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path2001 > Week 4 - Neoplasia > Flashcards

Week 4 - Neoplasia Flashcards

1
Q

Characteristics of benign neoplasm

A

Small, encapsulated, well differentiated, cells often retain normal function, no invasion, non lethal except if impinges on surrounding tissue and vessel, non metastasising, no pleomorphism

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2
Q

Characteristics of malignant neoplasm

A

Large, non encapsulated, show loss of differentiation, cells lose normal function, invasion of normal tissue, metastasise, potentially lethal, pleomorphic

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3
Q

Benign neoplasm nomenclature

A

-oma

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4
Q

Malignant neoplasm nomenclature

A

carcinoma, sarcoma

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5
Q

Carcinoma

A

Neoplasm arising from epithelial tissue

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6
Q

Sarcoma

A

Neoplasms arising in non-epithelial tissues

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7
Q

Screening methods used to assist in early diagnosis and treatment of breast cancer

A

Mammography and ultrasonography, fine needle aspiration cytology, core biopsy/vacuum assisted biopsy, self-palpitation/examination, clinical breast exam

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8
Q

Sessile

A

Absence of stalk

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9
Q

Pedunculated

A

Attached to the surface by a narrow elongated stalk

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10
Q

Importance of polyps recognition and treatment

A

Polyps = precursor to malignancy

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11
Q

Typical consequences of benign tumour in uterus

A

Abnormal uterine bleeding, urination frequency (increasing tumour puts pressure on urinary bladder), abdominal pain, pressure on colonic area

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12
Q

Tumour

A

Swelling

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13
Q

Neoplasm

A

Abnormal mass of tissue

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14
Q

Hyperplasia

A

Increased cell number

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15
Q

Hypertrophy

A

Increased cell size

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16
Q

Metaplasia

A

Change from normal cell type to another cell type in response to stimuli

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17
Q

Dysplasia

A

Disordered/abnormal cell growth

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18
Q

Carcinoma in-situ

A

Cancer that sits above the basement membrane, hasn’t invaded the tissue

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19
Q

Invasive carcinoma

A

Cells have invaded the basement membrane

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20
Q

Anaplastic

A

No differentiation

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21
Q

Pleomorphism

A

Variation in size and shape of cell or nucleus

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22
Q

Nuclear atypia in neoplastic cells

A

Hyperchromasia, Increased n:c ratio, mitotic activity, loss of polarity

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23
Q

Hyperchromasia

A

Dark nuclei due to increased amount of chromatin

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24
Q

Metastasis

A

Process by which primary malignant neoplasm gives rise to secondary tumours at other sites

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25
Q

Spread of malignant tumours

A

Direct invasion, lymphatic invasion, vascular invasion, transcoelomic spread

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26
Q

Vascular invasion

A

Invasion to other organs in the vascular pathway

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27
Q

Grade

A

Measure of how aggressively a tumour behaves (differentiation and mitotic activity)

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28
Q

Stage

A

How far the tumour has advanced at the time of diagnosis

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29
Q

Stage can be described through

A

Features of the tumour (size, extent of local invasion), nodal involvement, metastasis

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30
Q

Molecular techniques in clinical practice can be used for

A

Diagnosis, prognosis, therapeutics

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31
Q

FISH

A

Fluorescent In Situ Hybridization

32
Q

Techniques used to differentiate lipoma vs liposarcoma

A

FISH for specific translocations, immunohistochemistry, cytogenetics

33
Q

Techniques used to identify lymphoma

34
Q

Mutations that cause lung adenocarcinomas

A

EGFR mutations

35
Q

Mutations that cause melanomas

A

BRAF mutations

36
Q

Breast carcinoma molecular techniques

A

Tissue microarray (gene chips), microarray technology

37
Q

Carcinogenesis

A

Process that results in transformation of normal cells to neoplastic cells through permanent genetic alteration

38
Q

Carcinogen

A

Cancer causing agent

39
Q

Mechanism of carcinogenesis

A

Multistep process: Accumulation of permanent genetic alterations & tumour progression

40
Q

Proto-oncogenes

A

Promoters of cell growth

41
Q

Anti-oncogenes

A

Restrict cell growth

42
Q

Identification of carcinogens

A

Epidemiological studies, carcinogenic effects in laboratory animals, transforming effects on cell cultures and mutagenicity testing in bacteria

43
Q

Causes of cancer

A

Behavioural and occupational risks, chemicals, irradiation, hormones, physical agent (asbestos), diet, virus/bacterial preneoplastic dysplasia, autoimmune diseases

44
Q

Metabolic pathways for conversion of chemical procarcinogens into active ultimate carcinogen

A

Polycyclic aromatic hydrocarbons, aromatic amines, nitrosamines from ingested nitrates and nitrites

45
Q

Tumours caused by HPV

A

Common wart (squamous cell papilloma), cervical carcinoma

46
Q

Tumours caused by Epstein-Barr virus

A

Burkitt’s lymphoma, nasopharyngeal cancer

47
Q

Tumours caused by Hep B and C virus

A

Hepatocellular carcinoma

48
Q

Tumours caused by human herpesvirus-8

A

Kaposi’s sarcoma, primary effusion lymphoma

49
Q

Tumours caused by Human T-cell lymphotropic virus 1

A

Adult T-cell leukaemia/lymphoma

50
Q

Host factors in carcinogenesis

A

Race, diet, constitutional factors, premalignant lesions and conditions, transplacental exposure, congenital

51
Q

Cellular and molecular events in carcinogenesis

A

Multistep process, may require initiating and promoting agents, growth persists in the absence of the causative agents, genetic alterations of oncogenes and tumour suppressor genes

52
Q

Initiation

A

Where carcinogen induces genetic alteration(s) that give(s) transformed cells its neoplastic potential

53
Q

Promotion

A

Stimulation of clonal proliferation of the initiated transformed cell

54
Q

Progression

A

Process culminating in malignant behaviour characterised by invasion and its consequences

55
Q

How do abnormalities in genes regulating cell proliferation underpin neoplasia

A

Activation of oncogenes to stimulate growth, loss of genes controlling proliferation, loss of normal control mechanisms for eliminating genetically damaged cells, loss of gene products that repair damaged DNA => DNA instability and mutation in oncogenes and tumour suppressor genes

56
Q

Proto-oncogene

A

Genes that code for proteins involved in control of cell growth = switches for cell proliferation

57
Q

Viral oncogene

A

Genes within virus that code for a protein

58
Q

Cellular oncogene

A

Genes that code for protein in development of neoplasia

59
Q

Mechanisms of oncogene activation

A

Proto-oncogenes form oncogenes through point mutation, translocation or gene amplification

60
Q

Point mutation

A

Caused by a single nucleotide change resulting in changed amino acid

61
Q

Translocation

A

Moves a gene or part of a gene from one chromosome to another

62
Q

Gene amplification

A

Leads to raised protein levels

63
Q

Oncogene nomenclature

A

3 letter code of the cancer in which first found

64
Q

RAS

A

Rat sarcoma

65
Q

MYC

A

Myelocytomatosis retrovirus

66
Q

Prefix c

67
Q

Prefix v

A

Viral homologue

68
Q

Clinical applications of oncogenes

A

Predictive marker in some common cancers, production of drugs that target oncogene, production of drugs that target components of signalling pathways

69
Q

Example of proto-oncogene activated by point mutation

70
Q

Example of proto-oncogene activated by chromosomal translocation

A

bcl-2, abl

71
Q

BCR-ABL

A

Philadelphia gene - translocation (9:22) => CML

72
Q

Example of proto-oncogene activated by gene amplification

A

erb-B2 neu or HER2/neu, erb-B1

73
Q

HER2

A

Cell membrane surface bound receptor tyrosine kinase

74
Q

Function of HER2

A

Involved in signal transduction pathways leading to cell growth and differentiation

75
Q

Role of p53

A

Regulate cell proliferation and trigger apoptosis

76
Q

Cell cycle

A

M -> G1 -> S -> G2

path2001 (5 decks)

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