Comprehensive Table: Molecular Oncology Overview

Main Topic Subcategory Details & Examples

Description
Regulation of Cell Internal Control Controlled by Cyclin-CDK
Division Cyclins and Cyclin- complexes activate
Dependent Kinases progression to the
(CDKs), which next phase.
regulate cell cycle
checkpoints (G1, S,
G2, M phases).
Ensures proper DNA
replication and
prevents
propagation of
damaged DNA.
External Control Growth Factors and Growth Hormone,
Hormones bind to EGF (Epidermal
receptors on the cell Growth Factor), IGF
membrane, (Insulin-like Growth
triggering Factor).
intracellular
signaling pathways.
These pathways
activate Cyclin-CDK,
promoting cell cycle
progression.
Checkpoint G1 Checkpoint Checks for DNA Controlled by p53
Functions damage before and Cyclin-CDK
replication. inhibitors.
Prevents entry into
S phase if DNA is
damaged.
S Phase Checkpoint DNA synthesis
phase; ensures
correct replication
of DNA.
G2/M Checkpoint Checks for DNA
damage after
replication before
mitosis.
M Checkpoint Checks correct
spindle attachment
before
chromosomal
separation.
Tumor Suppressor Definition Genes that produce p53, RB
Genes (TSG) proteins to inhibit (Retinoblastoma),
 cell division, repair BRCA1/2.
DNA, or initiate
apoptosis when
damage is detected.
p53 Role Called 'Guardian of p53 prevents
the Genome.' proliferation of
Activates repair genetically damaged
enzymes, blocks S cells.
phase, or initiates
apoptosis if damage
is irreparable.
Mutated in over
50% of cancers.
RB Role Controls Retinoblastoma (eye
progression from G1 cancer in children).
to S phase by
binding E2F
transcription factor.
Mutation leads to
retinoblastoma and
other cancers.
Proto-Oncogenes & Proto-Oncogenes Normal genes RAS, MYC, EGFR.
Oncogenes coding for proteins
involved in growth
and division.
Essential for normal
cellular function.
Oncogenes Mutated proto- Mutant RAS found in
oncogenes; cause ~30% of cancers.
uncontrolled cell
division even in
absence of signals.
DNA Repair Genes Function Repair damaged BRCA1/BRCA2 in
DNA before cell breast and ovarian
division. Mutation cancer.
leads to
accumulation of
genetic errors.
Apoptosis-Related Function Regulate BAX (pro-
Genes programmed cell apoptotic), BCL-2
death to remove (anti-apoptotic).
damaged cells.
Inactivation allows
survival of defective
cells.
Multi-Step Mutation Cancer arises from Example: Colon
Carcinogenesis Accumulation sequential cancer involves APC
mutations: → KRAS → p53
Activation of mutation sequence.
 oncogenes,
Inactivation of TSGs,
DNA repair loss,
Apoptosis evasion.
Carcinogens Effects on Genes Activate oncogenes, Smoking:
Inactivate tumor carcinogens cause
suppressor genes, p53 mutation in
Block DNA repair, lung cancer.
Suppress apoptosis.
Analytical Targets in Tissue-Specific Reflect tissue origin Cytokeratin in
Molecular Testing Genes of tumor. May be gastric cancer, CEA
present in normal in breast cancer,
cells. TCR
rearrangements in
lymphoma.
Tumor-Specific Arise from unique Philadelphia
Genes genetic alterations Chromosome (BCR-
in cancer. More ABL fusion) in CML.
specific for
detecting tumors.
Applications of Clinical Uses Early cancer HER2 testing in
Molecular Oncology detection, Prognosis breast cancer; KRAS
prediction, mutation testing in
Monitoring disease colorectal cancer.
progression or
recurrence,
Predicting
therapeutic
response (targeted
therapy).