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Path 2 > neoplasm 4 > Flashcards

neoplasm 4 Flashcards

1
Q

define dysplasia

A
  • disordered growth = loss in uniformity of individual cells and loss in their architectural orientation
  • -> pleomorphism and mitoses are more prominent than in normal tissue
  • Dysplasia may be a precursor to cancer, but does NOT invariable progress to cancer
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2
Q

describe the spectrum of squamous neoplasia of the cervix

A
  • Grade of CIN is defined by proportion of the epithelium occupied by immature cells
  • invasive carcinoma occurs when the abnormal cells invade through (“breach”) the basement membrane
  • CIN 1 = 1/3 full thickness of immature cells (mild)
  • CIN 2 = 2/3 full thickness (moderate)
  • CIN 3 = 2/3-3/3 full thickness (severe)
  • carcinoma in situ(CIS) = full thickness
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3
Q

define carcinoma in situ (CIS)

A
  • full-thickness dysplasia extending from BM to surface of epithelium
  • applicable only to epithelial neoplasm
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4
Q

what occurs if oral leukoplakia undergoes dysplasia

A
  • squamous cell carcinoma
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5
Q

what occurs if barrett esophagus (metaplasia) undergoes dysplasia

A
  • Adeocarcinoma of esophagus
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6
Q

what occurs if chonric atrophic gastritis of pernicious anemia undergoes dysplasia

A
  • gastric adenocarcinoma
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7
Q

What occurs if chornic ulcerative colitis undergoes dysplasia

A
  • adenocarcinoma of colon
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8
Q

what occurs if hepatitis infection (B or C) undergo cirrhosis

A
  • macro-nodular cirrhosis develops and then hepato-cellular carcinoma
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9
Q

what occurs if simple/comlex hyperplasia occurs in endometrium

A
  • simple/complex hyperplasia develops into atypical hyperplasia (endometrical intra-epithelial neoplasia (EIN))
  • EIN develops into endometrial adenocarcinoma
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10
Q

what occurs if solar keratosis of skin undergoes dysplasia

A
  • skin cancer (usually squamous cell carcinoma)
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11
Q

what are the essential alterations for malignant transformation (some are needed)

A
  • self-sufficiency in growth signals
  • insensitivity to growth-inhibitory signals
  • evasion of apoptosis
  • limitless replicative potential
  • sustained angiogenesis
  • ability to invade and metastasize
  • defects in DNA repair
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12
Q

what are the 4 classes of normal regulatory genes

A
  • growth promoting proto-oncogenes
  • growth inhibiting tumor suppressor genes
  • genes regulating apoptosis
  • genes regulating DNA repair
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13
Q

define proto-oncogenes

A
  • responsible for regulation of growth and differentiation
  • once activated, proto-oncogene becomes oncogene
  • activation mechanism: mutation, chromosomal translocation and amplification
  • oncogene is the cancer causing gene
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14
Q

what mechanimism is involved in activation of oncogen

A
  • chemical carcinogen, radiation, infectious agent causes DNA damage
  • DNA damage leads to point mutation, translocation, amplification
  • leads to transformation with genetic defect
  • final effect is normal protein is overproduced or mutant protein is produced and has an aberrant function
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15
Q

define ERBB2 Receptor

A
  • growth factor receptor (EGF)
  • also known as (HER-2/NEU)
  • causes amplification
  • found in breast and ovarian cancer
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16
Q

define RET recetpor

A
  • receptor for neurotropic factors (GH)
  • causes point mutations
  • found in MEN 2A and 2B, familial meduallary thyroid carcinomas
17
Q

define KRAS receptor

A
  • GTP-binding receptor
  • causes point mutation in protein invovled in signal transduction
  • found in pancreas, colon and lung cancers
18
Q

define ABL receptor

A
  • non-receptor tyrosine kinase
  • causes translocation in proteins in signal transduction
  • found in chronic myeloid leukemia and actue lymphoblastic leukemia
19
Q

define B-catenin receptor

A
  • WNT signal transduction recetpor
  • causes point mutation and over-expression in protein involved in signal transduction
  • found in hepato-blastomas and hepatocellular carcinoma (LIVER CANCER)
20
Q

define BRAF

A
  • RAS signal transduction
  • causes point mutations in proteins involved in signal transduction
  • found in melanomas
21
Q

define C-myc receptor

A
  • transcriptional activator
  • causes translocation of nuclear-regulatory proteins
  • found in burkitt lymphoma
22
Q

define N-Myc receptor

A
  • transcriptional activator
  • casues amplification of nuclear-regulatory proteins
  • found in neuroblastoma, small-cell carcinoma of the lung
23
Q

define cyclin D

A
  • causes translocation of cell cycle regulators = found in mantle cell lymphoma
  • causes amplification of cell cycle regulators = found in breast and esophageal cancers
24
Q

describe Multiple endocrine neoplasia types 2a and 2b

A
  • caused by mutation of RET PROTO-ONCOGENE
  • involves lots of organs
  • -> thyroid, pancreas, parathyroid
  • -> can be hyperplasia or tumor
25
Q

describe chronic myelogenous leukemia (CML)

A
  • c-abl proto-oncogene on chromosome 9 is translocated to bcr (an oncogene on chromosome 22)
  • -> new chromosome referred to as philadelphia chromosome
  • -> increases tyrosine kinase activity causing stimulation of proliferation of granulocytic precursors giving rise to chronic myeloid leukemia (CML)
26
Q

describe imatinib mesylate

A
  • INHIBITS tyrosine kinase and can be used to treat CML
27
Q

describe burkitt lymphoma

A
  • translocation of C-MYC proto-oncogene from chromosome 8 to a site adjacent to Ig heavy chain locus on chromosome 14
  • leads to over-expression or amplification of C-MYC leads to excess transcription signals
28
Q

describe B-cell follicular lymphoma

A
  • BCL-2 genes produce gene products that PREVENT mitochondrial leakage of cytochrome C (signal for apoptosis)
  • BCL-2 = anti-apoptotic factor
  • Transolocation (14 to 18) leading to overexpression of BCL-2 protein product causing inhibition of apoptosis of B lymphocytes –> FOLLICULAR LYMPHOMA
  • *PATHOGENESIS is EXCLUSIVELY BY EVASION OF APOPTOSIS**
29
Q

Describe neuroblastoma

A
  • amplification of N-MYC

- only 40% are associated with amplification of N-MYC

Path 2 (11 decks)

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