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111 > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Choristoma
Heterotopia

A

Normal tissues in abnormal location

Ectopic Tissue

developmental abnormality, results in a lesion

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2
Q

Hyperplasia

A

increase in cell number in response to a stimulus

only in cells with capacity to divide

epithelial cells in breast during pregnancy
hepatocytes to regenerate liver parenchyma after partial resection
prostatic hyperplasia in older men from androgens
endometrial hyperplasia in postmenopausal women receiving estrogens

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3
Q

Metaplasia

A

replacement of one type of normal adult cell/tissue by another normal cell/tissue

squamous metaplasia in bronchial epithelium (smoking…)
intestinal metaplasia in stomach (H.pylori)

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4
Q

Epithelial tissues

A

Squamous, urothelium, glandular

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5
Q

Nomenclature of Neoplasms

Epithelial (most common)

Squamous

A

squamous papilloma - squamous cell carcinoma

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6
Q

Nomenclature of Neoplasms

Epithelial (most common)

urothelium

A

urothelial papilloma - urothelial carcinoma

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7
Q

Nomenclature of Neoplasms

Epithelial (most common)

glandular

A

adenoma, papillary adenoma - adenocarcinoma

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8
Q

Nomenclature of Neoplasms

Melanocytes

A

Nevus - melanoma

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9
Q

Nomenclature of Neoplasms

Germ Cells

A

benign cystic teratoma - dysgerminoma

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10
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)

Fibroblasts

A

fibroma - fibrosarcoma

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11
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)

Adipocytes (fat cells)

A

lipoma - liposarcoma

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12
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)
Smooth muscle cells:

A

leiomyoma - leiomyosarcoma

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13
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)

Endothelium

A

hemangioma - angiosarcoma

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14
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)

Osteocytes

A

Osteoma- osteosarcoma

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15
Q

What are the mesenchymal tissues?

A

Fibroblasts, adipocytes, smooth muscle cells, endothelium, osteocytes

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16
Q

Nomenclature of Neoplasms

Bone marrow/lymphoid

Hematopoietic cells

A

None - leukemia

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17
Q

Nomenclature of Neoplasms

Bone marrow/lymphoid

Lymphoid cells

A

None - lymphoma

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18
Q

Nomenclature of Neoplasms

Mixed Tumours

Breast

A

Fibroadenoma - phyllodes tumor

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19
Q

Microscopic morphology of neoplasias

A

Abnormal cytology/ cellular atypia or pleomorphism

Nucleus: hyperchromasia, increased size and N/C ratio, increased and abnormal mitoses (e.g.,tripolar), more prominent nucleoli

Cytoplasm: loss of normal features, more basophilic (more RNA)

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20
Q

Malignant neoplasms = cancers characteristics

A

aggressive and fast growing

  1. invasion (infiltrate and destroy surrounding tissues)
  2. metastatic potential
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21
Q

Nomenclature for neoplasms

A

oma = suffix for neoplasm

carcinoma = malignant epithelial neoplasm
sarcoma = malignant mesenchymal neoplasm

lymphoma, melanoma, seminoma, dygerminoma = malignant by definition

some carcinomas have VERY low metastasic potential, like basal cell carcinoma of the skin

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22
Q

Carcinoma vs Sarcoma

Incidence

A

Carcinoma: More common

Sarcoma: Less Common

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23
Q

Carcinoma vs Sarcoma

Age

A

Carcinoma: Increase with age

Sarcoma: Younger, bimodal

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24
Q

Carcinoma vs Sarcoma

Etiology

A

Carcinoma: generally known, environmental (drinking, smoking…) , viral

Sarcoma: viral unknown (maybe genetic?)

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25
Q

Carcinoma vs Sarcoma

Metastatic Spread

A

Carcinoma: Lymphatics, then hematogenous

Sarcoma: Hematogenous (BLOOD)

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26
Q

Carcinoma vs Sarcoma (morphology)

Macroscopy

A

Carcinoma: Variably hard

Sarcoma: Fleshy, firm

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27
Q

Carcinoma vs Sarcoma (morphology)

Microscopy
Histology

A

Carcinoma: Form islands of cells separated by stroma

Sarcoma: Sheets of spindle cells admixed with stroma between cells

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28
Q

Carcinoma vs Sarcoma (morphology)

Microscopy
Histochemistry

A

Carcinoma: Epithelial: e.g., mucin

Sarcoma: mesenchymal: fat, etc.

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29
Q

Carcinoma vs Sarcoma (morphology)

Microscopy
Immunohistochemistry

A

Carcinoma: Keratins

Sarcoma: Vimentin, muscle actin

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30
Q

How do we measure proliferation rates?

A

Using Ki67 proliferation marker

follicular lymphoma is SLOW
Burkitt lymphoma is FAST

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31
Q

Sequence of development of carcinoma of the cervix

well-defined sequence of development of carcinomas!

A
  1. Normal mucosa
  2. Dysplasia (some abnormality), aka CIN = cervical intraepithelial neoplasia
  3. Carcinoma-in-situ (whole layer is abnormal)
  4. Invasive squamous cell carcinoma (broken through basement membrane, can go to lymphatics and metastasize)
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32
Q

Grading of MALIGNANT neoplasms, purpose

A

determines degree of differentiation

differentiation = resemblance to normal

de-differentation: loss of resemblance, to a variable degree

anaplasia = complete de-differentation – no resemblance

prognostic and therapeutic implications

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33
Q

Grading of MALIGNANT neoplasms, HOW

A

light microscopy, based on cytology and histology

Grade 1: >75%
Grade 2: 50-75%
Grade 3: 25-50%
Grade 4: <25% differentiated

low grade = grade 1 = well differentiated= better prognosis

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34
Q

Grading parameters to assess in…

  1. Squamous CA
  2. Adenocarcinoma
A
  1. amount keratin, intercellular bridges
  2. quantity of glands, mucin
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35
Q

Routes of metastases (3)

A
  1. Lymphatic vessels to lymph nodes
  2. Blood vessels (hematogenous)
  3. Transcoelomic (seeding via body cavities)
36
Q

Staging of neoplasms

A

Determination of size and extent of spread

correlates to survival

37
Q

TNM system

A

Staging
Primary TUMOR size, characteristics
presence of absence of lymph NODE metastases
presence or absence of distant METASTASES

Distant metastases == automatically stage 4

38
Q

Tumor markers

A

CA in blood

CEA (carcinoembryonic antigen) in colon carcinoma
AFP (alpha-fetoprotein) in hepatocellular carcinoma, germ cell tumours
PSA (prostate specific antigen) in prostate carcinoma

39
Q

types of cancers with highest incidence in males

A
  1. Prostate
  2. Lung and Bronchus
  3. Colon and rectum
40
Q

types of cancers with highest incidence in females

A
  1. breast
  2. Lung and Bronchus
  3. Colon and rectum
41
Q

Cancer deaths

A
  1. Lung and Bronchus
  2. Prostate (males) and Breast (females)
  3. Colon and Rectum
42
Q

Exogenous Cancer Etiologies

A
  1. Chemical carcinogens
  2. Physical agents: radiation – electromagnetic, UV, and ionizing
  3. Biological agents: Viruses (e.g., HPV), bacteria, parasites
43
Q

Endogenous cancer etiologies

A
  1. Heredity
  2. Gender and Hormones
  3. Altered Immunity (Age, immunosuppressant drugs, immune deficiency states (e.g., AIDS…))
44
Q

Principal Causes of human cancer
(Top 3 are most important)

A

25% - Tobacco
25% - Diet
20% - Sexual behaviour, infections
7% - Industrial occupation, pollution
3% - Alcohol
3% - Radiation

45
Q

Chemical carcinogenesis

A
  1. Initiator - mutagenic and induce potentially heritable DNA damage

they can be direct, requiring NO metabolic conversion, or indirect, the opposite

  1. Promoters - not mutagenic, increase proliferation, including of cells with DNA mutations, favouring tumor growth
46
Q

What are the 3 classes of Medicinal Drugs that can act as carcinogens

A
  1. Anti-cancer drugs
  2. Horomones/related
  3. Immunosuppressants
47
Q

What are the 4 groups to classify carcinogens?

A

Group 1: carcinogenic to human (128)
Group 2: A(95)/B(323)- probably carcinogenic to humans
Group 3: not classifiable as to carcinogenicity in humans (500)

48
Q

Medicinal Drugs as carcinogens
Anti-cancer drugs

A

busulphan, chlorambucil, cyclophosphamide, etopside: leukemia ± bladder carcinoma

49
Q

Medicinal Drugs as carcinogens
Horomones/related

A

estrogens: breast, uterus…
tamoxifen: uterus
DES: cervix, vagina

50
Q

Medicinal Drugs as carcinogens
Immunosuppressants

A

cyclosporine: lymphoma, kaposi sarcoma
azathioprine: lymphoma, skin tumours

51
Q

Ionizing radiation and cancer

A

x rays, gamma rays, alpha and beta particles

hiroshima/nagasake = leukemia, breast, thyroid

radionuclides in occupation: lung, thyroid, liver CA, sarcomas and leukemias

Chernobyl = thyroid

how? through damaging chromosomes, translocations, mutations

52
Q

UV radiation

A

skin basal cell and squamous cell CA, melanomas

forming pyrimidine dimers, damaging DNA, overwhelming DNA repair mechanisms

53
Q

Electromagnetic fields (low frequency)

A

possibly carcinogenic (group 2bB): leukemia in children, data in adults is questionable

54
Q

Chronic infections and cancer

A

First link discovered by Rous, chicken sarcoma

18% of cancers worldwide, mostly developing countries

carcinogenicity may be: direct via oncogenic protein, indirect via inflammation, cell damage and regeneration with ensuing proliferation

55
Q

Asbestos

A

Occupational chemical carcinogen

causes lung and mesothelium cancer

lung: coetiological with smoking
mesothelium: good, they can get worker’s comp

industry: insulation, textiles

56
Q

Arsenic

A

occupational chemical carcinogen

causes skin and ling cancer

in glass, pesticides and metals

57
Q

HPV

A

Cervix, oral Ca, etc

58
Q

HBV and HCV

A

Liver CA

59
Q

EBV

A

lymphoma, nasopharyngeal CA

60
Q

HHV-8

A

Kaposi SA, lymphoma

61
Q

HTLV-1

A

Leukemia

62
Q

Merkel CA polyoma virus

A

Merkel cell carcinoma

63
Q

Schistomiasis

A

Bladder CA
indirect effect

64
Q

H. pylori

A

Gastric CA, lymphoma
indirect effect - bacteria, causing cell damage, inflammation, cytokines

65
Q

Liver flukes

A

cholangioCA
indirect effect

66
Q

HIV

A

lymphoma, Kaposi
indirect effect - immunosuppression

67
Q

Cancer stem cells

A

capable of self-renewal
potentially arise from transformation of normal or differentiated stem cells
must be eliminated to cure a cancer but are resistant to therapy: low rate of replication (bad with drugs that target rapidly diving cells), multiple drug resistance 1 expression (MDR-1) that counter drug effects

68
Q

Driver versus passenger mutations

A

Driver: alter function of cancer genes, with direct control, clustered

passenger: random, do not affect behaviour, but may provide a selective advantage e.g., after therapy

69
Q

Hallmarks of Cancer (8)

A
  1. Unrestricted proliferation w/o external stimuli - ONCOGENES
  2. Insensitivity to growth inhibitory signals
    - TUMOR SUPPRESSOR GENES
  3. Altered Cell Metabolism
  4. Evasion of Apoptosis
    alterations in tumor suppressor (p53) and anti-apoptotic genes (BCL2)
  5. Unlimited replicative potential
    activation of telomerase
    5.Sustained angiogenesis
  6. Invasion and metastasis
  7. Evasion of immune surveillance
  8. Defects in DNA repair, leading to genomic instability, facilitating mutations
70
Q

What is an autocrine loop? Provide an example

A

Cancer cells make their own growth factor to stimulate their own surface receptors

example: PDGF (platelet-derived growth factor) secreted by glioblastomas

71
Q

What can oncogenes be?

A
  1. Growth factors (PGDF)
  2. Growth factor receptors (Her2)
  3. Signal transduction proteins (Ras)
  4. Nuclear TFs (Myc)
  5. Cyclins and CDKs (breast hepatic and esophageal cancers and mantle cell lymphomas have cyclin D over expression)
72
Q

Burkitt lymphoma translocation

A

Translocation between chromosomes 8 and 14

MYC activity is regulated by IgH regulatory region = thus always on in the lymphocytes

73
Q

Roles of Wild p53 protein

A

Arrests cell cycle in late G1 via CDK inhibitor p21
Assists in DNA repair
Apoptosis if DNA cannot be repaired
Angiogenesis inhibitor via thrombospondin-1

74
Q

Mutated p53

A

Genetic: Li-Fraumeni syndrome, SAs, leukemias, breast and adrenal cortical CAs

Somatic, homozygous, in breast, lung and colon CAs

75
Q

Follicular lymphoma translocation

A

Translocation between chromosomes 18 and 14

BCL2 activity is regulated by IgH regulatory region = thus always on in the lymphocytes

BCL2 inhibits apoptosis = overexpression leads to rescue of lymphocytes == malignancy

helpful to identify follicular lymphoma versus follicular hyperplasia

76
Q

What is angiogenesis? What is it required for?

A

Process of BV neoformation from preexisting vasculature

Required for tumor to grow beyond 1-2mm in diameter

Occurs by disruption in balance between angiogenic factors and angiogenic inhibitors

77
Q

Angiogenic factors include…

A

Growth factors (VEGF, FGF2, PDGF)
Mutated p53

78
Q

Angiogenic inhibitors include…

A

Thrombospondin-1, endostatin, angiostatin
Wild p53

79
Q

5 stimuli for angiogenesis

A
  1. Tissue ischemia
  2. Tissue hypoxia
  3. Tissue injury
  4. Inflammation
  5. Shear stress
80
Q

chronology of neovasculatization (8 steps)

A
  1. basement membrane of parent vessel is DEGRADED
  2. ECs move to angiogenic stimulus (chemotaxis)
  3. elongation and alignment of ECs: capillary sprout
  4. EC proloferation in parent and offspring
  5. Lumen formation
  6. Anastomosis of 2 hollow sprouts to form loop
  7. Onset of blood flow
  8. Basement membrane produced, pericytes added
81
Q

Vascular endothelial growth factor (VEGF)
What is it?

A

growth factor acting on surface of endothelial cells via surface receptors (mains is VEGFR-2)

82
Q

Vascular endothelial growth factor (VEGF)
Sources?

A

Inflammatory cells, various neoplasms

83
Q

Vascular endothelial growth factor (VEGF)
Unregulated by?

A

Hypoxia (analogous to EPO)
Cytokines, hormones, other growth factors.

84
Q

Vascular endothelial growth factor (VEGF)
Actions?

A

Mitogenesis and maintenance ECS
Anti-immune: decrease maturation of dendritic cells
Vascular: vasodilation via NO pathways, fenestrations in EC

85
Q

Clinical applications of angiogenesis

A
  1. Radiologists use their properties to visualize them on angiograms, CT scans, etc
  2. abnormally permeable vessels explain high protein content (exudate) and hemorrhagic nature of malignant effusions in peritoneal, pericardial and pleural cavities – ascites in ovarian cancer
  3. inhibitor Avastin used in treatment
86
Q

DNA repair defects (3)

A
  1. mismatch excision repair (MMR) (MSH2, MLH1, PMS1, PMS2) - hereditary non-polyposis colon cancer
  2. nucleotide excision repair
  3. recombination repair
87
Q

Multistep carcinogenic sequence in gastric carcinoma

A
  1. Infection with H. pylori or pernicious anemia (immunologic)
  2. Chronic gastritis
  3. Intestinal metaplasia
  4. Dysplasia/CIS
  5. Adenocarcinoma

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