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path2001 > Week 4 - Neoplasia > Flashcards

Week 4 - Neoplasia Flashcards

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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
Spread of malignant tumours
Direct invasion, lymphatic invasion, vascular invasion, transcoelomic spread
26
Vascular invasion
Invasion to other organs in the vascular pathway
27
Grade
Measure of how aggressively a tumour behaves (differentiation and mitotic activity)
28
Stage
How far the tumour has advanced at the time of diagnosis
29
Stage can be described through
Features of the tumour (size, extent of local invasion), nodal involvement, metastasis
30
Molecular techniques in clinical practice can be used for
Diagnosis, prognosis, therapeutics
31
FISH
Fluorescent In Situ Hybridization
32
Techniques used to differentiate lipoma vs liposarcoma
FISH for specific translocations, immunohistochemistry, cytogenetics
33
Techniques used to identify lymphoma
PCR, FISH
34
Mutations that cause lung adenocarcinomas
EGFR mutations
35
Mutations that cause melanomas
BRAF mutations
36
Breast carcinoma molecular techniques
Tissue microarray (gene chips), microarray technology
37
Carcinogenesis
Process that results in transformation of normal cells to neoplastic cells through permanent genetic alteration
38
Carcinogen
Cancer causing agent
39
Mechanism of carcinogenesis
Multistep process: Accumulation of permanent genetic alterations & tumour progression
40
Proto-oncogenes
Promoters of cell growth
41
Anti-oncogenes
Restrict cell growth
42
Identification of carcinogens
Epidemiological studies, carcinogenic effects in laboratory animals, transforming effects on cell cultures and mutagenicity testing in bacteria
43
Causes of cancer
Behavioural and occupational risks, chemicals, irradiation, hormones, physical agent (asbestos), diet, virus/bacterial preneoplastic dysplasia, autoimmune diseases
44
Metabolic pathways for conversion of chemical procarcinogens into active ultimate carcinogen
Polycyclic aromatic hydrocarbons, aromatic amines, nitrosamines from ingested nitrates and nitrites
45
Tumours caused by HPV
Common wart (squamous cell papilloma), cervical carcinoma
46
Tumours caused by Epstein-Barr virus
Burkitt's lymphoma, nasopharyngeal cancer
47
Tumours caused by Hep B and C virus
Hepatocellular carcinoma
48
Tumours caused by human herpesvirus-8
Kaposi's sarcoma, primary effusion lymphoma
49
Tumours caused by Human T-cell lymphotropic virus 1
Adult T-cell leukaemia/lymphoma
50
Host factors in carcinogenesis
Race, diet, constitutional factors, premalignant lesions and conditions, transplacental exposure, congenital
51
Cellular and molecular events in carcinogenesis
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
Initiation
Where carcinogen induces genetic alteration(s) that give(s) transformed cells its neoplastic potential
53
Promotion
Stimulation of clonal proliferation of the initiated transformed cell
54
Progression
Process culminating in malignant behaviour characterised by invasion and its consequences
55
How do abnormalities in genes regulating cell proliferation underpin neoplasia
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
Proto-oncogene
Genes that code for proteins involved in control of cell growth = switches for cell proliferation
57
Viral oncogene
Genes within virus that code for a protein
58
Cellular oncogene
Genes that code for protein in development of neoplasia
59
Mechanisms of oncogene activation
Proto-oncogenes form oncogenes through point mutation, translocation or gene amplification
60
Point mutation
Caused by a single nucleotide change resulting in changed amino acid
61
Translocation
Moves a gene or part of a gene from one chromosome to another
62
Gene amplification
Leads to raised protein levels
63
Oncogene nomenclature
3 letter code of the cancer in which first found
64
RAS
Rat sarcoma
65
MYC
Myelocytomatosis retrovirus
66
Prefix c
Cellular
67
Prefix v
Viral homologue
68
Clinical applications of oncogenes
Predictive marker in some common cancers, production of drugs that target oncogene, production of drugs that target components of signalling pathways
69
Example of proto-oncogene activated by point mutation
ras
70
Example of proto-oncogene activated by chromosomal translocation
bcl-2, abl
71
BCR-ABL
Philadelphia gene - translocation (9:22) => CML
72
Example of proto-oncogene activated by gene amplification
erb-B2 neu or HER2/neu, erb-B1
73
HER2
Cell membrane surface bound receptor tyrosine kinase
74
Function of HER2
Involved in signal transduction pathways leading to cell growth and differentiation
75
Role of p53
Regulate cell proliferation and trigger apoptosis
76
Cell cycle
M -> G1 -> S -> G2

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