Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

111 > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Choristoma
Heterotopia

A

Normal tissues in abnormal location

Ectopic Tissue

developmental abnormality, results in a lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Epithelial tissues

A

Squamous, urothelium, glandular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Nomenclature of Neoplasms

Epithelial (most common)

Squamous

A

squamous papilloma - squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Nomenclature of Neoplasms

Epithelial (most common)

urothelium

A

urothelial papilloma - urothelial carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Nomenclature of Neoplasms

Epithelial (most common)

glandular

A

adenoma, papillary adenoma - adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Nomenclature of Neoplasms

Melanocytes

A

Nevus - melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Nomenclature of Neoplasms

Germ Cells

A

benign cystic teratoma - dysgerminoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)

Fibroblasts

A

fibroma - fibrosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)

Adipocytes (fat cells)

A

lipoma - liposarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)
Smooth muscle cells:

A

leiomyoma - leiomyosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)

Endothelium

A

hemangioma - angiosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Nomenclature of Neoplasms

Mesenchymal (solid tissues)

Osteocytes

A

Osteoma- osteosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the mesenchymal tissues?

A

Fibroblasts, adipocytes, smooth muscle cells, endothelium, osteocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nomenclature of Neoplasms

Bone marrow/lymphoid

Hematopoietic cells

A

None - leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Nomenclature of Neoplasms

Bone marrow/lymphoid

Lymphoid cells

A

None - lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Nomenclature of Neoplasms

Mixed Tumours

Breast

A

Fibroadenoma - phyllodes tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Malignant neoplasms = cancers characteristics

A

aggressive and fast growing

  1. invasion (infiltrate and destroy surrounding tissues)
  2. metastatic potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Carcinoma vs Sarcoma

Incidence

A

Carcinoma: More common

Sarcoma: Less Common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Carcinoma vs Sarcoma

Age

A

Carcinoma: Increase with age

Sarcoma: Younger, bimodal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Carcinoma vs Sarcoma

Etiology

A

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

Sarcoma: viral unknown (maybe genetic?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Carcinoma vs Sarcoma Metastatic Spread
Carcinoma: Lymphatics, then hematogenous Sarcoma: Hematogenous (BLOOD)
26
Carcinoma vs Sarcoma (morphology) Macroscopy
Carcinoma: Variably hard Sarcoma: Fleshy, firm
27
Carcinoma vs Sarcoma (morphology) Microscopy Histology
Carcinoma: Form islands of cells separated by stroma Sarcoma: Sheets of spindle cells admixed with stroma between cells
28
Carcinoma vs Sarcoma (morphology) Microscopy Histochemistry
Carcinoma: Epithelial: e.g., mucin Sarcoma: mesenchymal: fat, etc.
29
Carcinoma vs Sarcoma (morphology) Microscopy Immunohistochemistry
Carcinoma: Keratins Sarcoma: Vimentin, muscle actin
30
How do we measure proliferation rates?
Using Ki67 proliferation marker follicular lymphoma is SLOW Burkitt lymphoma is FAST
31
Sequence of development of carcinoma of the cervix well-defined sequence of development of carcinomas!
1. Normal mucosa 2. Dysplasia (some abnormality), aka CIN = cervical intraepithelial neoplasia 2. Carcinoma-in-situ (whole layer is abnormal) 4. Invasive squamous cell carcinoma (broken through basement membrane, can go to lymphatics and metastasize)
32
Grading of MALIGNANT neoplasms, purpose
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
33
Grading of MALIGNANT neoplasms, HOW
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
34
Grading parameters to assess in... 1. Squamous CA 2. Adenocarcinoma
1. amount keratin, intercellular bridges 2. quantity of glands, mucin
35
Routes of metastases (3)
1. Lymphatic vessels to lymph nodes 2. Blood vessels (hematogenous) 3. Transcoelomic (seeding via body cavities)
36
Staging of neoplasms
Determination of size and extent of spread correlates to survival
37
TNM system
Staging Primary TUMOR size, characteristics presence of absence of lymph NODE metastases presence or absence of distant METASTASES Distant metastases == automatically stage 4
38
Tumor markers
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
types of cancers with highest incidence in males
1. Prostate 2. Lung and Bronchus 3. Colon and rectum
40
types of cancers with highest incidence in females
1. breast 2. Lung and Bronchus 3. Colon and rectum
41
Cancer deaths
1. Lung and Bronchus 2. Prostate (males) and Breast (females) 3. Colon and Rectum
42
Exogenous Cancer Etiologies
1. Chemical carcinogens 2. Physical agents: radiation -- electromagnetic, UV, and ionizing 3. Biological agents: Viruses (e.g., HPV), bacteria, parasites
43
Endogenous cancer etiologies
1. Heredity 2. Gender and Hormones 3. Altered Immunity (Age, immunosuppressant drugs, immune deficiency states (e.g., AIDS...))
44
Principal Causes of human cancer (Top 3 are most important)
25% - Tobacco 25% - Diet 20% - Sexual behaviour, infections 7% - Industrial occupation, pollution 3% - Alcohol 3% - Radiation
45
Chemical carcinogenesis
1. Initiator - mutagenic and induce potentially heritable DNA damage they can be direct, requiring NO metabolic conversion, or indirect, the opposite 2. Promoters - not mutagenic, increase proliferation, including of cells with DNA mutations, favouring tumor growth
46
What are the 3 classes of Medicinal Drugs that can act as carcinogens
1. Anti-cancer drugs 2. Horomones/related 3. Immunosuppressants
47
What are the 4 groups to classify carcinogens?
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
Medicinal Drugs as carcinogens Anti-cancer drugs
busulphan, chlorambucil, cyclophosphamide, etopside: leukemia ± bladder carcinoma
49
Medicinal Drugs as carcinogens Horomones/related
estrogens: breast, uterus... tamoxifen: uterus DES: cervix, vagina
50
Medicinal Drugs as carcinogens Immunosuppressants
cyclosporine: lymphoma, kaposi sarcoma azathioprine: lymphoma, skin tumours
51
Ionizing radiation and cancer
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
UV radiation
skin basal cell and squamous cell CA, melanomas forming pyrimidine dimers, damaging DNA, overwhelming DNA repair mechanisms
53
Electromagnetic fields (low frequency)
possibly carcinogenic (group 2bB): leukemia in children, data in adults is questionable
54
Chronic infections and cancer
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
Asbestos
Occupational chemical carcinogen causes lung and mesothelium cancer lung: coetiological with smoking mesothelium: good, they can get worker's comp industry: insulation, textiles
56
Arsenic
occupational chemical carcinogen causes skin and ling cancer in glass, pesticides and metals
57
HPV
Cervix, oral Ca, etc
58
HBV and HCV
Liver CA
59
EBV
lymphoma, nasopharyngeal CA
60
HHV-8
Kaposi SA, lymphoma
61
HTLV-1
Leukemia
62
Merkel CA polyoma virus
Merkel cell carcinoma
63
Schistomiasis
Bladder CA indirect effect
64
H. pylori
Gastric CA, lymphoma indirect effect - bacteria, causing cell damage, inflammation, cytokines
65
Liver flukes
cholangioCA indirect effect
66
HIV
lymphoma, Kaposi indirect effect - immunosuppression
67
Cancer stem cells
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
Driver versus passenger mutations
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
Hallmarks of Cancer (8)
1. Unrestricted proliferation w/o external stimuli - ONCOGENES 2. Insensitivity to growth inhibitory signals - TUMOR SUPPRESSOR GENES 3. Altered Cell Metabolism 3. Evasion of Apoptosis alterations in tumor suppressor (p53) and anti-apoptotic genes (BCL2) 4. 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
What is an autocrine loop? Provide an example
Cancer cells make their own growth factor to stimulate their own surface receptors example: PDGF (platelet-derived growth factor) secreted by glioblastomas
71
What can oncogenes be?
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
Burkitt lymphoma translocation
Translocation between chromosomes 8 and 14 MYC activity is regulated by IgH regulatory region = thus always on in the lymphocytes
73
Roles of Wild p53 protein
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
Mutated p53
Genetic: Li-Fraumeni syndrome, SAs, leukemias, breast and adrenal cortical CAs Somatic, homozygous, in breast, lung and colon CAs
75
Follicular lymphoma translocation
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
What is angiogenesis? What is it required for?
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
Angiogenic factors include...
Growth factors (VEGF, FGF2, PDGF) Mutated p53
78
Angiogenic inhibitors include...
Thrombospondin-1, endostatin, angiostatin Wild p53
79
5 stimuli for angiogenesis
1. Tissue ischemia 2. Tissue hypoxia 3. Tissue injury 4. Inflammation 5. Shear stress
80
chronology of neovasculatization (8 steps)
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
Vascular endothelial growth factor (VEGF) What is it?
growth factor acting on surface of endothelial cells via surface receptors (mains is VEGFR-2)
82
Vascular endothelial growth factor (VEGF) Sources?
Inflammatory cells, various neoplasms
83
Vascular endothelial growth factor (VEGF) Unregulated by?
Hypoxia (analogous to EPO) Cytokines, hormones, other growth factors.
84
Vascular endothelial growth factor (VEGF) Actions?
Mitogenesis and maintenance ECS Anti-immune: decrease maturation of dendritic cells Vascular: vasodilation via NO pathways, fenestrations in EC
85
Clinical applications of angiogenesis
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
DNA repair defects (3)
1. mismatch excision repair (MMR) (MSH2, MLH1, PMS1, PMS2) - hereditary non-polyposis colon cancer 2. nucleotide excision repair 3. recombination repair
87
Multistep carcinogenic sequence in gastric carcinoma
1. Infection with H. pylori or pernicious anemia (immunologic) 2. Chronic gastritis 3. Intestinal metaplasia 3. Dysplasia/CIS 4. Adenocarcinoma

111 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions