Cancer Biology Articles

Understand how tumor suppressor genes — including TP53, BRCA1, PTEN, and RB1 — act as the genome's brakes, and what happens when they are lost in cancer.

A deep-dive into how EGFR mutations drive non-small-cell lung cancer, how downstream KRAS and BRAF amplify the signal, and why resistance to targeted therapy develops.

Learn how different types of gene mutations — point mutations, deletions, amplifications, and fusions — drive cancer and inherited disease, with real examples from TP53, KRAS, and BRCA1.

How the ATM–p53 signalling cascade detects DNA damage, how the MDM2–p53 feedback loop controls p53 stability, why TP53 mutations cause chemotherapy resistance, and how MDM2 inhibitors restore p53 signalling.

How ATM activates BRCA1 at DNA double-strand breaks, how BRCA1 orchestrates the homologous recombination repair cascade, why BRCA1 loss creates PARP inhibitor synthetic lethality, and germline mutation management.

How KRAS mutations lock the EGFR→KRAS→BRAF→MEK→ERK cascade in constitutive activation, why KRAS was undruggable for 40 years, how G12C covalent inhibitors work, and combination strategies overcoming EGFR-mediated resistance.

A complete guide to the PI3K/AKT/mTOR signalling axis — the most frequently altered pathway in human cancer — including PIK3CA mutations, PTEN loss, and approved inhibitors.

How BCL2-family proteins control the mitochondrial apoptosis decision, how cancer cells exploit BCL2/MCL1 overexpression for survival, and how venetoclax exploits BCL2 dependency.

How HER2 gene amplification drives constitutive receptor signalling, how trastuzumab and antibody-drug conjugates exploit HER2 overexpression, and emerging HER2-low treatment strategies.

How CDKN2A encodes two structurally unrelated tumor suppressors from the same locus, simultaneously protecting the pRb and p53 pathways, and why its deletion is so devastating in cancer.

How MYC functions as a universal transcriptional amplifier driving ribosome biogenesis, metabolic reprogramming, and cell cycle entry — why MYC-driven tumours require co-mutations in BCL2 or TP53 — and how BET inhibitors exploit super-enhancer dependency.

How BRAF V600E constitutively activates the MEK/ERK cascade, why BRAF and MEK inhibitors must be combined, and resistance mechanisms in melanoma, colorectal, and thyroid cancers.

How ATM detects and responds to DNA double-strand breaks, what germline ATM mutations cause, and how ATM loss in cancer creates sensitivity to PARP inhibitors and platinum chemotherapy.

How tumour hypoxia stabilises HIF-1α to drive VEGFA transcription, how VEGFA activates the VEGFR2 signalling cascade for vessel sprouting, and how bevacizumab and VEGFR TKIs block this angiogenic pathway.

How CDK4/6 inhibitors block the G1/S restriction point by protecting pRb from phosphorylation, their clinical evidence in breast cancer, and resistance mechanisms including RB1 loss.

How mTOR integrates growth, nutrient, and energy signals to drive protein synthesis and suppress autophagy, how mTOR inhibitors work, and why paradoxical AKT feedback limits their efficacy.

How proto-oncogenes become oncogenes through point mutation, amplification, and translocation — and how modern targeted therapies exploit oncogene dependency.

How cancers evolve through sequential mutation and clonal selection, how genomic instability accelerates this process, and what intratumoral heterogeneity means for treatment resistance.

How tumour cells exploit PD-1/PD-L1 and CTLA4 checkpoint signalling cascades to suppress T-cell activation, how KRAS and STAT3 drive intrinsic PD-L1 expression, and why MSI-high tumours respond to checkpoint blockade.

How mismatch repair corrects replication errors, how germline MLH1/MSH2/MSH6/PMS2 mutations cause Lynch syndrome, and why MSI-high tumours respond uniquely to PD-1 checkpoint blockade.