mutations
31
How does bp diol epoxide cause mutations
A)causes incorrect bases pairing when DNA replicates, may cause a point mutation in an oncogene/TSG B) can cause SOS repair, which has a high error rate- mutations in oncogene/TSG
32
What is the significance of AHH inducers
Genetically determined, high inducers are at higher risk of cancer
33
What gene mutation predisposes to breast cancer
BRCA1/2
34
What gene mutations predispose to colorectal cancer
APC | HNPCC
35
What is variable expression
Mutation in a single cancer gene can predispose to different rumours of the same individual
36
What is age related penetrance
Time needed for other outside hits to accumulate to cause a tumour
37
In what can inherited cancer predisposing genes occur
Protoncogenes Tumour supressor genes Mutator genes
38
Give two examples of mutations in protoncogenes
``` RET- multiple endocrine neoplasia type 2 Medullary thyroid cancer Parathyroid tumours Phaeochromocytoma MET-hereditary papillary renal carcinoma ```
39
Give four examples of mutations in tumour supressor genes
TP53 - li fraumeni syndrome BRCA1/2 APC-familial adenomatous polposis coli PTEN-breast cancer, particular skin tumours and thyroid cancer, together make Cowden syndrome
40
What is the difference between BRCA 1 and 2
1- cumulative risk of breast and ovarian cancer Contra lateral tumour risk Prostate cancer 2- cumulative risk of breast and ovarian cancer, also prostrate, pancreatic and male breast cancer
41
What is APC linked to p
Familial adenomatous polyposis coli -FAP Greater than 100 colorectal adenomatous polyps or fewer than 100 polyps + fdr with FAP 7% of untreated develop CRC by 21 Extra colorectal cancers- thyroid, duodenum, pancreas, liver
42
What mutations are in mutator genes?
hMLH1 and hMLH2, problems with mismatch DNA repair Causes colorectal, endometrial, ovarian, ureteric, or renal pelvis And brain cancer
43
What is HNPCC
Hereditary non-polyposis colorectal cancer. Ovarian Endometrial And bowel cancer
44
Name 6 key features when looking at familial cancer predisposition
``` Early onset rumours Multiple tumours in close relatives Multiple tumours in an individual Clusters of different tumours in a pattern Breast cancer in males First degree relatives with cancer ```
45
Name and uncommon cancer predisposition syndrome
``` Von Hippel-Lindau syndrome Cluster of: Harmangioblastomas Renal cell carcinoma/multiple renal cysts/ phaeochromocytoma Multiple pancreatic cysts/tumours ```
46
What options are there for reducing risk in familial predisposition
Surveillance Prophylactic surgery/chemo prevention Diagnostic and predictive molecular genetic testing
47
What mediators of growth control are there (5)
``` Secreted growth factors Environmental growth inhibitors Secreted growth inhibitors Intrinsic programme of differentiation/apoptosis Tumour immune response ```
48
For a tumour to become malignant what three things does it need
Limitless replication Angiogenesis Invasion and metastasis
49
Name 6 factors that lead to tumourigenesis
``` Evading apoptosis Tissue invasion and metastasis Insensitivity to anti-growth signals Sustained angiogenesis Limitless replicating potential Self sufficiency in growth signals ```
50
How can mutations occur
``` Sequence change Gene amplification Gene deletion Gene silencing (epigenetic) ```
51
How can a tumour gain self-sufficiency of growth signals
Mutations that cause: Increased secretion of GF's Up regulation of GF receptors Activation of GF Receptors
52
How might a mutation allow evasion of apoptosis
Up regulation of anti-apoptotic factors Down regulation of pro-apoptotic factors Loss of function of pro-apoptotic factors

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