GeneAnalyses Articleshttps://www.geneanalyses.com/articles2026-09-04T12:00:00ZSource-linked explanations of cancer genes, molecular pathways, mutations and research literature.How mTOR Inhibitors Work: Rapalogs and the Feedback Problemhttps://www.geneanalyses.com/articles/how-mtor-inhibitors-work2026-09-04T12:00:00Z2026-09-04T12:00:00ZEverolimus 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.How Alpelisib Works: Targeting the PI3K Alpha Isoformhttps://www.geneanalyses.com/articles/how-alpelisib-works2026-09-03T12:00:00Z2026-09-04T12:00:00ZAlpelisib selectively inhibits the p110-alpha catalytic subunit of PI3K encoded by PIK3CA. Why isoform selectivity matters, the hyperglycaemia mechanism, and resistance routes.How Selective RET Inhibitors Work: Selpercatinib and Pralsetinibhttps://www.geneanalyses.com/articles/how-selective-ret-inhibitors-work2026-09-03T12:00:00Z2026-09-04T12:00:00ZSelpercatinib and pralsetinib inhibit RET fusions and activating mutations far more selectively than older multikinase drugs, improving tolerability and CNS activity.How Larotrectinib and Entrectinib Work: TRK Fusion Inhibitorshttps://www.geneanalyses.com/articles/how-larotrectinib-and-entrectinib-work2026-09-02T12:00:00Z2026-09-04T12:00:00ZLarotrectinib 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.How Venetoclax Works: A BH3-Mimetic That Restores Apoptosishttps://www.geneanalyses.com/articles/how-venetoclax-works2026-09-02T12:00:00Z2026-09-04T12:00:00ZVenetoclax 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.How Antibody-Drug Conjugates Work: Targeted Chemotherapy Deliveryhttps://www.geneanalyses.com/articles/how-antibody-drug-conjugates-work2026-09-01T12:00:00Z2026-09-04T12:00:00ZAn 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.How Trastuzumab Works: Targeting the HER2 Receptorhttps://www.geneanalyses.com/articles/how-trastuzumab-works2026-08-31T12:00:00Z2026-09-04T12:00:00ZTrastuzumab 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.BRCA1 and Ovarian Cancer Risk: How to Read a Resulthttps://www.geneanalyses.com/articles/brca1-ovarian-cancer-risk2026-08-30T12:00:00Z2026-08-30T12:00:00ZLearn how germline BRCA1 results relate to ovarian cancer risk, why variant classification matters, and how to separate inherited-risk evidence from treatment claims.EGFR Exon 19 Deletions: What the Biomarker Meanshttps://www.geneanalyses.com/articles/egfr-exon-19-deletion2026-08-30T12:00:00Z2026-08-30T12:00:00ZA 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.EGFR L858R: Understanding the Exon 21 Mutationhttps://www.geneanalyses.com/articles/egfr-l858r2026-08-30T12:00:00Z2026-08-30T12:00:00ZUnderstand 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.EGFR T790M: A Gatekeeper Resistance Mutationhttps://www.geneanalyses.com/articles/egfr-t790m-resistance2026-08-30T12:00:00Z2026-08-30T12:00:00ZLearn 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.KRAS G12C in Colorectal Cancer: Biomarker Contexthttps://www.geneanalyses.com/articles/kras-g12c-colorectal-cancer2026-08-30T12:00:00Z2026-08-30T12:00:00ZUnderstand 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.TP53 and Li-Fraumeni Syndrome: Inherited-Risk Contexthttps://www.geneanalyses.com/articles/tp53-li-fraumeni-syndrome2026-08-30T12:00:00Z2026-08-30T12:00:00ZA careful guide to germline TP53 variants and Li-Fraumeni syndrome, including the difference between inherited and tumour-only findings, family testing, and NCI evidence.The Tumour Microenvironment: More Than Cancer Cellshttps://www.geneanalyses.com/articles/tumour-microenvironment-overview2026-08-29T12:00:00Z2026-09-04T12:00:00ZAn overview of the non-cancer cells and structures that surround a tumour, how they support or restrain growth, and why they influence treatment response.How CDK4/6 Inhibitors Work: Holding the Cell-Cycle Brakehttps://www.geneanalyses.com/articles/how-cdk4-6-inhibitors-work2026-08-28T12:00:00Z2026-09-04T12:00:00ZPalbociclib, 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.How PARP Inhibitors Work: Synthetic Lethality and Trappinghttps://www.geneanalyses.com/articles/how-parp-inhibitors-work2026-08-27T12:00:00Z2026-09-04T12:00:00ZPARP inhibitors kill homologous-recombination-deficient cells through two linked effects: blocking single-strand break repair and trapping PARP on DNA. Why BRCA context matters.The Adenosine Pathway: CD39, CD73 and A2A Receptorshttps://www.geneanalyses.com/articles/adenosine-cd73-immunosuppression2026-08-26T12:00:00Z2026-09-04T12:00:00ZHow tumours convert ATP into immunosuppressive adenosine through CD39 and CD73, how the A2A receptor dampens T and NK cells, and where inhibitors stand.ALK Inhibitor Generations Compared: Crizotinib to Lorlatinibhttps://www.geneanalyses.com/articles/alk-inhibitor-generations-compared2026-08-26T12:00:00Z2026-09-04T12:00:00ZFirst-generation crizotinib, second-generation alectinib, ceritinib and brigatinib, and third-generation lorlatinib differ in potency, CNS penetration and resistance-mutation coverage.How BRAF and MEK Inhibitors Work — and Why They Are Combinedhttps://www.geneanalyses.com/articles/how-braf-and-mek-inhibitors-work2026-08-25T12:00:00Z2026-09-04T12:00:00ZBRAF inhibitors block mutant V600 kinase but can paradoxically activate the MAPK pathway in normal cells. Adding a MEK inhibitor counters that and delays resistance.MTAP Deletion and PRMT5: A Metabolic Synthetic Lethalityhttps://www.geneanalyses.com/articles/mtap-prmt5-synthetic-lethality2026-08-24T12:00:00Z2026-09-04T12:00:00ZHow co-deletion of MTAP with CDKN2A creates a targetable dependence on the arginine methyltransferase PRMT5, and how MTA-cooperative inhibitors exploit it.Sotorasib vs Adagrasib: Two KRAS G12C Inhibitors Comparedhttps://www.geneanalyses.com/articles/sotorasib-vs-adagrasib2026-08-24T12:00:00Z2026-09-04T12:00:00ZBoth target KRAS G12C covalently, but sotorasib and adagrasib differ in half-life, CNS penetration, drug interactions and toxicity profile. What the differences mean.Glutamine Metabolism in Cancerhttps://www.geneanalyses.com/articles/glutamine-metabolism-cancer2026-08-22T12:00:00Z2026-09-04T12:00:00ZWhy many tumours consume large amounts of glutamine, how it feeds the TCA cycle and biosynthesis, and the status of glutaminase inhibitors.How Sotorasib Works: Locking KRAS G12C in Its Off Statehttps://www.geneanalyses.com/articles/how-sotorasib-works2026-08-21T12:00:00Z2026-09-04T12:00:00ZSotorasib 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.EGFR Inhibitor Generations Compared: First, Second and Thirdhttps://www.geneanalyses.com/articles/egfr-tki-generations-compared2026-08-20T12:00:00Z2026-09-04T12:00:00ZHow first-generation (gefitinib, erlotinib), second-generation (afatinib, dacomitinib) and third-generation (osimertinib) EGFR inhibitors differ in binding, selectivity and resistance.The Warburg Effect: Why Cancer Cells Ferment Glucosehttps://www.geneanalyses.com/articles/warburg-effect-cancer-metabolism2026-08-20T12:00:00Z2026-09-04T12:00:00ZWhy 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.How Osimertinib Works: A Third-Generation EGFR Inhibitorhttps://www.geneanalyses.com/articles/how-osimertinib-works2026-08-19T12:00:00Z2026-09-04T12:00:00ZOsimertinib 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.CAR T-Cell Therapy: Targets, Response Markers and Escapehttps://www.geneanalyses.com/articles/car-t-cell-therapy-biomarkers2026-08-18T12:00:00Z2026-09-04T12:00:00ZHow chimeric antigen receptor T cells are engineered to recognise a surface target, what predicts response and toxicity, and how tumours escape through antigen loss.Immune-Related Adverse Events: When the Immune System Overshootshttps://www.geneanalyses.com/articles/immune-related-adverse-events2026-08-16T12:00:00Z2026-09-04T12:00:00ZWhy checkpoint inhibitors cause inflammatory side effects in healthy organs, which organs are most often affected, and the general principles of recognition and management.Tumour-Infiltrating Lymphocytes: Prognosis and Predictionhttps://www.geneanalyses.com/articles/tumour-infiltrating-lymphocytes2026-08-14T12:00:00Z2026-09-04T12:00:00ZWhat 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.CTLA-4 Versus PD-1 Blockade: Different Brakes, Different Effectshttps://www.geneanalyses.com/articles/ctla4-vs-pd1-checkpoint-blockade2026-08-12T12:00:00Z2026-09-04T12:00:00ZHow 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.LAG-3, TIM-3 and TIGIT: Checkpoints Beyond PD-1 and CTLA-4https://www.geneanalyses.com/articles/lag3-tim3-tigit-checkpoints2026-08-10T12:00:00Z2026-09-04T12:00:00ZHow 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.Hot Versus Cold Tumours: What T-Cell Infiltration Meanshttps://www.geneanalyses.com/articles/hot-vs-cold-tumours2026-08-08T12:00:00Z2026-09-04T12:00:00ZWhat 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.HLA Loss of Heterozygosity: Losing Half the Presentation Repertoirehttps://www.geneanalyses.com/articles/hla-loss-of-heterozygosity2026-08-06T12:00:00Z2026-09-04T12:00:00ZHow 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.JAK1/JAK2 Loss and Interferon-Signalling Resistance to Immunotherapyhttps://www.geneanalyses.com/articles/jak1-jak2-interferon-resistance2026-08-04T12:00:00Z2026-09-04T12:00:00ZHow 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.B2M and MHC Class I Loss: Hiding From T Cellshttps://www.geneanalyses.com/articles/b2m-mhc-class-i-loss2026-08-02T12:00:00Z2026-09-04T12:00:00ZHow 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.Neoantigens and Tumour Immunogenicityhttps://www.geneanalyses.com/articles/neoantigens-and-tumour-immunogenicity2026-07-31T12:00:00Z2026-09-04T12:00:00ZHow 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.Hypomethylating Agents: Azacitidine and Decitabinehttps://www.geneanalyses.com/articles/hypomethylating-agents-explained2026-07-29T12:00:00Z2026-09-04T12:00:00ZHow azacitidine and decitabine deplete DNMT enzymes to reverse aberrant DNA methylation, where they are used in myeloid disease, and why response takes months.SMARCB1 Loss and Rhabdoid Tumourshttps://www.geneanalyses.com/articles/smarcb1-rhabdoid-tumours2026-07-27T12:00:00Z2026-09-04T12:00:00ZHow 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.Menin-KMT2A Inhibitors in Acute Leukaemiahttps://www.geneanalyses.com/articles/menin-kmt2a-leukaemia2026-07-25T12:00:00Z2026-09-04T12:00:00ZHow KMT2A rearrangements and NPM1 mutations create a dependence on the menin-KMT2A interaction, and how menin inhibitors such as revumenib exploit it.The CpG Island Methylator Phenotype (CIMP)https://www.geneanalyses.com/articles/cpg-island-methylator-phenotype2026-07-23T12:00:00Z2026-09-04T12:00:00ZWhat 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.DNA Methylation in Cancer: Silencing and Instabilityhttps://www.geneanalyses.com/articles/dna-methylation-cancer-overview2026-07-21T12:00:00Z2026-09-04T12:00:00ZHow cancers combine focal promoter hypermethylation that silences tumour suppressors with genome-wide hypomethylation, and how methylation is used for classification and detection.HDAC Inhibitors in Cancer: Where They Work and Where They Do Nothttps://www.geneanalyses.com/articles/hdac-inhibitors-cancer2026-07-19T12:00:00Z2026-09-04T12:00:00ZHow 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.BET Bromodomain Inhibitors: Targeting Transcriptional Addictionhttps://www.geneanalyses.com/articles/bet-bromodomain-inhibitors2026-07-17T12:00:00Z2026-09-04T12:00:00ZHow 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.Histone H3 G34 Mutations in Paediatric High-Grade Gliomahttps://www.geneanalyses.com/articles/histone-h3-g34-glioma2026-07-15T12:00:00Z2026-09-04T12:00:00ZHow 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.Histone H3 K27M and Diffuse Midline Gliomahttps://www.geneanalyses.com/articles/histone-h3-k27m-diffuse-midline-glioma2026-07-13T12:00:00Z2026-09-04T12:00:00ZHow 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.BAP1 Tumour Predisposition Syndromehttps://www.geneanalyses.com/articles/bap1-tumour-predisposition-syndrome2026-07-11T12:00:00Z2026-09-04T12:00:00ZHow germline BAP1 loss predisposes to mesothelioma, uveal melanoma, renal cell carcinoma and distinctive skin tumours, and how somatic BAP1 loss is used in pathology.SETD2: H3K36 Methylation, Transcription and Repairhttps://www.geneanalyses.com/articles/setd2-histone-methylation-cancer2026-07-09T12:00:00Z2026-09-04T12:00:00ZHow 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.KDM6A (UTX): An X-Linked Histone Demethylase Tumour Suppressorhttps://www.geneanalyses.com/articles/kdm6a-utx-cancer2026-07-07T12:00:00Z2026-09-04T12:00:00ZHow 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.KMT2D and KMT2C: Enhancer Regulators Lost in Many Cancershttps://www.geneanalyses.com/articles/kmt2d-kmt2c-chromatin-cancer2026-07-05T12:00:00Z2026-09-04T12:00:00ZWhy 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.EZH2 and Polycomb Repression in Cancerhttps://www.geneanalyses.com/articles/ezh2-polycomb-cancer2026-07-03T12:00:00Z2026-09-04T12:00:00ZHow 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.