https://www.geneanalyses.com/articles Source-linked explanations of cancer genes, molecular pathways, mutations and research literature. en-GB Fri, 04 Sep 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-mtor-inhibitors-work https://www.geneanalyses.com/articles/how-mtor-inhibitors-work 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. Fri, 04 Sep 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-alpelisib-works https://www.geneanalyses.com/articles/how-alpelisib-works Alpelisib selectively inhibits the p110-alpha catalytic subunit of PI3K encoded by PIK3CA. Why isoform selectivity matters, the hyperglycaemia mechanism, and resistance routes. Thu, 03 Sep 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-selective-ret-inhibitors-work https://www.geneanalyses.com/articles/how-selective-ret-inhibitors-work Selpercatinib and pralsetinib inhibit RET fusions and activating mutations far more selectively than older multikinase drugs, improving tolerability and CNS activity. Thu, 03 Sep 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-larotrectinib-and-entrectinib-work https://www.geneanalyses.com/articles/how-larotrectinib-and-entrectinib-work 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. Wed, 02 Sep 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-venetoclax-works https://www.geneanalyses.com/articles/how-venetoclax-works 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. Wed, 02 Sep 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-antibody-drug-conjugates-work https://www.geneanalyses.com/articles/how-antibody-drug-conjugates-work 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. Tue, 01 Sep 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-trastuzumab-works https://www.geneanalyses.com/articles/how-trastuzumab-works 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. Mon, 31 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/brca1-ovarian-cancer-risk https://www.geneanalyses.com/articles/brca1-ovarian-cancer-risk Learn how germline BRCA1 results relate to ovarian cancer risk, why variant classification matters, and how to separate inherited-risk evidence from treatment claims. Sun, 30 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/egfr-exon-19-deletion https://www.geneanalyses.com/articles/egfr-exon-19-deletion 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. Sun, 30 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/egfr-l858r https://www.geneanalyses.com/articles/egfr-l858r 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. Sun, 30 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/egfr-t790m-resistance https://www.geneanalyses.com/articles/egfr-t790m-resistance 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. Sun, 30 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/kras-g12c-colorectal-cancer https://www.geneanalyses.com/articles/kras-g12c-colorectal-cancer 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. Sun, 30 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/tp53-li-fraumeni-syndrome https://www.geneanalyses.com/articles/tp53-li-fraumeni-syndrome 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. Sun, 30 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/tumour-microenvironment-overview https://www.geneanalyses.com/articles/tumour-microenvironment-overview 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. Sat, 29 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-cdk4-6-inhibitors-work https://www.geneanalyses.com/articles/how-cdk4-6-inhibitors-work 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. Fri, 28 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-parp-inhibitors-work https://www.geneanalyses.com/articles/how-parp-inhibitors-work 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. Thu, 27 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/adenosine-cd73-immunosuppression https://www.geneanalyses.com/articles/adenosine-cd73-immunosuppression How tumours convert ATP into immunosuppressive adenosine through CD39 and CD73, how the A2A receptor dampens T and NK cells, and where inhibitors stand. Wed, 26 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/alk-inhibitor-generations-compared https://www.geneanalyses.com/articles/alk-inhibitor-generations-compared First-generation crizotinib, second-generation alectinib, ceritinib and brigatinib, and third-generation lorlatinib differ in potency, CNS penetration and resistance-mutation coverage. Wed, 26 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-braf-and-mek-inhibitors-work https://www.geneanalyses.com/articles/how-braf-and-mek-inhibitors-work 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. Tue, 25 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/mtap-prmt5-synthetic-lethality https://www.geneanalyses.com/articles/mtap-prmt5-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. Mon, 24 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/sotorasib-vs-adagrasib https://www.geneanalyses.com/articles/sotorasib-vs-adagrasib Both target KRAS G12C covalently, but sotorasib and adagrasib differ in half-life, CNS penetration, drug interactions and toxicity profile. What the differences mean. Mon, 24 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/glutamine-metabolism-cancer https://www.geneanalyses.com/articles/glutamine-metabolism-cancer Why many tumours consume large amounts of glutamine, how it feeds the TCA cycle and biosynthesis, and the status of glutaminase inhibitors. Sat, 22 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-sotorasib-works https://www.geneanalyses.com/articles/how-sotorasib-works 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. Fri, 21 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/egfr-tki-generations-compared https://www.geneanalyses.com/articles/egfr-tki-generations-compared How first-generation (gefitinib, erlotinib), second-generation (afatinib, dacomitinib) and third-generation (osimertinib) EGFR inhibitors differ in binding, selectivity and resistance. Thu, 20 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/warburg-effect-cancer-metabolism https://www.geneanalyses.com/articles/warburg-effect-cancer-metabolism 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. Thu, 20 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/how-osimertinib-works https://www.geneanalyses.com/articles/how-osimertinib-works 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. Wed, 19 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/car-t-cell-therapy-biomarkers https://www.geneanalyses.com/articles/car-t-cell-therapy-biomarkers 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. Tue, 18 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/immune-related-adverse-events https://www.geneanalyses.com/articles/immune-related-adverse-events Why checkpoint inhibitors cause inflammatory side effects in healthy organs, which organs are most often affected, and the general principles of recognition and management. Sun, 16 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/tumour-infiltrating-lymphocytes https://www.geneanalyses.com/articles/tumour-infiltrating-lymphocytes 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. Fri, 14 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/ctla4-vs-pd1-checkpoint-blockade https://www.geneanalyses.com/articles/ctla4-vs-pd1-checkpoint-blockade 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. Wed, 12 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/lag3-tim3-tigit-checkpoints https://www.geneanalyses.com/articles/lag3-tim3-tigit-checkpoints 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. Mon, 10 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/hot-vs-cold-tumours https://www.geneanalyses.com/articles/hot-vs-cold-tumours 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. Sat, 08 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/hla-loss-of-heterozygosity https://www.geneanalyses.com/articles/hla-loss-of-heterozygosity 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. Thu, 06 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/jak1-jak2-interferon-resistance https://www.geneanalyses.com/articles/jak1-jak2-interferon-resistance 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. Tue, 04 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/b2m-mhc-class-i-loss https://www.geneanalyses.com/articles/b2m-mhc-class-i-loss 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. Sun, 02 Aug 2026 12:00:00 GMT https://www.geneanalyses.com/articles/neoantigens-and-tumour-immunogenicity https://www.geneanalyses.com/articles/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. Fri, 31 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/hypomethylating-agents-explained https://www.geneanalyses.com/articles/hypomethylating-agents-explained How azacitidine and decitabine deplete DNMT enzymes to reverse aberrant DNA methylation, where they are used in myeloid disease, and why response takes months. Wed, 29 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/smarcb1-rhabdoid-tumours https://www.geneanalyses.com/articles/smarcb1-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. Mon, 27 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/menin-kmt2a-leukaemia https://www.geneanalyses.com/articles/menin-kmt2a-leukaemia How KMT2A rearrangements and NPM1 mutations create a dependence on the menin-KMT2A interaction, and how menin inhibitors such as revumenib exploit it. Sat, 25 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/cpg-island-methylator-phenotype https://www.geneanalyses.com/articles/cpg-island-methylator-phenotype 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. Thu, 23 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/dna-methylation-cancer-overview https://www.geneanalyses.com/articles/dna-methylation-cancer-overview How cancers combine focal promoter hypermethylation that silences tumour suppressors with genome-wide hypomethylation, and how methylation is used for classification and detection. Tue, 21 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/hdac-inhibitors-cancer https://www.geneanalyses.com/articles/hdac-inhibitors-cancer 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. Sun, 19 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/bet-bromodomain-inhibitors https://www.geneanalyses.com/articles/bet-bromodomain-inhibitors 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. Fri, 17 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/histone-h3-g34-glioma https://www.geneanalyses.com/articles/histone-h3-g34-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. Wed, 15 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/histone-h3-k27m-diffuse-midline-glioma https://www.geneanalyses.com/articles/histone-h3-k27m-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. Mon, 13 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/bap1-tumour-predisposition-syndrome https://www.geneanalyses.com/articles/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. Sat, 11 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/setd2-histone-methylation-cancer https://www.geneanalyses.com/articles/setd2-histone-methylation-cancer 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. Thu, 09 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/kdm6a-utx-cancer https://www.geneanalyses.com/articles/kdm6a-utx-cancer 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. Tue, 07 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/kmt2d-kmt2c-chromatin-cancer https://www.geneanalyses.com/articles/kmt2d-kmt2c-chromatin-cancer 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. Sun, 05 Jul 2026 12:00:00 GMT https://www.geneanalyses.com/articles/ezh2-polycomb-cancer https://www.geneanalyses.com/articles/ezh2-polycomb-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. Fri, 03 Jul 2026 12:00:00 GMT