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Phase 2a - ICS > Cellular and molecular events in carcinogenesis > Flashcards

Cellular and molecular events in carcinogenesis Flashcards

1
Q

Initiation

A

Carcinogen induces the genetic alteration that gives the transformed cell its neoplastic potential.

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2
Q

Promotion

A

Stimulation of clonal proliferation of the initiated transformed cell.

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3
Q

Progression

A

Culminating in malignant behaviour characterised by invasion and its consequences.

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4
Q

Chromosomal abnormalities

A

Translocation or additional chromosome.

Philadelphia chromosome. Translocation t(9;22) bcr-abl in CML.

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5
Q

Burkitt’s lymphoma

A

Translocation of c-myc oncogene (Cr 8) to Ig gene locus (Cr 14).

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6
Q

Follicle centre cell lymphoma

A

Translocation between Cr 14 (Ig locus) and 18 (bcl-2)

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7
Q

Ewing’s tumour and peripheral neuroectodermal tumour

A

Chromosom 11 (fli-1) and 22 (ews)

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8
Q

What is needed to transform tumour cells into neoplastic cells?

A

Expression of telomerase.

Loss/inactivation of tumour suppressor genes.

Activation/abnormal expression of oncogens.

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9
Q

Genetic instability can be inherited by which two major patterns?

A

Chromosomal instability - causing breaks

Microsatellite instability - defective DNA mismatch repair.

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10
Q

Tumour suppressor genes

A

Caretaker genes - repair DNA damage
Gatekeeper - promotes cell death with damaged DNA

Examples: RB1 and p53

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11
Q

Function of p53

A

Repair DNA damage before S phase (arresting cell in G1 until damage is repaired)

Apoptotic cell death in extensive DNA damage.

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12
Q

Examples of gatekeepers

A

p53, RB1, APC

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13
Q

Examples of caretakers

A

BRCA1, BRCA2, MSH2, MLH1, FANC genes, XP genes

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14
Q

How can p53 lose its normal function?

A

Mutation (non-sense, missense)

Complexes of normal and mutant p53 proteins inactivating or subverting the normal protein.

Binding to proteins encoded by oncogenic DNA viruses.

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15
Q

Transfection

A

Partially transformed cell cultures can be fully transformed by the addition of DNA bearing oncogenes.

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16
Q

Transduction

A

Oncogenic retroviruses can transform cells by transferring oncogenes from another cell.

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17
Q

Classification of oncogenes

A

GFs: sis - coding for PDGF

Receptors for GFs: erbB coding for EGFR

Signalling mediator with tyrosine kinase activity: src

Signalling mediator with nucleotide binding activity: ras

Nuclear-binding TF oncoproteins: myc

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18
Q

Oncogenes can be activated by

A

mutation: protein molecule is altered = excessively active

excessive production of a normal oncoprotein due to gene amplification, reduced degradation.

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19
Q

Epigenetic contribution to tumour growth:

A

Gene silencing by hypermethylation of promoter DNA sequence.

Histone modifications (methylation, acetylation).

Interference by microRNA.

Copy number changes to enhancer and silencer DNA sequences.

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20
Q

What is the most important criteria for metastasis?

A

Invasion

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21
Q

Invasion is due to…

A

Reduced cellular cohesion.

Production of proteolytic enzymes.

Abnormal cell motility.

22
Q

What are the common routes of metastasis?

A

Lymphatic vessels, blood vessels, and through body cavities.

23
Q

In epithelial neoplasms cells need to acquire motile and migratory properties…what is this process known as?

A

Epithelial-mesenchymal transition

24
Q

Invasion

A

Influenced by decreased cellular adhesion (E cadherin, dispersed integrins, loss of contact inhibition).

Secretion of proteolytic enzymes MMPs: interstitial collagenases, (I,II,III) gelatinases (IV, gelatin) stromelysins (IV, proteoglycans)

Abnormal or increased cellular motility.

25
Q

What are MMPs counteracted by?

A

TIMPs tissue inhibitors of metallopreoteinases.

26
Q

Invasion within epithelium is known as

A

Pagetoid infiltration

27
Q

Metastasis

A

Original tumour (primary tumour) spreads to form another tumour (secondary tumour).

28
Q

The metastatic sequence

A

Detachment: of tumour cells from their neighbours

Invasion: of the surrounding CT to reach conduits

Intravasation: into the lumen of vessels

Evasion: of host defence mechanisms such as NK cells

Adherence: to endothelium at remote locations.

Extravasation: of cells from the vessel lumen into surrounding tissue.

29
Q

Tumour cells proliferate in the new environment…what do they need to grow and why?

A

Blood vessels (angiogenesis) because nutrients and oxygen need to be delivered to all cells.

30
Q

Routes of metastasis

A

Haematogenous - by blood stream. Secondary tumours in organs that drains blood from primary site.

Lymphatic - regional lymph nodes

Transcoelomic - pleural, pericardial, and peritoneal cavities.

31
Q

What type of cancer prefers lymphatic spread…

A

Carcinomas

32
Q

What type of cancer prefers haematogenous spread…

A

Sarcomas

33
Q

What organs are commonly involved in haematogenous metastasis?

A

Liver
Lung
Bone
Brain

34
Q

What are the five carcinomas that favour bone metastasis?

A

Lung
Breast
Kidney
Thyroid
Prostate

35
Q

Lymph node metastases cause what?

A

Oedema - interrupt the flow.

36
Q

Transcoelomic tumours

A

Effusion of fluid into cavity - rich in protein and may contain fibrin.

Also contains neoplastic cells (aspiration of fluid as Dx).

Tumours often grow as nodules on mesothelial surfaces.

37
Q

What are the clinical effects of tumours?

A

Local effects (compression, invasion, ulceration{=blood loss and anaemia} or destruction of adjacent structures).

Metabolic effects.

Effects due to metastases, if tumour is malignant.

38
Q

Metabolic effects can be subdivided into:

A

Tumour type-specific effects and non-specific metabolic effects.

39
Q

Tumour type-specific effects

A

Endocrine tumours.

Thyroid adenoma - thyrotoxicosis

Adrenocortical adenoma - Cushing’s

Parathyroid adenoma - hyperparathyroidism

40
Q

Non-specific metabolic effects

A

Malignant tumours - weight loss.

41
Q

Cachexia

A

Catabolic clinical state of a CA PT. Due to tumour-derived humoral factors that interfere with protein metabolism.

42
Q

Warburg Effect

A

Producing energy by a high rate of glycolysis with fermentation of lactic acid (in normal cells low rate with oxidation of pyruvate in mitochondria).

PET uses FDG - FDG uptake is increased in tumours.

43
Q

Treatment is guided by

A

Tumour type
Grade or degree of differentiation
Stage or extent of spread

44
Q

Tumour grade it identified by

A

Mitotic activity
Nuclear size, hyperchromasia and pleomorphism
Degree of resemblance to normal tissue.

45
Q

Tumour stage

A

Extent of spread.

46
Q

Cuthbert Dukes staging system

A

For colorectal CA

Dukes’ A: invasion into, but not through the bowel muscular wall

Dukes’ B: invasion through the bowel muscular wall but without lymph node metastases

Dukes’ C: involvement of the local lymph nodes

Dukes’ D: hepatic metastases present.

47
Q

TNM system

A

T - tumour size

N - degree of lymph node involvement

M - extent of metastases

48
Q

Dormancy

A

Cancer patients are never fully cured - prognosis is given the probability of survival or the length of disease-free interval.

49
Q

Non-invasive carcinomas of the breast

A

Ductal carcinoma in situ and lobular (acini) carcinom in situ.

50
Q

Invasive carcinomas of the breast

A

Infiltrating ductal of no special type

Infiltrating lobular

Mucinous

Tubular

Medullary

Papillary

Others

51
Q

Paget’s disease of the nipple

A

Erosion of the nipple - looks similar to eczema.

Associated with underlying ductal carcinoma in situ or invasive carcinoma.

Roughening, reddening and slight ulceration of the nipple.

Within the epidermis of the nipple, large, pale-staining malignant cells histologically.

Phase 2a - ICS (43 decks)

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