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Principles of Neoplasia > Principles of Neoplasia > Flashcards

Principles of Neoplasia Flashcards

1
Q

Epithelium (Benign)

A

Adenoma and Papilloma

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2
Q

Epithelium (Malignant/Cancer)

A

Adenocarcinoma and Papillary carcinoma

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3
Q

Mesenchyme (Benign)

A

Lipoma

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4
Q

Mesenchyme (Malignant/Cancer)

A

Liposarcoma

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5
Q

Lymphocyte (Benign)

A

Does not exist

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6
Q

Lymphocyte (Malignant/Cancer)

A

Lymphoma/Leukemia

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7
Q

Melanocyte (Benign)

A

Nevus (mole)

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8
Q

Melanocyte (Malignant/Cancer)

A

Melanoma

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9
Q

Alfatoxins

A
  • hepatocellular carcinoma

- derived from Aspergillus, which can contaminate stored rice and grains

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10
Q

Alkylating agents

A
  • leukemia/lymphoma
  • side effect of chemotherapy
  • many chemotherapy agents are myelosuppresive
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11
Q

Alcohol

A
  • squamous cell carcinoma of oropharynx and upper esophagus

- hepatocellular carcinoma

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12
Q

Asbestos

A
  • lung carcinoma
  • mesothelioma
  • exposure to asbestos is more likely to lead to lung cancer than mesothelioma
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13
Q

Arsenic

A
  • squamous cell carcinoma of skin
  • lung cancer
  • angiosarcoma of liver
  • present in cigarette smoke
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14
Q

Cigarette smoke

A
  • carcinoma of oropharynx, esophagus, lung, kidney, bladder, and pancreas
  • most common carcinogen worldwide
  • polycyclic hydrocarbons are particularly carcinogenic
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15
Q

Nitrosamines

A
  • stomach cancer
  • found in smoked foods
  • responsible for high rate of stomach carcinoma in Japan
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16
Q

Naphthylamine

A
  • urothelial carcinoma of bladder

- derived from cigarette smoke

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17
Q

Vinyl chloride

A
  • angiosarcoma of liver
  • occupational exposure
  • used to make polyvinyl chloride (PVC) for use in pipes
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18
Q

Nickel, chromium, baryllium, or silica

A
  • lung carcinoma

- occupational exposure

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19
Q

EBV

A
  • oncogenic virus
  • nasopharyngeal carcinoma
  • Burkitt lymphoma
  • CNS lymphoma in AIDS
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20
Q

HHV-8

A
  • oncogenic virus

- Kaposi sarcoma

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21
Q

HBV and HCV

A
  • oncogenic virus

- hepatocellular carcinoma

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22
Q

HTLV-1

A
  • oncogenic virus

- adult T-cell leukemia/lymphoma

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23
Q

High-risk HPV (e.g. subtypes 16, 18, 31, 33)

A
  • oncogenic virus
  • squamous cell carcinoma of vulva, vagina, anus, and cervix
  • adenocarcinoma of cervix
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24
Q

Ionizing Radiation (nuclear reactor accidents and radiotherapy)

A
  • AML
  • CML
  • papillary carcinoma of the thyroid
  • generates hydroxyl free radicals
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25
Q

Nonionizing Radiation

A
  • basal cell carcinoma
  • squamous cell carcinoma
  • melanoma of skin
  • UVB sunlight is most common source
  • results in formation of pyrimidine dimers in DNA, which are normally excised by restriction endonucleases
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26
Q

PDGFB

A
  • platelet-derived growth factor
  • mechanism: overexpression, autocrine loop
  • associated tumor: astrocytoma
27
Q

ERBB2 (HER2/neu)

A
  • epidermal growth factor receptor
  • mechanism: amplification
  • associated tumor: subset of breast carcinomas
28
Q

RET

A
  • neural growth factor receptor
  • mechanism: point mutation
  • associated tumor: MEN2A, MEN2B and sporadic medullary carcinoma of thyroid
29
Q

KIT

A
  • stem cell growth factor receptor
  • mechanism: point mutation
  • associated tumor: gastrointestinal stromal tumor (GIST)
30
Q

RAS gene family

A
  • GTP-binding protein
  • mechanism: point mutation
  • associated tumor: carcinomas, melanoma, and lymphoma
31
Q

ABL

A
  • tyrosine kinase
  • mechanism: t(9;22) with BCR
  • associated tumor: CML and some types of ALL
32
Q

c-MYC

A
  • transcription factor
  • mechanism: t(8;14) involving IgH
  • associated tumor: Burkitt lymphoma
33
Q

N-MYC

A
  • transcription factor
  • mechanism: amplification
  • associated tumor: neuroblastoma
34
Q

L-MYC

A
  • transcription factor
  • mechanism: amplification
  • lung carcinoma (small cell)
35
Q

CCND1 (cyclin D1)

A
  • cyclin
  • mechanism: t(11;14) involving IgH
  • mantle cell lymphoma
36
Q

CDK4

A
  • cyclin-dependent kinase
  • mechanism: amplification
  • associated tumor: melanoma
37
Q

p53

A
  • regulates progression from G1 to S phase
  • DNA damage –> p53 slows the cell cycle and upregulates DNA repair enzymes
  • if DNA repair not possible –> induce apoptosis
  • p53 induces apoptosis by upregulating BAX, which disrupts Bcl2… this then causes cytochrome c to leak from mitochondria and thus activate apoptosis
  • both copies of the p53 gene must be knocked out for tumor formation
  • loss is seen in >50% of cancers
  • germline mutation results in Li-Fraumeni syndrome (2nd hit somatic), characterized by the propensity to develop multiple types of carcinomas and sarcomas
38
Q

Rb

A
  • regulates progression from G1 to S phase
  • “holds” the E2F transcription factor, which is necessary for transition to the S phase
  • E2F is released when Rb is phosphorylated by the cyclinD/cyclin-dependent kinase 4 (CDK4) complex
  • Rb mutation results in constitutively free E2F, allowing progression through the cell cycle and uncontrolled growth of cells
  • both copies of Rb gene must be knocked out for tumor formation
  • sporadic mutation (both hits are somatic) is characterized by unilateral retinoblastoma
  • germline mutation results in familial retinoblastoma (2nd hit is somatic), characterized by bilateral retinoblastoma and osteosarcoma
39
Q

Bcl2

A
  • prevent apoptosis in normal cells
  • promote apoptosis in mutated cells whose DNA cannot be repaired
  • normally stabilizes the mitochondrial membrane, blocking release of cytochrome c
  • disruption of Bcl2 allows cytochrome c to leave the mitochondria and activate apoptosis
40
Q

Bcl2 and Follicular Lymphoma

A
  • Bcl2 is overexpressed in follicular lymphoma
  • t(14,18) moves Bcl2 (chromosome 18) to the Ig heavy chain locus (chrom. 14), resulting in increased Bcl2
  • mitochondrial membrane is further stabilized, prohibiting apoptosis
  • B cells that would normally undergo apoptosis during somatic hyper-mutation in the lymph node germinal center accumulate, leading to lymphoma
41
Q

Telomerase and Tumor Development

A
  • telomerase is necessary for cell immortality
  • normally, telomeres shorten with serial cell divisions, eventually resulting in cellular senescence
  • cancers often have upregulated telomerase, which preserves telomeres
42
Q

Angiogenesis and Tumor Development

A
  • necessary for tumor survival and growth

- FGF and VEGF (angiogenic factors) are commonly produced by tumor cells

43
Q

Avoiding Immune Surveillance

A
  • necessary for tumor survival
  • mutations often result in production of abnormal proteins, which are expressed on MHC class I
  • CD8+ T cells detect and destroy such mutated cells
  • tumor cells can evade immune surveillance by downregulating expression of MHC class I
  • immunodeficiency (both primary and secondary) increases the risk for cancer
44
Q

Tumor Invasion and Spread

A
  • epithelial tumor cells are normally attached to one another by cellular adhesion molecules (e.g. E-cadherin)
  • downregulation of E-cadherin leads to dissociation of attached cells
  • cells attach to laminin and destroy basement membrane (collagen type IV) via collagenase
  • cells attach to fibronectin in the extracellular matrix and spread locally
  • entrance into vascular or lymphatic spaces allows for metastasis (distant spread)
45
Q

Routes of Metastasis (lymphatic spread)

A
  • lymphatic spread is characteristic of carcinomas

- initial spread is to regional draining lymph nodes

46
Q

Routes of Metastasis (hematogenous spread)

A
  • hematogenous spread is characteristic of sarcomas and some carcinomas
  • renal cell carcinoma (often invades renal vein)
  • hepatocellular carcinoma (often invades hepatic vein)
  • follicular carcinoma of the thyroid
  • choriocarcinoma
47
Q

Seeding

A

-seeding of body cavities is characteristic of ovarian carcinoma, which often involves the peritoneum

48
Q

Clinical Features (Benign and Malignant Tumors)

A
  • benign tumors tend to be slow growing, well circumscribed, distinct, and mobile
  • malignant tumors are usually rapid growing, poorly circumscribed, infiltrative, and fixed to surrounding tissues and local structures
  • biopsy or excision is generally required before a tumor can be classified as benign or malignant with certainty
  • some benign tumors can grow in a malignant-like fashion, and some malignant tumors can grow in a benign-like fashion
49
Q

Histological Features (benign tumors)

A
  • usually well differentiated
  • organized growth
  • uniform nuclei
  • low nuclear to cytoplasmic ratio
  • minimal mitotic activity
  • lack of invasion (of basement membrane or local tissue)
  • no metastatic potential
50
Q

Histological Features (metastatic tumors)

A
  • classically poorly differentiated (anaplastic)
  • disorganized growth (loss of polarity)
  • nuclear pleomorphism and hyperchomasia
  • high nuclear to cytoplasmic ratio
  • high mitotic activity with atypical mitosis
  • invasion (through basement membrane or into local tissue)
  • metastatic potential is the hallmark of malignancy - benign tumors never metastasize
  • immunohistochemistry is used to characterize tumors that are difficult to classify on histology
51
Q

Serum Tumor Markers

A
  • proteins released by tumor into serum (e.g. PSA)
  • useful for screening, monitoring response to treatment, and monitoring recurrence
  • elevated levels require tissue biopsy for diagnosis of carcinoma (e.g. biopsy of prostate with elevated PSA)
52
Q

Grading of Cancer

A
  • microscopic assessment of differentiation (i.e. how much a cancer resembles the tissue in which it grows); takes into account architectural and nuclear features
  • well differentiated (low grade) resembles normal parent tissue
  • poorly differentiated (high grade) does not resemble parent tissue
  • important for determining prognosis; well-differentiated cancers have better prognosis than poorly-differentiated cancers
53
Q

Staging of Cancer

A
  • assessment of size and spread of a cancer
  • key prognostic factor; more important than grade
  • determined after final surgical resection of the tumor
  • utilizes TNM staging system
  • T: tumor (size and/or depth of invasion)
  • N: spread to regional lymph nodes; second most important prognostic factor
  • M: metastasis; single most important prognostic factor
54
Q

Immunohistochemical Stain (keratin)

A

-epithelium

55
Q

Immunohistochemical Stain (vimentin)

A

-mesenchyme

56
Q

Immunohistochemical Stain (GFAP)

A

-neuroglia

57
Q

Immunohistochemical Stain (desmin)

A

-muscle

58
Q

Immunohistochemical Stain (neurofilament)

A

-neurons

59
Q

Immunohistochemical Stain (PSA)

A

-prostatic epithelium

60
Q

Immunohistochemical Stain (ER)

A

-breast epithelium

61
Q

Immunohistochemical Stain (thyroglobulin)

A

-thyroid follicular cells

62
Q

Immunohistochemical Stain (chromogranin)

A

-neuroendocrine cells (e.g. small cell carcinoma of lung and carcinoid tumors)

63
Q

Immunohistochemical Stain (S-100)

A

-melanoma, Schwannoma and Langerhans cell histiocytes

Principles of Neoplasia (1 decks)

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