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Mol Med Final Exam > Oncology > Flashcards

Oncology Flashcards

0
Q

Hypertrophy

A

Increase in the number of organelles and subsequently the size of cells

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1
Q

Hyperplasia

A

Increase in the number of cells in an organ or tissue

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2
Q

What cells can undergo hyperplasia

A

Cells capable of synthesizing DNA. Therefore, heart, skeletal muscle and nerve almost pure hypertrophy under stress or hormone stimulation

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3
Q

Four types of hyperplasia

A

Physiologic
Hormonal (estrogen on endometrium)
Compensatory (liver after partial lobectomy)
Pathologic

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4
Q

Define pathologic hyperplasia

A

Increase in cell number in response to external stimulus. Growth stops when stimulus abates (different to neoplasia) However, fertile ground for cancerous proliferation eg. Cervical cancer/endometrial

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5
Q

Define choristoma

A

Excess of tissue in an abnormal location

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6
Q

Define hamartoma

A

Benign disorganized tissue that grows at the same rate of surrounding tissue that is composed of tissue usually found at that site.

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7
Q

Define metaplasia

A

A reversible change in which one adult cell type is replaced by another

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8
Q

Define dysplasia

A

Disorderly but non-neoplastic tissue growth.

Often seen as precursor to carcinoma (‘in situ’)

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9
Q

Dysplasia characterized by..

A

Ploemorphism
Hyperchromatism
Loss of normal orientation

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10
Q

Define neoplasia

A

Abnormal growth of tissue that is virtually autonomous and exceeds that of surrounding tissue. Growth persists after cessation of stimuli.

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11
Q

Two broad categories of neoplasia

A

Benign

Malignant

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12
Q

Two broad categories of malignancy

A

Carcinoma

Sarcoma

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13
Q

Factors used to differentiate beni and malignant tumours.

A

Differentiation/ anaplasia
Rate of growth
Local invasion
Metastasis

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14
Q

Cytologic features that characterize anaplastic tumours

A 
Nuclear and cellular pleomorphism
Hyperchromatism
Nuclear:cytoplasmic ratio approaches 1:1
Abundant mitoses
Tumour giant cells
Disarray of tissue architecture
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15
Q

Three routes of distant spread by tumours

A

Into body cavities eg. Transperitoneal
Invasion of lymphatics
Haematogenous

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16
Q

Most likely route of spread of carcinomas

A

Lymphatic

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17
Q

Most likely route of spread of sarcomas

A

Blood

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18
Q

Two causes of LN enlargement in metastatic carcinoma

A

Proliferation of carcinoma cells

Reactive hyperplasia in response to Ags

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19
Q

Six hallmarks of cancer

A 
Limitless replicative potential
Self sufficiency in growth signals
Insensitivity to anti growth signals
Evades apoptosis
Sustained angiogenesis
Tissue invasion and metastisis
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20
Q

Two emerging hallmarks of cancer

A

Deregulating cellular energetics

Avoiding immune destruction

21
Q

Two enabling characteristics

A

Genome instability and mutation

Tumour-promoting inflammation

22
Q

What is the generally accepted model of tumorigenesis

A

Multi step and multigene

23
Q

Why is RAS a good candidate for being involved in cancer

A

Has many downstream effects and is involved in many cellular processes

24
Q

Examples of mechanisms for each hallmark of cancer

A

Self sufficient growth signals - activate H-Ras oncogene
Insensitive to anti growth signals - lose Rb suppressor
Evade apoptosis - produce IGF survival factors
Limitless replication - turn on telomerase
Sustained angiogenesis - produce VEGF inducer
Invasion/ metastasis - inactivate E-cadherin

25
Q

Factors that cause cancer

A

Hereditary
Chemicals
Radiation
Viral/bacterial

26
Q

End points of DNA damage

A

Repair and cell survival
Block replication -> apoptosis
Gene/chromosomal change -> cancer

27
Q

Normal regulation of G1/S control point

A

CyclinD/cdk4,6 complex phosphorylates Rb.E2F.
Rb.E2F is then further phosphorylated by cyclinE/cdk2 which causes release of E2F and the subsequent transcription of proliferation genes.

28
Q

How HPV causes cancer

A

E6 inactivates p53 therefore less p21
E7 causes E2F release from Rb

Therefore proliferation despite DNA damage

29
Q

Process of metastisis

A

Break BM, induce angiogenesis, invade blood or lymph, adhere to cap wall in target tissue, invade normal tissue, proliferate forming 2ndry tumour(more angiogenesis)

30
Q

Various products formed by cisplatin

A

Intrastrand cross link
Interstrand cross link
Monoadducts (either with one monoadduct still available for reaction or monoadduct linked to small molecule or nuclear protein)

31
Q

Mutations in these gene classes can lead to cancer

A

Tumour suppressor
Protooncogenes
DNA repair genes
Cell cycle genes

32
Q

Define microsatellites

A

Highly conserved, stably inherited, short tandem repeats/motifs

33
Q

Increase or decrease in microsatellites =

A

Microsatellites instability (MSI)

34
Q

MSI arises due to..

A

DNA slippage
Backward slippage = more repeats
Forward slippage = less repeats

35
Q

Name DNA repair genes

A

MLH1
MSH2,3,6
PMS1,2

36
Q

How DNA repair genes work

A 
Binds incorrect pairing or adduct.
Helicase unwinds DNA 
Endonuclease 'cuts' out fragment 
DNA polymerase fills the gap
DNA lipase reseals remaining nick
37
Q

How is MSI tested for

A

DNA extracted from normal and tumour tissue.
Amplify DNA with PCR
Add Bethesda markers. Analyse fragment sizes
If loss of heterozygosity = MSI

(Can only be done in heterozygotes)

38
Q

Knudson’s two hit hypothesis

A

Loss of tumour suppression requires LOF of both alleles of a relevant gene

39
Q

What is the Fearon and Vogelstein pathway

A

The adenoma-carcinoma sequence that is caused by sequential genetic alterations (clonal evolution) that causes colorectal cancer.

Possible 5-hit scenario [5q mutation, DNA hypo methylation, 12p = k-Ras mutation, 18q loss, 17p = p53 loss)

40
Q

What is the other genetic pathway in CRC other that FV

A

MSI

41
Q

What CRCs is MSI seen in

A

HNPCC - hereditary nonpolyposis colorectal cancer

Sporadic CRC

42
Q

Clinical description of HNPCC

A 
Inherited
Early onset
Multiple
Mutation in MMR
Accelerated adenoma to carcinoma
Right sided 
Mucinous with signet cells
43
Q

Three types of MSI status

A

MSS
MSI-L
MSI-H

44
Q

Two forms of instability in MMR

A

CIN

MSI

45
Q

What is CIN

A

Chromosome instability.
Many chromosomal abnormalities
Linked to APC mutations
Mediated by stepwise accumulation of cytogenetic changes

46
Q

How does one test for MMR gene defects

A

Direct test of hMSH2 and hMLH1
Indirect staining for hMSH2 and hMLH1 proteins

MSI test (Bethesda markers)

47
Q

Sporadic MSI + CRC due to..

A

Promotor hypomethylation of hMLH1

NB NO MUTATION, common in elderly/female

48
Q

HNPCC MSI+ tumours due to..

A

Germline mutation of DNA MMR gene

Early onset

49
Q

What is MSI-H termed

A

Lynch syndrome associated MSI

50
Q

Two classes of chemical carcinogens

A

Genotoxic

Non genotoxic

51
Q

Possible drug targets for anti metastisis

A

Molecules over expressed (tenascin-C)
Intracellular signaling (rac/rho)
Provide anti motility signals (CXCR3, decorin)

Mol Med Final Exam (6 decks)

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