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Foundations of Medicine > Genetic Predisposition to Cancer > Flashcards

Genetic Predisposition to Cancer Flashcards

1
Q

<p>What do a small proportions of cancers happen due to?</p>

A

<p>Increased inherited predisposition to cancer (genetic)</p>

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2
Q

<p>What are the 2 different kinds of gene mutations that cancer can arise from?</p>

A

<p>Somatic mutations</p>

<p>Germline mutations</p>

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3
Q

<p>Where to somatic mutations occur?</p>

A

<p>In somatic tissue, nongermline</p>

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4
Q

<p>What can you say about the inheritability of somatic and germline mutations?</p>

A

<p>Somatic cannot be inherited and germline can</p>

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5
Q

<p>Where are germline mutations present?</p>

A

<p>In egg or sperm</p>

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6
Q

<p>What are some genetic processes associated with cancer?</p>

A

<p>Oncogenes</p>

<p>Tumour suppresor genes</p>

<p>DNA damage response genes</p>

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7
Q

<p>What are proto-oncogenes?</p>

A

<p>Normal gene that codes for proteins to regulate cell growth and differentiation</p>

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8
Q

<p>What can mutations change into oncogenes and what does this do?</p>

A

<p>Proto-oncogenes which accerlerates cell division</p>

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9
Q

<p>What are tumour suppresor genes?</p>

A

<p>Genes that inhibit cell cycle or promotes apoptosis</p>

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10
Q

<p>What happens when tumour suppresor genes fail?</p>

A

<p>Cancer arises</p>

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11
Q

<p>What are DNA damage response genes?</p>

A

<p>Repair mechanism for DNA</p>

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12
Q

<p>What happens when DNA damage response genes fail?</p>

A

<p>Cancer arises due to speeding the accumulation of mutations in other critical genes</p>

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13
Q

<p>What is an example of a DNA damage response gene?</p>

A

<p>Mismatch repair genes (MMR genes)</p>

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14
Q

<p>What do mismatch repair (MMR) genes do?</p>

A

<p>Corrects errors that spontaneously occur during DNA replication like single base mismatches or short insertions and deletions</p>

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15
Q

<p>What does mismatch repair failure lead to?</p>

A

<p>Microsatellite instability (MSI) where there is the addition of nucleotide repeats, which is the phenotypic evidence that MMR is not functioning normally</p>

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16
Q

<p>What is microsatellite instability (MSI)?</p>

A

<p>Where there is an addition of nucleotide repeats, which is phenotypic evidents that mismatch repair genes (MMR) are not working correctly</p>

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17
Q

<p>What are the 3 kinds of tumours?</p>

A

<p>Benign</p>

<p>Malignant</p>

<p>Dysplastic</p>

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18
Q

<p>What are some properties of benign tumours?</p>

A

<p>Lack the ability to metastasize</p>

<p>Rarely or never become cancerous</p>

<p>Can cause negative health benefits due to pressure on other organs</p>

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19
Q

<p>What are some properties of dysplastic tumours?</p>

A

<p>Benign but could progress to malignancy</p>

<p>Cells show abnormalities of appearance and cell maturation</p>

20
Q

<p>What is a unique property of malignant tumours?</p>

A

<p>Able to metastasize</p>

21
Q

<p>What are some other causes of cancer in relation to genes?</p>

A

<p>Autosomal recessive syndromes</p>

<p>Multiple modifier genes of lower genetic risk</p>

22
Q

<p>What are de novo mutations?</p>

A

<p>Occur in germ cells of parents with no family history of hereditary cancer syndrome</p>

23
Q

<p>What are de novo mutations common in?</p>

A

<p>Famial adenomatous polyposis</p>

<p>Multiple endocrine neoplasia 2B</p>

<p>Hereditary retinoblastoma</p>

24
Q

<p>What is hereditory retinoblastoma?</p>

A

<p>Most common eye tumour in children</p>

25
Q

<p>What is the type of inheritence of most cancer susceptability genes?</p>

A

<p>Dominant</p>

26
Q

<p>What are some risk factors for breast cancer?</p>

A

<p>Ageing</p>

<p>Family history</p>

<p>Late menopause</p>

<p>Early menarche</p>

<p>Nulliparty (condition where woman cannot give birth)</p>

<p>Estrogen use</p>

<p>Dietary factors (alcohol)</p>

<p>Lack of exercise</p>

27
Q

<p>What is nulliparty?</p>

A

<p>Condition where woman cannot give birth</p>

28
Q

<p>What are some genes that increase hereditory susceptability to breast cancer?</p>

A

<p>BRCA1</p>

<p>BRCA2</p>

<p>TP53</p>

<p>PTEN</p>

29
Q

<p>Which of BRCA1 and BRCA2 increases the risk of breast cancer the most?</p>

A

<p>BRCA1 (20-40%) whereas BRCA2 is only 10-30%</p>

30
Q

<p>What are functions of the BRCA1 gene?</p>

A

<p>Checkpoint mediatory</p>

<p>DNA damage signalling and repair</p>

<p>Chromatin remodelling</p>

<p>Transcription</p>

31
Q

<p>What is the main function of the BRCA2 gene?</p>

A

<p>DNA repair by homologous recombination</p>

32
Q

<p>What do BRCA1 mutations increase the risk of?</p>

A

<p>Breast cancer (50-85%)</p>

<p>Second primary breast cancer (40-60%)</p>

<p>Ovarian cancer (15-45%)</p>

<p>Other cancers</p>

33
Q

<p>What do BRCA2 gene mutations increase the risk of?</p>

A

<p>Breast cancer (50-85%)</p>

<p>Ovarian cancer (10-20%)</p>

<p>Male breast cancer (6%)</p>

<p>Other cancers</p>

34
Q

<p>What are some risk factors for colorectal cancer?</p>

A

<p>Ageing</p>

<p>Personal history of colorectal cancer or adenomas</p>

<p>High fat, low fibre diet</p>

<p>Inflammatory bowel disease</p>

<p>Family history of colorectal cancer</p>

35
Q

<p>What are the 2 possible hereditary colorectal cancer syndromes?</p>

A

<p>Non-polyposis (few to no adenomas)</p>

<p>Polyposis (multiple adenomas)</p>

36
Q

<p>What is an example of a non-polyposis hereditary colorectal cancer?</p>

A

<p>HNPCC</p>

37
Q

<p>What are examples of polyposis hereditary colorectal cancers?</p>

A

<p>FAP</p>

<p>AFAP</p>

<p>MAP</p>

38
Q

<p>What are adenomas?</p>

A

<p>A beneign tumour formed from glandular structures in epithelial tissue</p>

39
Q

<p>What are some clinical features of HNPCC?</p>

A

<p>Early but variable age in CRC diagnosis (about 45 years)</p>

<p>Tumour site through colon rather than descending colon</p>

40
Q

<p>What is a clinical feature of familial adenomatous polyposis (FAP)?</p>

A

<p>Risk of extracolonic tumours (upper GI, thyroid, brain)</p>

41
Q

<p>What is a milder form of FAP?</p>

A

<p>Recessive MYH polyposis</p>

42
Q

<p>What do multiple modifier genes of lower genetic risk explain?</p>

A

<p>Families with history of cancer and no identified mutation</p>

<p>Different in cancer penetrance in families with the same mutation</p>

43
Q

<p>What can cancer risk for patients with FAP be managed by?</p>

A

<p>Surveillance</p>

<p>Surgery</p>

<p>Chemoprevention</p>

44
Q

<p>What are predictive gene tests used for?</p>

A

<p>To test who has genes that are associated with an increased risk in developing cancer</p>

45
Q

<p>What is it important to remember about inherited mutations causing cancer compared to other causes?</p>

A

<p>Most cancers are sparodic, with only a small proportion being due to inherited mutations</p>

Foundations of Medicine (167 decks)

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