Research Articles

Cancer Biology Articles

Expert explanations of tumor suppressor genes, oncogenic signalling, and targeted therapy — grounded in peer-reviewed science.

Quick Answer

This article library focuses on cancer genes, driver mutations, signalling pathways, and therapy resistance, with contextual links into curated gene profiles and pathway mechanisms.

How cancer drugs work → — a dedicated section on targeted-therapy mechanisms.

Flagship Guide

Gene Function Explained: A Complete Guide to Cancer Biology

From the basics of how genes control cell division to the mechanisms of tumor suppressors, oncogenes, and targeted therapy — with detailed examples from TP53, BRCA1, and EGFR.

15 min readComprehensive · Internally linked

Topic clusters

Explore connected research guides

Each pillar connects 15 focused explainers into one navigable mechanism-to-interpretation pathway.

DNA Repair and Genomic Instability

A source-linked guide to DNA repair pathways, mutational signatures, telomere maintenance, chromothripsis, whole-genome doubling and HRD scars.

15 articles

Cancer Epigenetics and Chromatin Regulators

Explore DNA methylation, histone marks, SWI/SNF and Polycomb biology, chromatin-regulator mutations and the therapies designed around them.

15 articles

Immuno-Oncology and Tumour Metabolism

A guide to tumour immunogenicity, antigen presentation, immune escape, checkpoint biology, T-cell biomarkers and cancer metabolic dependencies.

15 articles

All Articles

190 articles

Cancer Biology 6 min read

Top Tumor Suppressor Genes Explained

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.

TP53BRCA1PTENRB1

Precision Oncology 5 min read

EGFR Mutations in NSCLC: Testing, Inhibitors and Resistance

Understand sensitising EGFR mutations in NSCLC, how molecular testing is interpreted, and how T790M, C797S, MET amplification and other resistance mechanisms differ.

EGFRKRASBRAFPIK3CA

Genetics 5 min read

Gene Mutations That Cause Disease

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.

TP53KRASBRCA1BRAF

Cancer Biology 6 min read

TP53 Mutations in Cancer: Function, Hotspots and Interpretation

Understand TP53 loss of function, dominant-negative effects, hotspot mutations, p53 immunohistochemistry limits, inherited-risk context and experimental strategies.

TP53MDM2ATMCDKN2A

Cancer Genetics 7 min read

BRCA1: Homologous Recombination, Inherited Risk and HRD

Understand BRCA1 in homologous recombination, how germline and tumour findings differ, what HRD can and cannot establish, and why PARP evidence is context-specific.

BRCA1ATMCHEK2TP53

Oncogenic Signalling 6 min read

KRAS Mutations: Constitutive MAPK Signalling and Targeted Therapy

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.

KRASBRAFPIK3CAEGFR

Precision Oncology 5 min read

PIK3CA, PTEN and AKT1 Alterations Compared

Compare PIK3CA hotspot mutations, PTEN loss and AKT1 E17K: where each acts, what assays detect and why the biomarkers are not interchangeable.

PIK3CAPTENAKT1MTOR

Signalling Pathways 4 min read

The PI3K/AKT/mTOR Pathway in Cancer

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.

PIK3CAPTENAKT1MTOR

Cancer Biology 5 min read

BCL2 Family Proteins and Cancer Cell Survival

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

BCL2TP53AKT1MYC

Targeted Therapy 4 min read

HER2 Amplification: Mechanism, Targeted Therapy, and Resistance

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

HER2EGFRPIK3CAAKT1

Cancer Genetics 4 min read

CDKN2A: Two Tumor Suppressors from One Locus

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.

CDKN2ACDK4RB1TP53

Oncogenic Signalling 5 min read

How MYC Drives Oncogenic Transcriptional Amplification in Cancer

How MYC reshapes transcription, ribosome biogenesis, metabolism and cell-cycle control—and why MYC dependencies and therapeutic strategies vary by context.

MYCBCL2TP53CDKN2A

Oncogenic Signalling 4 min read

BRAF V600E in Cancer: Mechanism and Targeted Treatment

How BRAF V600E activates MEK–ERK signalling, why treatment evidence differs by tumour lineage, and how feedback and resistance shape interpretation.

BRAFKRASMEKEGFR

DNA Repair 4 min read

ATM Kinase and the DNA Damage Response

How ATM coordinates the DNA-damage response, what germline and tumour alterations mean, and why ATM loss is not interchangeable with BRCA deficiency.

ATMTP53BRCA1CHEK2

Tumor Biology 4 min read

How Tumour Hypoxia Drives VEGFA Angiogenic Signalling

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.

VEGFAHIF1AAKT1MTOR

Targeted Therapy 4 min read

CDK4/6 Inhibitors in Breast Cancer

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.

CDK4RB1CDKN2AAKT1

Signalling Pathways 4 min read

mTOR Signalling and Cancer Therapy

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.

MTORAKT1PIK3CAPTEN

Cancer Biology 4 min read

Oncogenes in Cancer: Mechanisms and Targeted Therapy

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

KRASMYCHER2BRAF

Cancer Biology 4 min read

Clonal Evolution and Genomic Instability in Cancer

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

TP53BRCA1ATMKRAS

Immunology 4 min read

How Tumours Suppress T-Cell Activation: PD-1, PD-L1, and CTLA4 Checkpoint Signalling

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.

STAT3TP53MYCVEGFA

Cancer Genetics 4 min read

DNA Mismatch Repair and Lynch Syndrome

How mismatch repair, MSI and Lynch syndrome relate—and why tumour screening, germline testing and immunotherapy evidence answer different questions.

ATMBRCA1TP53MLH1

Cancer Biology 6 min read

TP53, RB1, CDKN2A and MDM2: Tumour-Suppressor Pathways Compared

Compare the p53 and RB tumour-suppressor systems, see how CDKN2A connects them, and learn why MDM2 amplification is not the same as a TP53 mutation.

TP53RB1CDKN2AMDM2

Precision Oncology 4 min read

EGFR Exon 19 Deletions: What the Biomarker Means

A clear, evidence-linked guide to EGFR exon 19 deletions in non-small-cell lung cancer: what the alteration is, how it is tested, and what the FDA label does and does not establish.

EGFRKRASBRAFPIK3CA

Precision Oncology 3 min read

EGFR L858R: Understanding the Exon 21 Mutation

Understand EGFR L858R in exon 21, how laboratories detect it, why it is grouped with sensitising EGFR alterations, and where treatment claims must stay label-specific.

EGFRKRASBRAFPIK3CA

Precision Oncology 3 min read

EGFR T790M: A Gatekeeper Resistance Mutation

Learn how EGFR T790M can alter drug binding after an earlier EGFR therapy, why resistance testing is contextual, and how to read the FDA label without overgeneralising.

EGFRKRASBRAFPIK3CA

Precision Oncology 4 min read

KRAS G12C in Colorectal Cancer: Biomarker Context

Understand what KRAS G12C means in colorectal cancer, why EGFR biology matters, how testing is reported, and the exact population covered by the FDA treatment announcement.

KRASEGFRBRAFPIK3CA

Cancer Genetics 3 min read

TP53 and Li-Fraumeni Syndrome: Inherited-Risk Context

A careful guide to germline TP53 variants and Li-Fraumeni syndrome, including the difference between inherited and tumour-only findings, family testing, and NCI evidence.

TP53CHEK2ATMBRCA1

Cancer Genetics 6 min read

Homologous Recombination Deficiency: BRCA, ATM and HRD Testing

Compare germline BRCA results, tumour BRCA or ATM alterations and genomic-scar HRD tests—and learn what each finding can and cannot establish.

BRCA1ATMCHEK2TP53

Cancer Genetics 3 min read

BRCA1 and Ovarian Cancer Risk: How to Read a Result

Learn how germline BRCA1 results relate to ovarian cancer risk, why variant classification matters, and how to separate inherited-risk evidence from treatment claims.

BRCA1BRCA2PALB2ATM

Cancer Genetics 2 min read

EGFR C797S: What This Resistance Alteration Means

A source-linked explanation of EGFR C797S, why its molecular context matters, and how to read a resistance report.

EGFRKRASBRAFHER2

Cancer Genetics 2 min read

MET Amplification in EGFR-Mutant Cancer: A Resistance Mechanism

Understand how MET amplification can bypass EGFR signalling, why assays differ, and how to interpret this resistance-associated finding.

EGFRHER2KRASBRAF

Oncogenes 2 min read

KRAS G12D Mutation: Biology, Testing and Context

A mechanism-first guide to KRAS G12D: molecular switching, report interpretation and why tumour context matters.

KRASBRAFEGFRPIK3CA

Oncogenes 2 min read

KRAS G12V Mutation: How to Interpret the Finding

Learn what KRAS G12V denotes, how it affects KRAS signalling, and what to preserve from a molecular report.

KRASBRAFEGFRPIK3CA

Oncogenes 2 min read

KRAS G12C vs G12D: Similar Gene, Different Alterations

Compare KRAS G12C and G12D at the protein level, in molecular reporting, and in the limits of cross-variant conclusions.

KRASBRAFEGFRPIK3CA

Oncogenes 2 min read

BRAF V600E vs Non-V600 Alterations: Why Classification Matters

A clear comparison of BRAF V600E and non-V600 alterations, their signalling logic, and limits of applying one result to another.

BRAFKRASEGFRHER2

Oncogenes 2 min read

BRAF Class 2 vs Class 3 Alterations: A Mechanism Guide

Understand the functional distinction between BRAF class 2 and class 3 alterations and why it should not be oversimplified.

BRAFKRASEGFRHER2

Oncogenes 2 min read

HER2 Mutation vs Amplification: Different Biomarker Questions

Learn the difference between HER2 sequence mutations, ERBB2 amplification and protein expression, including testing boundaries.

HER2EGFRKRASBRAF

Oncogenes 2 min read

EGFR, HER2, HER3 and HER4: The ERBB Receptor Family

A practical explanation of the ERBB receptor family, receptor pairing and how EGFR-family biomarker results differ.

EGFRHER2KRASPIK3CA

Oncogenes 2 min read

MAPK Pathway Resistance: A Framework for Reading Resistance Reports

Understand pathway reactivation, bypass signalling and tumour heterogeneity when reading MAPK resistance reports.

EGFRKRASBRAFHER2

Tumour Suppressors 2 min read

PTEN Loss Testing: Sequence, Copy Number and Protein Expression

A practical guide to the different ways PTEN loss can be measured and why results should not be treated as interchangeable.

PTENPIK3CAAKT1MTOR

Tumour Suppressors 2 min read

RB1 Loss in Cancer: Cell-Cycle Biology and Testing

Understand RB1 loss, the G1–S checkpoint, and the difference between genetic and protein-level test results.

RB1CDK4CDKN2ATP53

Cell Cycle 2 min read

CDKN2A and MTAP Co-Deletion: Understanding the 9p21 Region

Learn why CDKN2A and MTAP can be lost together, what a copy-number report measures, and the limits of emerging biomarker claims.

CDKN2AMTAPCDK4RB1

Tumour Suppressors 2 min read

MDM2 Amplification: Its Relationship to TP53

A source-linked explanation of MDM2 amplification, p53 regulation and the importance of TP53 context.

MDM2TP53RB1CDKN2A

Apoptosis 2 min read

BCL2 vs MCL1: Two Anti-Apoptotic Proteins Compared

Compare BCL2 and MCL1, their role in apoptosis and why expression alone does not establish functional dependency.

BCL2TP53MYCBRAF

Cancer Genetics 2 min read

BRCA1 vs BRCA2: Different Roles in DNA Repair

Compare BRCA1 and BRCA2 in homologous recombination, testing and inherited-risk interpretation.

BRCA1BRCA2PALB2ATM

Cancer Genetics 2 min read

PALB2: DNA Repair, Inherited Risk and Tumour Findings

An evidence-led guide to PALB2's role between BRCA1 and BRCA2, and how to interpret germline and tumour findings.

PALB2BRCA1BRCA2ATM

Cancer Genetics 2 min read

RAD51C vs RAD51D: Inherited-Risk Evidence in Context

Compare RAD51C and RAD51D roles in homologous recombination and how evidence supports genetics-led risk interpretation.

BRCA1BRCA2PALB2ATM

Cancer Genetics 2 min read

Germline vs Somatic Testing: Two Different Cancer Questions

Understand what germline and somatic testing measure, why a tumour result may need follow-up, and what each cannot answer.

BRCA1BRCA2TP53ATM

Cancer Genetics 2 min read

Variant of Uncertain Significance: How to Read a VUS Result

A clear guide to what a VUS means, why it is not a diagnosis, and how laboratory reclassification works.

BRCA1BRCA2TP53ATM

DNA Repair 2 min read

Mismatch-Repair Protein Loss Patterns: What IHC Can Show

Learn how mismatch-repair immunohistochemistry is read, why patterns guide follow-up, and why it does not replace germline testing.

MLH1MSH2MSH6PMS2

DNA Repair 2 min read

MSI-High vs TMB-High: Two Different Tumour Biomarkers

Compare microsatellite instability and tumour mutational burden, their assay limits and why one result does not imply the other.

MLH1MSH2MSH6PMS2

DNA Repair 2 min read

ATM vs ATR: Two DNA-Damage Response Kinases

Compare ATM and ATR functions in DNA-damage signalling, replication stress and genetic-testing interpretation.

ATMCHEK2BRCA1TP53

Cancer Immunology 2 min read

PD-L1 Testing Explained: Assays, Scores and Limits

Understand PD-L1 immunohistochemistry, why assays and scoring systems differ, and what a result does and does not show.

STAT3HIF1ATP53

Cancer Immunology 2 min read

Tumour Mutational Burden: How TMB Is Measured

A source-linked guide to tumour mutational burden, panel differences and why a TMB value needs assay context.

TP53BRCA1ATM

Cancer Genetics 2 min read

Liquid Biopsy vs Tissue Testing: What Each Sample Can Tell You

Compare circulating-tumour-DNA testing with tissue profiling, including sensitivity, sampling and interpretation boundaries.

EGFRKRASBRAFTP53

Oncogenes 2 min read

HIF-1α and Tumour Hypoxia: A Signalling Guide

Learn how HIF-1α links low oxygen to transcription, angiogenesis and metabolic adaptation in tumours.

HIF1AVEGFASTAT3PIK3CA

Cell Cycle 4 min read

Cell-Cycle Checkpoints Explained: G1/S, Intra-S, G2/M and Mitosis

How the G1/S, intra-S, G2/M and spindle-assembly checkpoints keep cell division accurate, and why cancers disable them yet become dependent on those that remain.

TP53RB1ATMCDK4

Cell Cycle 3 min read

The Cyclin D-CDK4/6-RB Axis: How Cells Enter the Division Cycle

How D-type cyclins, CDK4/6, the INK4 and CIP/KIP inhibitors and the retinoblastoma protein control G1 progression, and how the axis is disrupted in cancer.

CDK4RB1CDKN2AMDM2

Cell Cycle 3 min read

The G1/S Restriction Point: Where a Cell Commits to Dividing

What the restriction point is, how the RB-E2F switch makes cell-cycle entry irreversible, and why loss of this control is near-universal in cancer.

RB1CDK4CDKN2ATP53

Cell Cycle 3 min read

The G2/M DNA-Damage Checkpoint: ATR, CHK1 and WEE1

How ATM, ATR, CHK1, CHK2 and WEE1 hold a damaged cell out of mitosis, and why p53-deficient tumours depend on this checkpoint.

ATMTP53RB1

Cell Cycle 3 min read

The Spindle-Assembly Checkpoint and Chromosomal Instability

How the spindle-assembly checkpoint prevents chromosome missegregation, how a weakened checkpoint drives chromosomal instability, and why cancers still need it.

TP53RB1

Cell Cycle 3 min read

E2F Transcription Factors: Activators, Repressors and Cancer

How the eight E2F family members split into activators and repressors, how RB pocket proteins control them, and why E2F activity is raised in nearly all cancers.

RB1CDK4CDKN2ATP53

Cell Cycle 3 min read

CCNE1 Amplification and Cyclin E: Biology and Testing Context

What CCNE1 amplification means, how cyclin E-CDK2 drives S-phase entry, its link to CDK4/6 inhibitor resistance, and emerging synthetic-lethal strategies.

RB1CDK4TP53

Cancer Biology 3 min read

Oncogene-Induced Senescence: A Built-In Barrier to Cancer

How an activated oncogene can trigger a permanent growth arrest, the roles of p16/RB and p53/p21, the senescence-associated secretory phenotype, and senescence escape.

BRAFKRASTP53CDKN2A

Apoptosis 3 min read

Intrinsic vs Extrinsic Apoptosis: Two Routes to Cell Death

How the mitochondrial (intrinsic) and death-receptor (extrinsic) apoptosis pathways are triggered, where they converge, and how cancers evade both.

BCL2TP53MYC

Apoptosis 3 min read

BAX and BAK: Mitochondrial Gatekeepers of Apoptosis

How the effector proteins BAX and BAK are activated, how they permeabilise mitochondria, how anti-apoptotic proteins restrain them, and what this means for cancer.

BCL2TP53MYC

Apoptosis 3 min read

BH3 Mimetics Explained: Drugging the BCL-2 Family

How BH3 mimetics such as venetoclax free pro-apoptotic proteins from BCL-2, where they are used, why MCL1 and BCL-XL matter, and how resistance develops.

BCL2TP53MYC

Cell Cycle 3 min read

p21 and p27: The CIP/KIP CDK Inhibitors

How the CIP/KIP proteins p21 and p27 restrain cyclin-dependent kinases, why they are rarely mutated in cancer, and how their function is lost by other means.

TP53CDK4RB1MDM2

Tumour Suppressors 3 min read

MDM2 and MDM4: The Dual Brake on p53

How MDM2 and MDM4 together restrain p53, why the autoregulatory loop matters, what amplification means, and why MDM2 inhibitors need wild-type TP53.

MDM2TP53CDK4CDKN2A

Cell Cycle 3 min read

Aurora Kinases in Cancer: Mitotic Regulators as Drug Targets

What Aurora A, B and C do in cell division, how their overexpression contributes to cancer, and where Aurora-kinase inhibitors stand in development.

MYCTP53RB1

Cell Cycle 3 min read

PLK1: A Mitotic Kinase and Its Role in Cancer

What Polo-like kinase 1 does across mitosis, why its overexpression is common in cancer, its context-dependent tumour-suppressor side, and the status of PLK1 inhibitors.

TP53MYCRB1

Precision Oncology 3 min read

mTORC1 vs mTORC2: Two Complexes, Different Jobs

How the two mTOR complexes differ in composition, inputs and outputs, why rapamycin mainly hits mTORC1, and what this means for mTOR-pathway drugs.

MTORPTENAKT1PIK3CA

Precision Oncology 3 min read

PI3K Pathway Biomarkers: PIK3CA, PTEN, AKT1 and Beyond

What PIK3CA mutations, PTEN loss and AKT1 alterations mean as biomarkers, how the tests differ, and why pathway status is not a single number.

PIK3CAPTENAKT1MTOR

Oncogenes 3 min read

STAT3 Signalling in Cancer: The IL-6/JAK/STAT3 Axis

How the IL-6/JAK/STAT3 pathway is activated in tumours, what STAT3 switches on, its effect on anti-tumour immunity, and why it has been hard to drug.

STAT3HIF1AMYC

Precision Oncology 3 min read

The AKT1 E17K Mutation: A Direct Activator of AKT

How the AKT1 E17K mutation activates AKT independently of PI3K, which cancers carry it, and how it is used in AKT-inhibitor trials.

AKT1PIK3CAPTENMTOR

Precision Oncology 3 min read

PIK3CA Mutation Hotspots: Helical and Kinase Domain Changes

Why most PIK3CA mutations fall at a few hotspots, how helical and kinase domain changes activate PI3K by different routes, and what this means for testing.

PIK3CAPTENAKT1

Tumour Suppressors 3 min read

TSC1 and TSC2: The Brake Upstream of mTORC1

How the TSC1-TSC2 complex restrains mTORC1, what happens when it is lost in tuberous sclerosis and in sporadic tumours, and the role of mTOR inhibitors.

MTORPTEN

Cancer Genetics 3 min read

PTEN Hamartoma Tumour Syndrome: Germline PTEN Loss

What PTEN hamartoma tumour syndrome is, the cancers and benign features associated with germline PTEN variants, and why this is a genetics-led diagnosis.

PTENPIK3CAAKT1MTOR

Cancer Biology 3 min read

VEGFA vs VEGFR2: Ligand and Receptor in Tumour Angiogenesis

How the VEGFA ligand and its main receptor VEGFR2 drive new blood-vessel growth in tumours, and how different drugs target each side of the interaction.

VEGFAHIF1ASTAT3

Cancer Biology 3 min read

Tumour Angiogenesis: How Cancers Build a Blood Supply

The angiogenic switch, sprouting and non-sprouting vessel growth, vessel abnormality and normalisation, and why tumour vasculature is a therapeutic target.

VEGFAHIF1A

Cancer Biology 2 min read

Resistance to Anti-Angiogenic Therapy: Why Tumours Adapt

How tumours evade VEGF-targeted drugs through alternative angiogenic factors, vessel co-option, stromal changes and metabolic adaptation.

VEGFAHIF1A

Oncogenes 3 min read

HIF-1alpha vs HIF-2alpha: Related but Distinct Hypoxia Factors

How HIF-1alpha and HIF-2alpha differ in target genes, timing and tumour context, and why HIF-2alpha is a drug target in renal cell carcinoma.

HIF1AVEGFA

Cancer Biology 3 min read

Vessel Co-option: When Tumours Borrow Existing Blood Vessels

How some tumours grow by hijacking pre-existing vessels instead of making new ones, where it occurs, and why it matters for anti-angiogenic therapy.

VEGFAHIF1A

Cancer Biology 2 min read

Angiopoietin-TIE2 Signalling: Stabilising and Destabilising Vessels

How ANG1 and ANG2 act through the TIE2 receptor to control vessel stability, why ANG2 rises in tumours, and how this pathway is being targeted.

VEGFA

Oncogenes 3 min read

The JAK-STAT Pathway in Cancer: Signalling from Cytokines to Genes

How cytokine receptors, JAK kinases and STAT transcription factors relay signals, how JAK2 mutations drive myeloproliferative neoplasms, and where JAK inhibitors fit.

STAT3MYC

Precision Oncology 3 min read

PI3K Isoforms Explained: p110-alpha, -beta, -gamma and -delta

How the four class I PI3K catalytic isoforms differ in tissue distribution and function, why isoform-selective inhibitors exist, and their toxicity trade-offs.

PIK3CAPTENAKT1

Cancer Genetics 3 min read

Lynch Syndrome: Tumour Screening vs Germline Confirmation

How mismatch-repair tumour testing screens for possible Lynch syndrome, why a germline test is needed to confirm it, and what causes false leads.

MLH1MSH2MSH6PMS2

Cancer Genetics 3 min read

BRIP1 and Cancer Risk: What the Evidence Supports

What BRIP1 does in DNA repair, the ovarian cancer risk associated with pathogenic variants, and why the breast cancer link is weaker than once thought.

BRCA1BRCA2PALB2ATM

Cancer Genetics 3 min read

CHEK2 and Cancer Risk: A Moderate-Penetrance Gene

How CHEK2 functions in the DNA-damage response, the breast and other cancer risks linked to pathogenic variants, and why the 1100delC variant is treated specially.

ATMBRCA1BRCA2TP53

Cancer Genetics 3 min read

Multigene Panel Testing for Hereditary Cancer: What It Adds

How hereditary-cancer gene panels work, the trade-off of more variants of uncertain significance, and why gene content and interpretation matter.

BRCA1BRCA2ATMPALB2

Cancer Genetics 3 min read

Penetrance in Hereditary Cancer: Why a Variant Is Not a Diagnosis

What penetrance means, why lifetime risk estimates vary between studies, and how family history and modifiers change an individual carrier's risk.

BRCA1BRCA2ATMTP53

Cancer Genetics 3 min read

How to Read an Inherited-Cancer Genetic Testing Report

What the sections of a hereditary-cancer genetic test report mean, how variant classifications work, and which findings do and do not change management.

BRCA1BRCA2ATM

Cancer Genetics 3 min read

Cascade Testing: Extending a Genetic Result Through a Family

How cascade testing offers targeted genetic testing to relatives of someone with a known pathogenic variant, its benefits, and its practical barriers.

BRCA1BRCA2

Precision Oncology 3 min read

EGFR Exon 20 Insertions: A Distinct Group in Lung Cancer

Why EGFR exon 20 insertion mutations behave differently from classical EGFR mutations, how they are detected, and which targeted drugs address them.

EGFR

Precision Oncology 3 min read

HER2 (ERBB2) Exon 20 Insertions in Lung Cancer

What HER2 exon 20 insertion mutations are, how they differ from HER2 amplification, and how antibody-drug conjugates changed their treatment.

HER2EGFR

Precision Oncology 3 min read

MET Exon 14 Skipping: A Splicing Change That Activates MET

How mutations that cause MET exon 14 to be skipped stabilise the MET receptor, how this differs from MET amplification, and which inhibitors target it.

EGFRKRAS

Precision Oncology 3 min read

KRAS vs NRAS vs HRAS: Three RAS Genes, Different Cancers

How the three RAS genes differ in tissue distribution, the cancers each is mutated in, and why they are not interchangeable in testing or treatment.

KRASBRAF

Precision Oncology 3 min read

Uncommon EGFR Mutations: G719X, S768I and L861Q

What the uncommon EGFR mutations G719X, S768I and L861Q are, how their drug sensitivity differs from classical mutations, and how compound mutations complicate reports.

EGFR

Precision Oncology 3 min read

ALK Rearrangements in Lung Cancer: Fusions and Their Inhibitors

How ALK gene fusions create a constitutively active kinase in lung cancer, how they are detected, and how successive generations of ALK inhibitors address resistance.

EGFR

Precision Oncology 3 min read

ROS1 Rearrangements in Lung Cancer: A Rare but Targetable Driver

What ROS1 gene fusions are, how they overlap biologically with ALK, how they are detected, and which inhibitors are used including for brain disease.

EGFR

Precision Oncology 3 min read

RET Alterations in Cancer: Fusions and Activating Mutations

How RET fusions in lung and thyroid cancer differ from activating RET point mutations in medullary thyroid cancer, and how selective RET inhibitors changed treatment.

RETKRASBRAFEGFR

Precision Oncology 3 min read

Clinical Trial Phases Explained: From First-in-Human to Confirmation

What phase 1, 2 and 3 cancer trials are designed to test, how modern biomarker-driven and adaptive designs blur the boundaries, and how to read trial evidence.

KRASEGFR

Cancer Genetics 3 min read

Biomarker Assay Validation: Why the Test Behind a Result Matters

What analytical and clinical validation of a molecular assay involves, the difference between the two, and why an unvalidated result should be treated cautiously.

EGFRKRASBRCA1

Cancer Biology 3 min read

Tumour Heterogeneity: Why One Biopsy May Not Represent the Whole Cancer

How spatial and temporal heterogeneity arise from clonal evolution, why a single biopsy can miss important subclones, and what this means for molecular results.

EGFRKRASTP53

Cancer Genetics 3 min read

Tumour Purity and Sequencing: How Much Cancer Is in the Sample

Why the fraction of cancer cells in a specimen affects which mutations can be detected, how low purity causes false negatives, and how reports handle it.

TP53EGFRKRAS

Cancer Genetics 3 min read

Variant Allele Fraction: What the Percentage on a Report Means

How variant allele fraction is calculated, how tumour purity, copy number and clonality shape it, and why a low fraction is not automatically less important.

TP53EGFRKRAS

Cancer Genetics 3 min read

Interpreting Copy-Number Changes: Amplification, Gain, Loss and Deletion

What amplification, gain, heterozygous loss and homozygous deletion mean on a molecular report, how thresholds and purity affect the call, and common pitfalls.

MYCCDK4MDM2HER2

Cancer Genetics 3 min read

Gene Fusion Testing: FISH, Immunohistochemistry, DNA and RNA Sequencing

How the main methods for detecting gene fusions differ in what they measure, their blind spots, and why RNA-based sequencing is often preferred.

EGFR

Cancer Genetics 3 min read

RNA vs DNA Sequencing in Cancer: Complementary, Not Interchangeable

What DNA sequencing and RNA sequencing each capture in tumour profiling, where each is stronger, and why some laboratories run both.

EGFR

Cancer Genetics 3 min read

NGS Panels vs Hotspot Testing: Breadth Versus Focus

How targeted hotspot assays differ from broad next-generation sequencing panels in what they detect, turnaround and cost, and when a negative result is incomplete.

EGFRKRASBRAF

Cancer Genetics 3 min read

Whole-Exome vs Whole-Genome Sequencing: What Each Covers

How whole-exome and whole-genome sequencing differ in coverage, cost and the variant types they detect, and where each is used in cancer and inherited disease.

TP53BRCA1

Cancer Genetics 3 min read

Confirming Sequencing Results: When Is Orthogonal Testing Needed

Why some next-generation sequencing calls are confirmed by a second method such as Sanger sequencing, which calls need it, and what confirmation does and does not prove.

EGFRKRAS

Cancer Genetics 3 min read

Molecular Residual Disease: Using ctDNA to Detect Cancer That Imaging Cannot

How circulating tumour DNA is used to detect molecular residual disease after curative-intent treatment, the assay approaches, and the current limits of the evidence.

EGFRKRASTP53

Precision Oncology 3 min read

Companion Diagnostics: Tests Tied to Specific Treatments

What a companion diagnostic is, how it differs from a complementary diagnostic, why drug-test pairs are co-developed, and what off-label testing means.

EGFRBRAFHER2KRAS

Cancer Genetics 3 min read

Reference Genome Builds: Why GRCh37 vs GRCh38 Appears on Reports

What a reference genome build is, how GRCh37 and GRCh38 differ, why coordinates and transcript versions matter, and how this affects comparing variant reports.

BRCA1TP53

Cancer Genetics 3 min read

Limit of Detection: The Smallest Signal a Molecular Assay Can Call

What the limit of detection of a sequencing or PCR assay means, how it is set, and why a negative result only rules out what the assay was designed to see.

EGFRKRAS

Oncogenes 3 min read

The Wnt/beta-Catenin Pathway in Cancer

How the Wnt/beta-catenin pathway controls the beta-catenin destruction complex, how APC or CTNNB1 mutations switch it on, and why it has been hard to drug.

MYCTP53

Oncogenes 3 min read

Notch Signalling in Cancer: Oncogene or Tumour Suppressor

How the Notch pathway transmits a signal by regulated proteolysis, why it drives some cancers and suppresses others, and how context determines its role.

MYC

Oncogenes 3 min read

The Hedgehog Pathway in Cancer: From Basal Cell Carcinoma to Resistance

How the Hedgehog pathway signals through PTCH1, SMO and GLI, why PTCH1 or SMO mutations drive basal cell carcinoma and medulloblastoma, and how SMO inhibitors work.

TP53

Cancer Biology 3 min read

TGF-beta Signalling in Cancer: Suppressor Early, Promoter Late

How TGF-beta signals through SMAD proteins, why it restrains early tumours but promotes invasion and immune evasion later, and how this shapes drug strategy.

TP53MYC

Tumour Suppressors 3 min read

NF1 and Neurofibromin: A Brake on RAS

How the NF1 protein neurofibromin switches off RAS, what happens when NF1 is lost in neurofibromatosis type 1 and in sporadic cancers, and the role of MEK inhibitors.

KRASBRAF

Oncogenes 3 min read

IDH1 and IDH2 Mutations: A Metabolic Change That Rewires the Epigenome

How mutant IDH enzymes produce the oncometabolite 2-hydroxyglutarate, how this blocks cell differentiation in glioma and AML, and how IDH inhibitors act.

TP53

Tumour Suppressors 3 min read

The VHL-HIF Pathway: Oxygen Sensing and Kidney Cancer

How the VHL protein controls HIF degradation under normal oxygen, why VHL loss defines clear cell renal cell carcinoma, and how the pathway is targeted.

HIF1AVEGFA

Tumour Suppressors 3 min read

ARID1A and the SWI/SNF Complex: Chromatin Remodelling in Cancer

What the SWI/SNF (BAF) chromatin-remodelling complex does, why ARID1A and other subunits are among the most mutated genes in cancer, and emerging vulnerabilities.

TP53ATM

Precision Oncology 3 min read

MEK-ERK Feedback: Why Blocking the MAPK Pathway Is Not Simple

How negative feedback from ERK keeps the MAPK pathway in check, why inhibitors relieve that feedback and cause rebound signalling, and how combinations respond.

BRAFKRAS

Precision Oncology 3 min read

RAF Dimerisation and Paradoxical Activation by BRAF Inhibitors

Why first-generation BRAF inhibitors can paradoxically activate the MAPK pathway in RAS-mutant cells, how RAF dimerisation causes it, and how newer inhibitors address it.

BRAFKRAS

Oncogenes 3 min read

The MYC Family: MYC, MYCN and MYCL

How the three MYC-family genes share a function as universal transcriptional amplifiers, which cancers each is amplified in, and why MYC has been so hard to drug.

MYC

Precision Oncology 3 min read

FGFR Alterations in Cancer: Fusions, Mutations and Amplifications

How FGFR1-4 alterations differ, why FGFR2 fusions and FGFR3 mutations are the most actionable, and where FGFR inhibitors are approved.

EGFR

Precision Oncology 3 min read

NTRK Fusions Explained: A Tumour-Agnostic Target

What NTRK1/2/3 gene fusions are, why they are rare in common cancers but enriched in some rare ones, how they are detected, and how TRK inhibitors perform.

EGFR

Precision Oncology 3 min read

KIT and PDGFRA in Gastrointestinal Stromal Tumours

How mutually exclusive KIT and PDGFRA mutations drive most gastrointestinal stromal tumours, why the exact exon matters for drug choice, and how resistance develops.

KITPDGFRAKRASBRAF

DNA Repair 3 min read

POLE and POLD1 Proofreading Mutations: Ultramutated Tumours

How exonuclease-domain mutations in POLE and POLD1 drive extremely high mutation counts, and how germline and somatic findings differ in interpretation.

TP53ATMMLH1MSH2

Cancer Genetics 3 min read

MUTYH-Associated Polyposis: Recessive Base-Excision-Repair Risk

Why MUTYH-associated polyposis is inherited recessively, how biallelic base-excision-repair loss drives colorectal adenomas, and what a monoallelic result does not establish.

MLH1MSH2APC

DNA Repair 3 min read

Base Excision Repair: Small Lesions, Large Consequences

How base excision repair corrects oxidised, alkylated and deaminated bases, its links to MUTYH and PARP, and why it is described as a synthetic-lethal partner of homologous recombination.

ATMBRCA1MLH1

DNA Repair 3 min read

Nucleotide Excision Repair, Xeroderma Pigmentosum and Platinum Response

How nucleotide excision repair removes bulky DNA lesions such as UV photoproducts and platinum adducts, its link to xeroderma pigmentosum, and why ERCC1 has been hard to use as a biomarker.

TP53ATM

DNA Repair 3 min read

Translesion Synthesis: Damage Tolerance and Mutagenesis

How specialised polymerases let replication continue past unrepaired DNA damage, why this tolerance pathway is error-prone, and how it contributes to chemotherapy resistance.

ATMBRCA1

DNA Repair 3 min read

The Fanconi Anaemia Pathway: Interstrand Crosslink Repair

How the Fanconi anaemia pathway coordinates repair of DNA interstrand crosslinks, its overlap with BRCA-linked homologous recombination, and what pathway membership does and does not imply.

BRCA1ATMBRCA2PALB2

DNA Repair 3 min read

RECQ Helicases: Bloom, Werner and Genome Maintenance

How the RECQ family of DNA helicases protects replication and recombination, why their loss causes distinct predisposition syndromes, and the WRN synthetic-lethal link to MSI-high cancers.

ATMBRCA1TP53

DNA Repair 3 min read

MGMT Promoter Methylation: A Glioma Treatment Biomarker

What MGMT does, why promoter methylation silences it, and how methylation status is used as a predictive and prognostic biomarker in glioblastoma alkylating-agent treatment.

TP53MDM2

DNA Repair 3 min read

Mutational Signatures: Reading a Tumour's History

How the patterns of mutations across a tumour genome record past exposures and repair defects, what single-base-substitution signatures mean, and the limits of signature analysis.

TP53BRCA1

DNA Repair 3 min read

APOBEC Mutagenesis: An Internal Source of Cancer Mutations

How APOBEC3 cytidine deaminases generate clustered mutations in many cancers, why the signature is often subclonal, and its emerging link to treatment resistance.

TP53PIK3CAHER2

Cancer Biology 3 min read

TERT Promoter Mutations: Switching Telomerase Back On

How recurrent non-coding mutations in the TERT promoter reactivate telomerase, which cancers carry them, and how they relate to alternative lengthening of telomeres.

TP53BRAF

Cancer Biology 3 min read

Alternative Lengthening of Telomeres: Telomerase-Independent Immortality

How some cancers maintain telomeres without telomerase using a recombination-based mechanism, the link to ATRX and DAXX loss, and which tumour types rely on it.

ATRXDAXXTP53RB1

Cancer Biology 3 min read

Chromothripsis: One Catastrophe, Many Rearrangements

How a single catastrophic shattering-and-reassembly event rearranges one or a few chromosomes, how it is recognised in sequencing data, and why it matters for cancer evolution.

TP53MDM2MYC

Cancer Biology 3 min read

Whole-Genome Doubling: A Macro-Evolutionary Step in Cancer

How a one-off doubling of the entire chromosome set buffers further mutations, its association with TP53 loss and poorer prognosis, and how it is inferred from sequencing.

TP53RB1MYC

DNA Repair 3 min read

HRD Scores and Genomic Scars: What an HRD-Positive Result Means

How homologous recombination deficiency is inferred from genome-wide scarring, what the component metrics measure, and why HRD-positive is not the same as a BRCA mutation.

BRCA1ATMBRCA2PALB2

Cancer Genetics 3 min read

DNMT3A and TET2 in Clonal Haematopoiesis

TP53ATM

Cancer Biology 3 min read

EZH2 and Polycomb Repression in Cancer

How EZH2, the enzymatic core of polycomb repressive complex 2, silences genes through H3K27 methylation, why it can act as an oncogene or a tumour suppressor, and where inhibitors are used.

MYCRB1CDKN2A

Cancer Biology 3 min read

KMT2D and KMT2C: Enhancer Regulators Lost in Many Cancers

Why the histone methyltransferases KMT2D and KMT2C are among the most frequently mutated genes across cancer, how they mark active enhancers, and what loss means for interpretation.

TP53CDKN2AKRAS

Cancer Biology 3 min read

KDM6A (UTX): An X-Linked Histone Demethylase Tumour Suppressor

How KDM6A removes the repressive H3K27me3 mark, why its location on the X chromosome contributes to sex differences in some cancers, and where its loss is common.

RB1CDKN2ATP53

Cancer Biology 3 min read

SETD2: H3K36 Methylation, Transcription and Repair

How SETD2 writes the H3K36me3 mark that guides transcription, splicing and DNA repair, and why its loss is a recurrent event in clear cell renal cell carcinoma and other cancers.

TP53MTOR

Cancer Genetics 3 min read

BAP1 Tumour Predisposition Syndrome

How germline BAP1 loss predisposes to mesothelioma, uveal melanoma, renal cell carcinoma and distinctive skin tumours, and how somatic BAP1 loss is used in pathology.

BRCA1TP53

Cancer Biology 3 min read

Histone H3 K27M and Diffuse Midline Glioma

How a single lysine-to-methionine change in histone H3 reprogrammes the epigenome of diffuse midline glioma, why it defines the tumour type, and what is being tried therapeutically.

TP53CDKN2A

Cancer Biology 3 min read

Histone H3 G34 Mutations in Paediatric High-Grade Glioma

How glycine-34 substitutions in histone H3.3 define a distinct group of hemispheric paediatric high-grade gliomas, how they differ from K27M, and their effect on chromatin and repair.

TP53ATM

Precision Oncology 3 min read

BET Bromodomain Inhibitors: Targeting Transcriptional Addiction

How BET proteins such as BRD4 read acetylated histones to drive transcription of genes like MYC, why BET inhibitors were developed, and the challenges seen in trials.

MYCBCL2

Precision Oncology 3 min read

HDAC Inhibitors in Cancer: Where They Work and Where They Do Not

How histone deacetylase inhibitors change gene expression, why they are approved mainly in T-cell lymphomas and myeloma, and why they have underperformed in solid tumours.

TP53BCL2

Cancer Biology 3 min read

DNA Methylation in Cancer: Silencing and Instability

How cancers combine focal promoter hypermethylation that silences tumour suppressors with genome-wide hypomethylation, and how methylation is used for classification and detection.

CDKN2AMLH1TP53

Cancer Biology 3 min read

The CpG Island Methylator Phenotype (CIMP)

What it means when a tumour has widespread coordinated promoter methylation, how CIMP relates to BRAF mutation and MLH1 silencing in colorectal cancer, and its limits as a category.

BRAFMLH1KRAS

Precision Oncology 3 min read

Menin-KMT2A Inhibitors in Acute Leukaemia

How KMT2A rearrangements and NPM1 mutations create a dependence on the menin-KMT2A interaction, and how menin inhibitors such as revumenib exploit it.

MYC

Cancer Genetics 3 min read

SMARCB1 Loss and Rhabdoid Tumours

How loss of the SWI/SNF subunit SMARCB1 causes rhabdoid tumours despite a near-silent genome, the link to the rhabdoid predisposition syndrome, and the EZH2 dependency it creates.

CDKN2AMYC

Precision Oncology 3 min read

Hypomethylating Agents: Azacitidine and Decitabine

How azacitidine and decitabine deplete DNMT enzymes to reverse aberrant DNA methylation, where they are used in myeloid disease, and why response takes months.

TP53

Cancer Immunology 3 min read

Neoantigens and Tumour Immunogenicity

How tumour mutations create new peptides the immune system can recognise, why only a fraction become effective targets, and how this links to mutational burden and treatment response.

TP53STAT3

Cancer Immunology 3 min read

B2M and MHC Class I Loss: Hiding From T Cells

How loss of beta-2-microglobulin or other antigen-presentation components lets tumours evade CD8 T cells, and why it is a recognised mechanism of checkpoint-inhibitor resistance.

STAT3TP53

Cancer Immunology 3 min read

JAK1/JAK2 Loss and Interferon-Signalling Resistance to Immunotherapy

How loss-of-function mutations in JAK1 or JAK2 make tumour cells unresponsive to interferon gamma, and why this is a mechanism of primary and acquired checkpoint-inhibitor resistance.

STAT3TP53

Cancer Immunology 3 min read

HLA Loss of Heterozygosity: Losing Half the Presentation Repertoire

How tumours delete one parental copy of the HLA locus to narrow which antigens they can present, how it is detected, and why it matters for immunotherapy and neoantigen prediction.

STAT3TP53

Cancer Immunology 3 min read

Hot Versus Cold Tumours: What T-Cell Infiltration Means

What makes a tumour immunologically hot or cold, how infiltration patterns relate to checkpoint-inhibitor response, and why the label is a simplification of a spectrum.

STAT3TP53

Cancer Immunology 3 min read

LAG-3, TIM-3 and TIGIT: Checkpoints Beyond PD-1 and CTLA-4

How the next-generation inhibitory receptors LAG-3, TIM-3 and TIGIT contribute to T-cell exhaustion, and where blocking them has and has not shown benefit.

STAT3

Cancer Immunology 3 min read

CTLA-4 Versus PD-1 Blockade: Different Brakes, Different Effects

How CTLA-4 and PD-1 inhibitors act at different stages of the T-cell response, why the combination is more active and more toxic, and what that means clinically.

STAT3

Cancer Immunology 3 min read

Tumour-Infiltrating Lymphocytes: Prognosis and Prediction

What tumour-infiltrating lymphocytes are, how they are scored in pathology, why they carry prognostic weight in several cancers, and the difference between prognostic and predictive value.

STAT3TP53

Cancer Immunology 3 min read

Why checkpoint inhibitors cause inflammatory side effects in healthy organs, which organs are most often affected, and the general principles of recognition and management.

STAT3

Cancer Immunology 3 min read

CAR T-Cell Therapy: Targets, Response Markers and Escape

How chimeric antigen receptor T cells are engineered to recognise a surface target, what predicts response and toxicity, and how tumours escape through antigen loss.

MYC

Cancer Biology 3 min read

The Warburg Effect: Why Cancer Cells Ferment Glucose

Why many tumours take up large amounts of glucose and produce lactate even with oxygen available, what this supports biosynthetically, and how it underlies FDG-PET imaging.

MYCPIK3CAHIF1A

Cancer Biology 3 min read

Glutamine Metabolism in Cancer

Why many tumours consume large amounts of glutamine, how it feeds the TCA cycle and biosynthesis, and the status of glutaminase inhibitors.

MYCPIK3CA

Precision Oncology 3 min read

MTAP Deletion and PRMT5: A Metabolic Synthetic Lethality

How co-deletion of MTAP with CDKN2A creates a targetable dependence on the arginine methyltransferase PRMT5, and how MTA-cooperative inhibitors exploit it.

CDKN2AMTAP

Cancer Immunology 3 min read

The Adenosine Pathway: CD39, CD73 and A2A Receptors

How tumours convert ATP into immunosuppressive adenosine through CD39 and CD73, how the A2A receptor dampens T and NK cells, and where inhibitors stand.

HIF1ASTAT3

Cancer Biology 3 min read

The Tumour Microenvironment: More Than Cancer Cells

An overview of the non-cancer cells and structures that surround a tumour, how they support or restrain growth, and why they influence treatment response.

VEGFAHIF1ASTAT3

Cancer Drugs 4 min read

How Osimertinib Works: A Third-Generation EGFR Inhibitor

Osimertinib is a covalent EGFR inhibitor designed to hit sensitising mutations and the T790M resistance mutation while sparing wild-type EGFR. How that shapes its use and its own resistance.

EGFRMETTP53

Cancer Drugs 4 min read

EGFR Inhibitor Generations Compared: First, Second and Third

How first-generation (gefitinib, erlotinib), second-generation (afatinib, dacomitinib) and third-generation (osimertinib) EGFR inhibitors differ in binding, selectivity and resistance.

EGFRHER2MET

Cancer Drugs 4 min read

How Sotorasib Works: Locking KRAS G12C in Its Off State

Sotorasib covalently binds the mutant cysteine of KRAS G12C and traps the protein in its inactive, GDP-bound form. Why that only works for G12C, and how resistance develops.

KRASEGFRTP53

Cancer Drugs 3 min read

Sotorasib vs Adagrasib: Two KRAS G12C Inhibitors Compared

Both target KRAS G12C covalently, but sotorasib and adagrasib differ in half-life, CNS penetration, drug interactions and toxicity profile. What the differences mean.

KRASEGFRTP53

Cancer Drugs 3 min read

How BRAF and MEK Inhibitors Work — and Why They Are Combined

BRAF inhibitors block mutant V600 kinase but can paradoxically activate the MAPK pathway in normal cells. Adding a MEK inhibitor counters that and delays resistance.

BRAFKRASNRAS

Cancer Drugs 3 min read

ALK Inhibitor Generations Compared: Crizotinib to Lorlatinib

First-generation crizotinib, second-generation alectinib, ceritinib and brigatinib, and third-generation lorlatinib differ in potency, CNS penetration and resistance-mutation coverage.

ALKROS1EGFR

Cancer Drugs 3 min read

How PARP Inhibitors Work: Synthetic Lethality and Trapping

PARP inhibitors kill homologous-recombination-deficient cells through two linked effects: blocking single-strand break repair and trapping PARP on DNA. Why BRCA context matters.

BRCA1BRCA2ATMPALB2

Cancer Drugs 3 min read

How CDK4/6 Inhibitors Work: Holding the Cell-Cycle Brake

Palbociclib, ribociclib and abemaciclib block the CDK4/6 kinases that release the RB brake on cell division. Why an intact RB pathway is needed and how the three drugs differ.

CDK4RB1CDKN2ACCND1

Cancer Drugs 4 min read

How Trastuzumab Works: Targeting the HER2 Receptor

Trastuzumab is a monoclonal antibody that binds HER2 on the cell surface, blocking signalling and flagging the cell for immune destruction. Why HER2 status testing is essential.

HER2EGFRPIK3CA

Cancer Drugs 4 min read

How Antibody-Drug Conjugates Work: Targeted Chemotherapy Delivery

An antibody-drug conjugate links a targeting antibody, a chemical linker and a potent cytotoxic payload. How the pieces work together, the bystander effect, and why HER2-low matters.

HER2TROP2EGFR

Cancer Drugs 4 min read

How Venetoclax Works: A BH3-Mimetic That Restores Apoptosis

Venetoclax mimics a pro-death BH3 protein to displace BIM from BCL2, freeing the apoptosis machinery. Why BCL2-dependent cancers respond and how tumour lysis and resistance arise.

BCL2TP53MCL1

Cancer Drugs 4 min read

How Larotrectinib and Entrectinib Work: TRK Fusion Inhibitors

Larotrectinib and entrectinib inhibit the TRK kinases produced by NTRK gene fusions, wherever the tumour arises. How tumour-agnostic approval works and how resistance mutations emerge.

NTRK1ROS1ALK

Cancer Drugs 3 min read

How Selective RET Inhibitors Work: Selpercatinib and Pralsetinib

Selpercatinib and pralsetinib inhibit RET fusions and activating mutations far more selectively than older multikinase drugs, improving tolerability and CNS activity.

RETALKROS1

Cancer Drugs 3 min read

How Alpelisib Works: Targeting the PI3K Alpha Isoform

Alpelisib selectively inhibits the p110-alpha catalytic subunit of PI3K encoded by PIK3CA. Why isoform selectivity matters, the hyperglycaemia mechanism, and resistance routes.

PIK3CAAKT1PTENMTOR

Cancer Drugs 3 min read

How mTOR Inhibitors Work: Rapalogs and the Feedback Problem

Everolimus and temsirolimus are rapalogs that partially inhibit mTORC1. Why they only block part of the pathway, the AKT feedback loop, and where TSC and PI3K pathway context matters.

MTORTSC1PIK3CAAKT1

All articles are based on analysis of peer-reviewed scientific literature, including PubMed, UniProt, and TCGA data. Content is for educational purposes and does not constitute medical advice.

Clinical Trials News

A daily, plain-language digest of new oncology and life-sciences clinical trials, with a weekly deep-dive roundup — every update linked to its trial registry or primary source.