This quiz explores the molecular basis of precancerous conditions through clinical scenarios. It assesses understanding of genetic mutations and molecular changes leading to cancer, enhancing knowledge crucial for medical practitioners and researchers.
ERBB2
P53
RAS
MYC
APC
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Desmin
Telomerase
P selectin
E cadherin
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MYC
APC
RAS
ERBB2
Sis
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BCL1 (cyclin gene)
BCL2 (anti-apoptosis gene)
K-RAS (GTP-binding protein gene)
N-MYC (transcription factor gene)
P53 ( DNA damage response gene)
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BRCA1
P53
Rb
VHL
WT-1
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K-RAS mutation in neoplastic cells
Immuno-histochemical stain positive for vimentin in the neoplastic cells
Translocation between chromosomes 9 and 22
Translocation between chromosomes 8 and 14
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Increased tyrosine kinase activity
Lack of apoptosis
Gene amplification
Reduced DNA repair
Loss of cell cycle inhibition
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Chromosomal translocation
Exon deletion
Frame-shift mutation
Gene amplification
Expansion of a tri-nucleotide repeat
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Activation of telomerase
Activation of BCL2 gene
Activation of VEGF
Inability to repair errors in DNA replication
Activation of cyclin gene
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ABL
BCL-1
BCL-2
MYC
Retinoic acid receptor (RAR)
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Balanced translocation
Expansion of tri-nucleotide repeat
Gene amplification
Loss of heterozygosity
Maternal non-disjunction
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Atrophy
Hydropic swelling
Hyperplasia
Hypertrophy
Metaplasia
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Apoptosis
Cell adhesion
DNA repair
Gene transcription
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P53
PTEN
Rb
RET
WT-1
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Hyperplasia
Metaplasia
Dysplasia
Carcinoma in situ
Carcinoma
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Point mutation
Chromosomal translocation
Gene amplification
Deletion
Epigenetic modification
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Mutation in mismatch repair genes
Inability to hydrolyze GTP-bound RAS
Activation of WNT signaling pathway
Loss of heterozygosity affecting p53 gene
Translocation of BCL2 from mitochondria to cytoplasm
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BCL2
Beta-catenin
MYC
P53
TGF-beta
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Quiz Review Timeline (Updated): Feb 2, 2025 +
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