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neoplasia Flashcards

1
Q

5 characteristics of anaplasia

A
  1. pleomorphism (variation in cell shape and size
  2. nuclear hyperchromatism (intensely basophilic nuclei)
  3. increased nuclear/cytoplasmic ratio compared to normal cells
  4. atypical nuclei (variation in shape and size)
  5. numerous and atypical mitoses
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2
Q

most severe form of epithelial dysplasia which has all of the microscopic features of cancer, but the atypical cells have not invaded into the host

A

carcinoma-in-situ

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3
Q

____ tumors tend to have a capsule, which is a compressed band of _____ at the periphery of the tumor

A

benign; fibrous connective tissue

hemangioma and neurofibroma are common exceptions

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4
Q

the ____ quality is the most reliable means for distinguishing the malignant nature of a tumor

A

infiltrative

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5
Q

____ is considered the best indicator of malignancy

A

presence of metastasis

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6
Q

3 ways that malignancies spread

A
  1. seeding within body cavities (like the peritoneal cavity)
  2. lymphatic spread (commonly seen in carcinomas, resulting in lymph node metastases)
  3. hematogenous spread- favored by sarcomas; lung and liver frequent sites of metastasis in this case
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7
Q

3 well-defined genetic influences on cancer

A
  1. inherited cancer syndromes, AD (Rb, MEN)
  2. defective DNA repair syndromes, AR (xeroderma pigmentosum, ataxia telangiectasia)
  3. familial cancers (colon, breast, ovarian)
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8
Q

acquired preneoplastic disorders (persistent regenerative cell replication)

A
  1. squamous metaplasia and dysplasia of bronchial mucosa
  2. endometrial hyperplasia and dysplastic proliferations
  3. leukoplakia of the oral mucosa, vulva, penis
  4. villous adenomas of the colon
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9
Q

3 classes of normal regulatory genes - principal targets of genetic damage

A
  1. protooncogenes
  2. cancer suppressor genes
  3. apoptosis regulatory genes
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10
Q

____ are also important in carcinogenesis; if these genes are disabled, the _____ increases and the _____ increases

A

DNA repair genes; frequency of mutations; rate of neoplastic transformation

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11
Q

6 hallmarks of cancer

A
  1. self-sufficiency in growth signals
  2. insensitivity to growth inhibitory signals
  3. evasion of cell death
  4. limitless replicative potential
  5. development of sustained angiogenesis
  6. ability to invade and metastasize
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12
Q

factors susceptible to cancer in development of self-sufficiency in growth signals

A
  1. growth factors
  2. growth factor receptors
  3. signal-transduction proteins
  4. nuclear transcription factors
  5. cyclins and cyclin-dependent kinases (CDKs)
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13
Q

growth factor receptor commonly overexpressed

A

epidermal growth factor receptor family
ERBB-1 in squamous cell carcinoma of the lung
ERBB-2 (HER/NEU) amplified in some breast cancers

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14
Q

most commonly mutated proto-oncogene

A

RAS gene (normal cytoplasmic signal-transducing protein)

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15
Q

most common overexpressed nuclear transcription factor

A

MYC gene (activates transcription of cyclin D1, a gene whose product drives cells into the cell cycle)

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16
Q

first tumor suppressor gene to be discovered

A

retinoblastoma (Rb) gene

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17
Q

single most common target for genetic alteration in human tumors

A

TP53 tumor suppressor gene

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18
Q

___ loss of ____ is found in virtually every type of cancer; usually due to _____

A

homozygous loss of TP53; somatic mutation

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19
Q

condition in which families have one aberrant TP53 gene, resulting in a markedly increased rate of cancer for affected individuals

A

Li-Fraumeni syndrome

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20
Q

____ is the prototypic anti-apoptosis gene activated by ____; found in ____

A

BCL2; translocation; low-grade lymphomas

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21
Q

2 major phases of metastasis

A
  1. invasion of the ECM

2. vascular dissemination and adhesion/homing of tumor cells

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22
Q

steps of invasion of ECM

A
  1. detachment of tumor cells from one another
  2. attachment of tumor cells to matrix components
  3. degradation of ECM
  4. migration of tumor cells
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23
Q

once in the circulation, tumor cells adhere to _____, followed by _____

A

vascular endothelium; basement membrane transmigration

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24
Q

the dist of tumor metastases can generally be predicted by the _____ and _____

A

location of the primary tumor and its vascular or lymphatic drainage

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25
Q

2 methods of organ tropism

A
  1. organ specific endothelial adhesion molecules bind tumor cell ligands
  2. chemokine receptors on tumor cells home to sites where specific ligands are readily produced
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26
Q

conditions with inherited defects in DNA repair

A
  1. hereditary nonpolyposis colon cancer syndrome
  2. xeroderma pigmentosum
  3. bloom syndrome, ataxia telangiectasia, fanconi anemia
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27
Q

HNPCC syndromes are familial cancers of the colon resulting from defective genes involved in ______ and evidence of ______

A

DNA mismatch repair; microsatellite instability (MSI)

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28
Q

xeroderma pigmentosum involves a defective _______; sunlight (UV light) causes _____ in DNA, halting replication with inability to repair these altered residues

A

nucleotide excision repair system; pyrimidine cross-linking

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29
Q

Bloom syndrome, ataxia telangiectasia, and fanconi anemia are ____ disorders characterized by _____; called _____

A

AR; hypersensitivity to Dna damage; fragile dna disorders

30
Q

familial breast cancer genes (BRCA1 and BRCA2) involved with _____, may also have _____ roles

A

dsDNA breaks; tumor suppressor

31
Q

karyotypic changes in tumors

A
  1. balanced translocations
  2. deletions
  3. gene amplifications
32
Q

balanced translocations extremely common especially in _____ (example is _____ in ____)

A

hematopoietic neoplasms; philadelphia chromosome; chronic myelogenous leukemia

33
Q

most carcinogens are ____ and require some _____

A

indirect; metabolic conversion

34
Q

indirect carcinogens are called _____ and active end-products are termed _____

A

procarcinogens (i.e. polycyclic hydrocarbons); ultimate carcinogens

35
Q

all carcinogens are highly reactive _____, interacting with the _____ and inducing genetic damage

A

electrophiles; electron-rich DNA molecule

36
Q

3 major classes of carcinogenic agents

A
  • chemicals
  • radiation
  • oncogenic viruses
37
Q

some carcinogens can be augmented by ____, agents that have little inherent transforming ability

A

promoters (carcinogen serves as initiator of mutagenic event)

38
Q

example of an RNA oncogenic virus

A

HTLV-I (human T cell leukemia virus type I)

39
Q

HTLV-I is associated with a form of _____ in certain parts of ____ and the _____

A

T cell leukemia/lymphoma (develops in about 3-5% of infected people after a long 20-50 year latent period)

40
Q

DNA oncogenic viruses are transforming DNA viruses that form ____ associations with the host cell _____

A

stable; genome

41
Q

3 types of DNA oncogenic viruses

A
  1. human papillomavirus (HPV)
  2. epstein-barr virus (EBV)
  3. hepatitis B virus (HBV)
42
Q

some types of HPV (1, 2, 4, 7) cause _____ or _____

A

benign squamous papillomas; verruca vulgaris (wart)

43
Q

HPV types 16 and 18 are associated with the development of _____ and _____

A

uterine cancer; oropharyngeal (tonsillar) cancer

44
Q

EBV implicated in pathogenesis of:

A

Burkitt lymphoma, B-cell lymphoma in immunosuppressed patients, Hodgkin lymphoma, and nasopharyngeal carcinoma

45
Q

HBV linked to development of ______

A

hepatocellular carcinoma

46
Q

the concept of _____ refers to the recognition and destruction of non-self tumor cells when they appear

A

immune surveillance

47
Q

antigens only associated with tumor cells

A

tumor-specific antigens

48
Q

2 examples of tumor-specific antigens

A

cancer-testis antigens

MAGE-1 (melanoma-associated antigen)

49
Q

these are antigens that may be found on normal cells, but may be overexpressed or represent a specialized function of the cells

A

tumor-associated antigens

50
Q

tumor-associated antigens that represent a specialized function of the cells

A

differentiation-specific antigens

51
Q

example of a differentiation-specific antigen

A

prostate-specific antigen (PSA)

52
Q

4 antitumor effector mechanisms

A
  1. cytotoxic (CD8+) T lymphocytes
  2. natural killer (NK) cells
  3. macrophages
  4. humoral mechanisms
53
Q

CD8+ T lymphocytes play a role against ____ neoplasms, such as ____

A

virus-induced; Burkitt’s lymphoma

54
Q

NK cells are lymphocytes that can kill tumor cells without _____; may be the ___ line of defense against tumors

A

prior sensitization; first

55
Q

macrophages may collaborate with ____ and ____ to destroy tumor cells; may act by mechanisms used to destroy ____ or by producing ____

A

T cells; NK cells; microbes; TNF-alpha

56
Q

humoral mechanisms include either activation of _____ or induction of _____ by NK cells

A

complement; antibody-dependent cytotoxicity

57
Q

3 host defenses against tumors

A
  1. tumor antigens
  2. antitumor effector mechanisms
  3. immunosurveillance
58
Q

how cancers develop in immune competent individuals

A
  1. selective outgrowth of antigen-negative variants
  2. loss or reduced expression of histocompatibility antigens
  3. lack of co-stimulation
  4. immunosuppression
59
Q

tumor cells do not express normal levels of _____, thereby escaping attack by _____

A

HLA class I; cytotoxic T cells

60
Q

effects of tumor on host

A
  1. location
  2. hormone production
  3. ulceration
  4. cachexia
  5. paraneoplastic syndromes
61
Q

____ and _____ arising from the beta cells of the pancreatic islets may produce _____ which may be fatal

A

adenomas; carcinomas; hyperinsulinism

62
Q

hormone production is more frequent in _____ tumors

A

well-differentiated, benign

63
Q

cachexia may involve ___ and ____

A

TNF; IL-1

64
Q

examples of paraneoplastic syndromes

A

hypercalcemia
cushing’s syndrome
nonbacterial thrombotic endocarditis
paraneoplastic pemphigus

65
Q

attempt to assess the aggressiveness of a malignancy based on such criteria as the degree of cytologic differentiation of the tumor cells and the number of mitoses

A

grading (can range from I to IV)
I - most differentiated
IV- least differentiated

66
Q

a method of estimating the size or extent usually done using clinical examination coupled with imaging studies (plain radiographs, CT, MRI)

A

staging

67
Q

used primarily as a screening method for cervical Ca. Now being supplemented by HPV testing

A

cytologic (papanicolaou) smears

68
Q

specific antibody-guided detection of tumor-specific or associated antigens to determine the precise classification or subclassification of a tumor

A

immunocytochemistry

69
Q

Used routinely in classification of leukemias and lymphomas. Surface markers and DNA ploidy analysis

A

flow cytometry

70
Q

looking for tumor-associated enzymes, hormones and other tumor markers in the blood. Prostate-specific antigen (PSA) is a good example

A

biochemical assays

71
Q

use of fluorescent in-situ hybridization (FISH) or polymerase chain reaction(PCR)-based methods gives important diagnostic and prognostic information. “Personalized” medicine

A

molecular diagnosis

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