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Principles of disease Jess > Tumour Pathology > Flashcards

Tumour Pathology Flashcards

1
Q

What is haemoptysis?

A

Coughing up blood

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2
Q

Epithelium glandular benign

A

Adenoma

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3
Q

Epithelium glandular malignant

A

Adenocarcinoma

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4
Q

Epithelium squamous benign

A

Squamous papilloma

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5
Q

Epithelium squamous malignant

A

Squamous carcinoma

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6
Q

Tissue, Bone benign

A

Osteoma

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7
Q

Tissue, Bone, malignant

A

Osteo- sarcoma

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8
Q

Tissue, fat, benign

A

Lipoma

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9
Q

Tissue, fat, malignant

A

Lipo-sarcoma

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10
Q

Tissue, fibrous-tissue, benign

A

Fibroma

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11
Q

Tissue, Fibrous-tissue, malignant

A

Fibro-sarcoma

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12
Q

Blood, white blood cells, malignant

A

Leukaemia

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13
Q

Lymphoid tissue, malignant

A

Lymphoma

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14
Q

Melanocytes, benign

A

Naevus

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15
Q

Melanocytes, malignant

A

Melanoma

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16
Q

Neural tissue, central nervous system, malignant

A

Astrocytoma

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17
Q

Neural tissue, peripheral nervous system, malignant

A

Schwannoma

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18
Q

What is dysplasia?

A

Presence of cells of an abnormal type within a tissue

No invasion but can progress to cancer

19
Q

Intraepithelial neoplasia

A

Development of a benign neoplasia or high-grade dysplasia in epithelium

20
Q

Properties of cancer cells?

A

Loss of tumour suppressor genes - e.g Rb, APC

Gain of function of oncogenes

Altered cellular function

Abnormal morphology

Cells capable of independent growth

Tumour biomarkers

21
Q

What are tumour biomarkers?

A

Alpha - feta protein

Carcino-embryonic antigen

Oestrogen receptor

Prostate specific antigen

22
Q

What can biomarkers be used for?

A

Screening, diagnosis, prognostic, or predictive

23
Q

What is retinoblastoma?

A

Tumour in eyes

Normally found in children

Around 40-50 children each year

High cure level

24
Q

2 forms of retinoblastoma

A

Inherited - younger, more tumours (both eyes),
2 abnormal copies (one from birth, then another mutation)

Sporadic - older, just one eye
Just 1 abnormal copy (point mutations)

25
Q

What are anti-oncogenes?

A

Tumour suppressor genes

Follows ‘2 hit hypothesis’ - needs two mutations

Genes that Normally regulate cell cycle.

26
Q

Inherited cancer syndromes

A

Account for just 5 -10%

Genetic predispositions to develop cancer

Earlier onset and multiple tumours

27
Q

Inherited to predisposition of cancer

A

Familial retinoblastoma

Familial adenomatous polyposis of colon - 100% risk of invasive colon cancer by 50 (bowel removal)

Hereditary breast and ovarian cancer syndrome

Hereditary non-polyposis colorectal cancer syndrome

Li-fragment syndrome

Multiple endocrine neoplasia

Van hipped-Linda syndrome

28
Q

List of tumour suppressor genes

A

APC - colon cancer

P53

Rb - retinoblastoma

P16

29
Q

What is another name for a tumour suppressor gene?

A

Anti - oncogene

30
Q

What are proto-oncogenes?

A

Normal genes coding for normal growth regulating proteins

Abnormal - GAIN of function (one abnormal copy) activated

31
Q

Tumour suppressor genes (antioncogenes)

A

Abnormal = loss of function

32
Q

Proto-oncogenes

A

GAIN of function = abnormal

33
Q

List of Porto-oncogenes

A

Growth factors

Growth factor receptors

Signal transducers

Regulatory proteins

Cell cycle regulators - cyclins/ cyclin dependant kinases

34
Q

Example of oncogenes activation

A

HER2 and breast cancer

35
Q

What are translocations?

A

Chromosomal rearrangements

Burritos lymphoma (malignancy of B cells)

36
Q

Chemical carcinogenesis

A

Carcinogens react with DNA - purine and pyridimine bases in DNA are critical targets for radiation damage.

Activation of oncogenes and loss of anti-oncogenes

37
Q

Radiation carcinogenesis

A

Purine and my ride mine bases in DNA -critical targets

UVB present in sunlight
CT scans

38
Q

Viral carcinogenesis

A

Oncoviruses

Virus inserts oncogene into host DNA causing cell division

HPV (genital, throat and anal cancers)
Hep B (liver cancer)
EBV (lymphoma)

39
Q

HPV

A

Human papilloma virus

Causes cervical cancer

40
Q

Multi step carcinogenesis hypothesis

A

Mutations accumulate with time

Mutations of many oncogenes and anti-oncogenes to cause cancer

With age - Repair less effective

41
Q

Bronchial mucosa bad cigarettes

A

(Chemical carcinogenesis - multi step carcinogenesis)

Progressive accumulation of mutations: cyclins, p53.

Cyclins = cell cycle control 
P53 = apoptosis and cell cycle control
42
Q

Colorectal adenoma-carcinoma sequence

A

Dysplastic cells - adenoma, losing cell cycle control

Normal —— adenoma ———- carcinoma

43
Q

Summary of molecular basis of cancer

A

Mutations can be inherited or sporadic

Mutations accumulate over time - explains cancer being very prominent in the elderly

Loss of cell cycle control key to malignant transformation

Key regulators include p16, cyclin D, CDK4, Rb - mutated in MAJORity of cancers

Loss mutations of p53 allow genetically damaged cells to proliferate, forming malignant neoplasms

Principles of disease Jess (36 decks)

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