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pathology exam 1 > Lectures 12-17 > Flashcards

Lectures 12-17 Flashcards

1
Q

characteristics of benign tumors

A

usually resemble normal tissue, slow growth rate

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2
Q

cell of origin: adeno-

A

epithelial; glandular

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3
Q

cell of origin: lipo-

A

mesenchymal; fat

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4
Q

cell of origin: fibro-

A

mesenchymal; connective tissue-making

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5
Q

cell of origin: leio

A

mesenchymal; smooth muscle

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6
Q

cell of origin: rhabdomyo-

A

mesenchymal; skeletal muscle

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7
Q

cell of origin: osteo-

A

mesenchymal; bone

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8
Q

cell of origin: chondro-

A

mesenchymal; cartilage

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9
Q

cell of origin: angio-

A

mesenchymal; blood vessel

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10
Q

what are mixed tumors?

A

tumors with epithelial and mesenchymal compartments

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11
Q

what are teratomas?

A

tumors composed of tissue derived from multiple germ layers; predominantly benign

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12
Q

what are hamartomas?

A

mass of disorganized, mature tissue, not necessarily neoplastic conditions

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13
Q

what are choriostomas?

A

ectopic tissue in a foreign location, an anomaly of development (not tumor)

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14
Q

cell of origin: carcino-

A

epithelial

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15
Q

cell of origin: sarcoma

A

mesenchymal

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16
Q

define “well-differentiated”

A

resembles normal tissue

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17
Q

carcinoma in situ

A

malignant cells do not penetrate beyond basement membrane

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18
Q

define dysplasia

A

disordered growth of epithelium

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19
Q

characteristics of dysplasia (4)

A

loss of polarity, loss of maturation, loss of organization, abnormally located mitoses

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20
Q

malignant tumors that don’t metastasize (2)

A

basal cell carcinoma, gliomas (brain tumors)

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21
Q

most common pathway for sarcoma spread

A

hematogenous

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22
Q

most common pathway for carcinoma spread

A

lymphatics

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23
Q

seeding of peritoneal cavity is a frequent finding of what cancers?

A

ovarian and peripheral lung cancers

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24
Q

TNM staging system

A

T=tumor size; N=nodal involvement; M=metastasis

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25
Q

histologic examination: process

A

portions of tissue are sectioned into cassettes, fixed in formalin and embedded in paraffin overnight, cut into thin sections and H&E stained the next day

26
Q

indications for frozen tissues

A

surgical margin assessment and sentinel lymph node involvement

27
Q

karyotype analysis: process

A

dependent on isolation of chromosomes in metaphase, following stimulation with a mitogen, chromosomes are stained and arranged in pairs

28
Q

describe the exogenous pathway of tumor antigen processing

A

APCs capture tumor proteins from the microenvironment, process them, and present them on class II MHCs for CD4 T cells

29
Q

describe the endogenous pathway of tumor antigen processing

A

tumor cells process cytoplasmic proteins into peptides and present them on MHC class I for CD8 T cells

30
Q

tumor-infiltrating lymphocytes (TILs): mechanism

A

lymphocytes are cultured from tumors removed by surgery, expanded, then given back to patients

31
Q

chimeric antigen receptors (CARs): what are they

A

fuse antibody/binding portion of BCRs to internal portion of TCR which contains T cell signaling motifs

32
Q

chimeric antigen receptors (CARs): process

A

extract total white cells from patient, extract T cells, activate with cytokines, expand, transduce with CAR, return to patient

33
Q

allogeneic T cells as cancer immunotherapy: mechanism

A

donor T cells become activated to host alloantigens, can eliminate residual host cancer cells that express the alloantigens

34
Q

only one mutant allele required

A

oncogene (gain of function gene)

35
Q

ERB B2 gene (Her-2-Neu): mechanism, what type of gene is this

A

ERB B2 gene (Her-2-Neu) is a growth factor receptor that is amplified in breast cancer; protooncogene

36
Q

role of RAS in oncogenesis

A

Ras proteins are GTP-binding proteins and point mutations cause reduced GTPase activity –> continuous ON signal

37
Q

role of ABL in oncogenesis

A

ABL is normally a transient tyrosine kinase; t(9;22) Philadelphia Chromosome creates a BCR-ABL fusion product –> constitutive activity –> CML and ALL

38
Q

role of MYC in oncogenesis

A

normally MYC expression is increased following signal to replicate; mutated form leads to overexpression or amplification

39
Q

Burkitt lymphoma: mechanism

A

increased c-MYC expression via t(8;14), myc is placed under the control of Ig heavy chain locus –> B cell cancer

40
Q

n-MYC: clinical relevance

A

amplified in neuroblastoma; amplification is associated with poor prognosis; amplifies within chromosome or as little pieces of DNA

41
Q

role of cyclin D1 in oncogenesis

A

mantle cell lymphoma: t(11;14), cyclin D1-IgH fusion leading to overexpression of cyclin D1 –> CDK4 constitutively activated

42
Q

mantle cell lymphoma: two genes responsible

A

cyclin D1 and IgH

43
Q

increased c-MYC expression

A

Burkitt lymphoma

44
Q

what is the model for the two-hit hypothesis?

A

retinoblastoma (familial and sporadic forms)

45
Q

role of RB in oncogenesis

A

RB gene encodes for a tumor suppressor protein, mutations cause a failure of E2F regulation, allowing for uncontrolled E2F activation and unregulated cell growth –> retinoblastoma

46
Q

retinoblastoma: mechanism

A

mutations in RB cause a failure of E2F regulation allowing for uncontrolled E2F activation and unregulated cell growth

47
Q

role of APC in oncogenesis

A

APC gene encodes for a tumor suppressor that downregulates beta-catenin; mutations in APC cause beta-catenin accumulation and beta-catenin can complex with a transcription factor that stimulates the transcription of other growth factors –> hundreds of adenomas

48
Q

familial adenomatous polyposis (FAP): mechanism

A

mutations in APC cause beta-catenin accumulation and beta-catenin can complex with a transcription factor that stimulates the transcription of other growth factors –> hundreds of mucosal polyps carpet the colon of adolescents; need prophylactic colectomy

49
Q

hundreds of mucosal polyps carpet the colon of adolescents: what disease, mechanism

A

familial adenomatous polyposis (FAP); mutations in APC cause beta-catenin accumulation and beta-catenin can complex with a transcription factor that stimulates the transcription of other growth factors

50
Q

Li-Fraumeni syndrome: mechanism

A

inheritance of a mutated p53 allele, second mutation acquired later in life

51
Q

role of BCL-2 in oncogenesis

A

BCL-2 is an antiapoptotic protein, overexpressed in many lymphomas; t(14;18) causes IgH-bcl-2 fusion –> overexpression of BCL-2 –> follicular lymphoma

52
Q

follicular lymphoma: mechanism

A

t(14;18) causes IgH-bcl-2 fusion –> overexpression of BCL-2 (antiapoptotic protein)

53
Q

initiator and promoter chemical carcinogens

A

initiator: cause permanent DNA damage; promoter: enhances proliferation of mutated cells (Ex: hormones)

54
Q

role of EBV in oncogenesis

A

infected B cells in lymphoid tissue of oropharynx –> in immunocompromised patients, B cells are not checked by T cells so the infected B cells continue to grow and accumulate more mutations –> Burkitt lymphoma

55
Q

what kind of tumors are more likely to form in immunocompromised patients?

A

EBV-driven B cell tumors

56
Q

role of Hepatitis viruses in oncogenesis

A

chronic liver injury leads to regeneration, which leads to increased potential for genetic abnormalities; HBx (a viral protein from Hepatitis B) activates growth genes and inhibits p53

57
Q

role of Helicobacter pylori in oncogenesis

A

host inflammatory response leads to carcinogenesis; regeneration, metaplasia, dysplasia –> adenocarcinoma; treatment with eradication of H. pylori

58
Q

a constant dose of drug kills a constant ??? of tumor cells

A

fraction

59
Q

tumor size predicts what component of therapy?

A

duration

60
Q

to be a curative, a chemotherapy regimen must have a ??? efficiency and be repeated for ??? cycles

A

2-4 log-kill; 4-12 cycles

61
Q

cell cycle-specific, phase nonspecific drugs (3)

A

cyclophosphamide, cisplatin, doxorubicin

pathology exam 1 (4 decks)

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