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A growth-signal receptor. Some cancers make far too much of it, and drugs that block it or use it as a docking site have transformed those cancers. This dossier gathers the 44 products (19 approved), 278 trials, 9 pathways and 6 resistance routes in the corpus that involve it, with external identifiers so it can be joined to UniProt, ChEMBL, Open Targets and the rest of biology.
Ligand-less receptor that heterodimerises with HER3/EGFR to drive PI3K and MAPK signalling. Amplification is a true oncogenic driver; low expression is merely a delivery address for ADCs.
| Cancer | Prevalence | Measure | Note | Source |
|---|---|---|---|---|
| HER2-positive breast cancer | 100% | IHC 3+ or ISH-amplified (defining) | Nature | |
| HR-positive / HER2-negative breast cancer | 55-65% | HER2-low (IHC 1+ or 2+/ISH-) | Nature | |
| Triple-negative breast cancer | 38% | HER2-ultralow (IHC 0 with faint membrane staining in 10% or fewer cells) | 37.6% ultralow, 38.4% null and 24.0% low among 367 non-metastatic TNBCs; ultralow tumours were smaller and lower grade and more often carried BRCA1 promoter methylation, and HER2 category did not affect relapse-free survival over 10.3 years (Boissiere-Michot 2026). | doi.org |
| Triple-negative breast cancer | 30-40% | HER2-low (IHC 1+ or 2+/ISH-) | Nature | |
| Triple-negative breast cancer | 24-37% | HER2-low (IHC 1+ or 2+/ISH-negative) | 36.6% of triple-negative against 65.4% of hormone receptor-positive disease among 3,689 HER2-negative patients (Schettini 2021); 395 of 1,162 hormone receptor-negative tumours, 34.0%, in four German neoadjuvant trials (Denkert 2021); 24.0% of 367 chemotherapy-naive non-metastatic TNBCs (Boissiere-Michot 2026); 63 of 557 DESTINY-Breast04 patients, 11.3%, were hormone receptor-negative (Modi 2022). cBioPortal: IHC 1+ or 2+ recorded for 34 of 166 scored triple-negative samples, 20%, with a further 66 recorded as 0 to 1+ (breast_msk_2018); ERBB2 mutation in 10 of 299, 3.3%, in brca_metabric. | doi.org |
| Gallbladder cancer | 9-31% | Protein overexpression (IHC) | 31.3% HER2-positive among 80 resected Japanese gallbladder carcinomas scored by the gastro-oesophageal guideline (Hiraoka 2020); 12.8% overexpression among 187 Chilean cases scored by ASCO/CAP breast criteria, with 20% equivocal (Roa 2014); 9.4% of 53 Italian gallbladder carcinomas HER2-positive by HERIZON-BTC-01 criteria (Angerilli 2026). | doi.org |
| Gastric & gastro-oesophageal junction cancer | 15-20% | IHC 3+ or 2+/ISH+ | ToGA screening | Wikipedia |
| Biliary tract cancer | 10-20% | IHC 3+ or amplification | Higher in gallbladder/extrahepatic | Wikipedia |
| Gallbladder cancer | 8-10% | Amplification | 8% amplification alone plus 1.5% amplification with a mutation among 260 patients (Mondaca 2024); about 8% of 376 Indian patients (Suryavanshi 2025); high-level amplification in 25 of 244 samples, 10.2%, in cBioPortal gbc_mskcc_2022 and 7 of 103, 6.8%, in gbc_msk_2018. ERBB2 alterations of any kind: 15% (Giraldo 2022), 16% of 85 (Javle 2016), 14% overall and 15% versus 9% in the American and Chilean cohorts (Mondaca 2024). | doi.org |
| Gallbladder cancer | 4-8% | Activating mutation (S310F/Y hotspot) | 4% mutation alone, 1.5% with amplification and 0.4% fusion among 260 patients (Mondaca 2024); S310F/Y hotspot predominance among Indian ERBB2 alterations (Suryavanshi 2025); mutations in 19 of 244 samples, 7.8%, in cBioPortal gbc_mskcc_2022; 9.4% of 32 exomes in gbc_shanghai_2014. | doi.org |
| Colorectal cancer | 4-6% | Activating mutation (not amplification) | cBioPortal: 378 of 7,237, 5.2%, in crc_msk_2026; 53 of 1,134, 4.7%, in crc_msk_2017; 64 of 1,516, 4.2%, in crc_eo_2020; 20 of 534, 3.7%, in coadread_tcga_pan_can_atlas_2018; 38 of 619, 6.1%, in coadread_dfci_2016. ERBB3 mutations were among the recurrent receptor kinase events of the Genentech exome series (Seshagiri 2012). | cBioPortal (TCGA) |
| Colorectal cancer | 3-5% | Amplification/IHC 3+ | RAS wild-type enriched | Wikipedia |
| Pancreatic ductal adenocarcinoma | 1-5% | Amplification (mutation in a further 1%) | cBioPortal high-level amplification: 9 of 183, 4.9%, in paad_tcga_pan_can_atlas_2018; 12 of 109, 11.0%, in paad_utsw_2015; 28 of 2,336, 1.2%, plus 18 mutations in pdac_msk_2024; 4 of 395 in pancreas_msk_2024. Focal amplifications of ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA were found at low individual prevalence in 100 whole genomes (Waddell 2015); ERBB2 amplification in 2.2% of 266 KRAS wild-type tumours (Philip 2022). | cBioPortal (TCGA) |
| Non-small-cell lung cancer | 2-4% | Exon 20 insertion and kinase-domain missense | cBioPortal, samples with an exon 20 insertion: 58 of 2,653, 2.2%, in luad_mskcc_2023_met_organotropism; 51 of 2,621, 1.9%, in nsclc_ctdx_msk_2022; 20 of 915, 2.2%, in lung_msk_2017; 8 of 232, 3.4%, in lung_nci_2022; 5 of 302, 1.7%, in luad_oncosg_2020. Any ERBB2 mutation reaches 110 of 2,653 (4.1%) and 103 of 2,621 (3.9%). Y772_A775dup is the dominant allele, 42 of 110 records in luad_mskcc_2023_met_organotropism. The Lung Cancer Mutation Consortium found ERBB2 in 19 of 733, 3% (Kris 2014). | cBioPortal (TCGA) |
| Non-small-cell lung cancer | 2-3% | ERBB2 exon 20 mutation | cBioPortal (TCGA) | |
| Colorectal cancer | 2-3% | High-level amplification | cBioPortal high-level amplification: 198 of 7,237, 2.7%, in crc_msk_2026; 35 of 1,134, 3.1%, in crc_msk_2017; 47 of 1,516, 3.1%, in crc_eo_2020; 20 of 592, 3.4%, in coadread_tcga_pan_can_atlas_2018; 8 of 257 in coadread_tcga_pub; 32 of 1,015 in crc_sysucc_2022. ERBB2 amplification was among the potentially drug-targetable recurrent copy-number events named in the TCGA analysis (Cancer Genome Atlas Network 2012). Immunohistochemical overexpression was 2.2% of 1,342 stage IV and 1.3% of 1,914 stage II-III patients, with 27 of 28 stage IV overexpressing cases amplified on fluorescence in situ hybridisation (Richman 2016). | cBioPortal (TCGA) |
| Non-small-cell lung cancer | 1-3% | High-level amplification | cBioPortal high-level amplification: 51 of 2,422, 2.1%, in luad_mskcc_2023_met_organotropism; 29 of 915, 3.2%, in lung_msk_2017; 33 of 2,621, 1.3%, in nsclc_ctdx_msk_2022; 9 of 511, 1.8%, in luad_tcga_pan_can_atlas_2018; 12 of 487, 2.5%, in lusc_tcga_pan_can_atlas_2018. | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
| Residue | Kind | How common | What it does | Addressed by | Defeats | Source |
|---|---|---|---|---|---|---|
| Exon 20 insertions (A775_G776insYVMA) 776 to 781 | Activating | About 2 to 4% of non-squamous NSCLC carries a HER2 mutation, mostly exon 20 insertions | Not amplification: HER2 IHC is often low. Trastuzumab deruxtecan and the mutant-selective TKIs zongertinib and sevabertinib are the approved routes. | - | DESTINY-Lung01, NEJM 2022 | |
| S310F / S310Y 310 | Activating | not sourced | Extracellular domain II; the most common HER2 point mutation across tumour types, sensitive to HER2 TKIs in basket trials. | - | Cancer Hotspots (MSK) | |
| L755S / V777L / D769H 755 | Activating | not sourced | Kinase-domain alleles enriched in HR-positive lobular breast cancer after endocrine therapy; L755S resists lapatinib but not irreversible TKIs. | SUMMIT, Nature 2018 |
Frequencies are quoted from the source on each row; a blank means no figure was sourced, not that it is rare. Domain boundaries are approximate. Sources for the map: Cancer Hotspots (MSK) · COSMIC: ERBB2.
| Modality | Approved | Phase 3 | Phase 2 | Phase 1 | Withdrawn or failed |
|---|---|---|---|---|---|
| ADC 13 | - | ||||
| Antibody 12 | - | - | |||
| Small molecule 11 | - | ||||
| Bispecific antibody 3 | - | - | - | ||
| Vaccine or virus 2 | - | - | - | - | |
| fusion protein 1 | - | - | - | - | |
| Small-molecule pan-ErbB TKI 1 | - | - | - | - | |
| Test or device 1 | - | - | - | - |
| Trial | Setting | Result | Products | ||
|---|---|---|---|---|---|
MOUNTAINEER-03 NCT05253651 | 3 | Recruiting | First-line HER2-positive, RAS wild-type metastatic colorectal cancer: tucatinib with trastuzumab and mFOLFOX6 against mFOLFOX6 with bevacizumab or cetuximab | - | |
HERIZON-GEA-01 NCT05152147 | 3 | Positive | First-line HER2-positive advanced gastro-oesophageal adenocarcinoma: zanidatamab + chemotherapy ± tislelizumab vs trastuzumab + chemotherapy | PFS 12.4 vs 8.1 months (HR 0.63-0.65); OS significantly improved. | |
DESTINY-Breast05 NCT04622319 | 3 | Positive | High-risk HER2+ early breast cancer with residual invasive disease after neoadjuvant therapy: T-DXd vs T-DM1 | 3-year iDFS 92.4% vs 83.7%, HR 0.47. | |
DESTINY-Breast09 NCT04784715 | 3 | Positive | First-line HER2+ metastatic breast cancer: T-DXd + pertuzumab vs THP | PFS HR 0.56. | |
DESTINY-Breast11 NCT05113251 | 3 | Positive | Neoadjuvant high-risk HER2+ early breast cancer: T-DXd followed by THP vs ddAC-THP | pCR 67.3% vs 56.3%. | |
DESTINY-Gastric04 NCT04704934 | 3 | Positive | Second-line HER2-positive gastric/GEJ cancer after trastuzumab: T-DXd vs ramucirumab + paclitaxel | OS 14.7 vs 11.4 months, HR 0.70. | |
HER2CLIMB-05 NCT05132582 | 3 | Positive | First-line HER2+ metastatic breast cancer after induction with taxane + trastuzumab + pertuzumab: maintenance tucatinib + HP vs placebo + HP | PFS 24.9 vs 16.3 months, HR 0.64. | |
HORIZON-Breast01 NCT05424835 | 3 | Positive | HER2+ metastatic breast cancer after trastuzumab and taxane (China): trastuzumab rezetecan (SHR-A1811) vs pyrotinib + capecitabine | PFS 30.6 vs 8.3 months, HR 0.22. | |
| ACE-Breast-02 | 3 | Positive | HER2+ advanced breast cancer after trastuzumab and taxane (China): ARX788 vs lapatinib + capecitabine | PFS 11.3 vs 8.2 months, HR 0.64. | |
DESTINY-Breast06 NCT04494425 | 3 | Positive | HR+ HER2-low/ultralow breast cancer after endocrine therapy, chemotherapy-naive: T-DXd vs chemotherapy | PFS HR 0.62. | |
DESTINY-Breast12 NCT04739761 | 3 | Positive | HER2+ metastatic breast cancer with or without brain metastases: single-arm T-DXd | CNS ORR 71.7%; 12-month PFS 61.6% in brain-metastasis cohort. | |
PATINA NCT02947685 | 3 | Positive | Hormone receptor-positive, HER2-positive metastatic breast cancer after induction chemotherapy with anti-HER2 therapy: maintenance anti-HER2 therapy and endocrine therapy with or without palbociclib | Palbociclib added to maintenance anti-HER2 and endocrine therapy lengthened progression-free survival. | |
| 3 | Completed | A Randomized Phase III Trial Evaluating Pathologic Complete Response Rates in Patients With Hormone Receptor-Positive, HER2-Positive, Large Operable and Locally Advanced Breast Cancer Treated With Neoadjuvant Therapy of Docetaxel, Carboplatin, Trastuzumab, and Pertuzumab (TCHP) With or Without Estrogen Deprivation | - | ||
HER2CLIMB-02 NCT03975647 | 3 | Mixed | HER2+ metastatic breast cancer after trastuzumab and taxane: tucatinib + T-DM1 vs placebo + T-DM1 | PFS 9.5 vs 7.4 months, HR 0.76; OS no benefit. | |
| 3 | Completed | A Multi-centre, Open-label, Randomized Clinical Trial Comparing the Efficacy and Safety of the Antibody-drug Conjugate SYD985 to Physician's Choice in Patients With HER2-positive Unresectable Locally Advanced or Metastatic Breast Cancer | - | ||
DESTINY-Breast04 NCT03734029 | 3 | Positive | HER2-low metastatic breast cancer after chemotherapy: T-DXd vs chemotherapy | OS HR 0.64. | |
| 3 | Completed | A Phase 3, Randomized Study of Margetuximab Plus Chemotherapy vs Trastuzumab Plus Chemotherapy in the Treatment of Patients With HER2+ Metastatic Breast Cancer Who Have Received Prior Anti-HER2 Therapies and Require Systemic Treatment | - | ||
| 3 | Completed | A Phase III Clinical Trial Comparing Trastuzumab Given Concurrently With Radiation Therapy and Radiation Therapy Alone for Women With HER2-Positive Ductal Carcinoma In Situ Resected by Lumpectomy | - | ||
DESTINY-Breast03 NCT03529110 | 3 | Positive | HER2+ metastatic breast cancer after trastuzumab and taxane: T-DXd vs T-DM1 | PFS HR 0.33; OS HR 0.64. | |
KEYNOTE-811 NCT03615326 | 3 | Positive | Untreated HER2-positive advanced gastric or gastro-oesophageal junction adenocarcinoma: trastuzumab and fluoropyrimidine-platinum chemotherapy with pembrolizumab or placebo | Higher response rate and longer progression-free survival with pembrolizumab added to trastuzumab and chemotherapy, with benefit concentrated in PD-L1-positive tumours; accelerated approval in May 2021, later limited to PD-L1 combined positive score of 1 or more. | |
| 3 | Completed | A Randomized Phase III Trial of Adjuvant Therapy Comparing Chemotherapy Alone (Six Cycles of Docetaxel Plus Cyclophosphamide or Four Cycles of Doxorubicin Plus Cyclophosphamide Followed by Weekly Paclitaxel) to Chemotherapy Plus Trastuzumab in Women With Node-Positive or High-Risk Node-Negative HER2-Low Invasive Breast Cancer | - | ||
NALA NCT01808573 | 3 | Positive | HER2-positive metastatic breast cancer after two or more HER2-directed regimens: neratinib plus capecitabine against lapatinib plus capecitabine | Neratinib plus capecitabine improved progression-free survival over lapatinib plus capecitabine and reduced interventions for central nervous system disease; approved in February 2020. | |
PERSEPHONE NCT00712140 | 3 | Positive | Adjuvant HER2+ early breast cancer: 6 vs 12 months of trastuzumab | 4-year DFS 89.4% vs 89.8%, non-inferior. | |
KATHERINE NCT01772472 | 3 | Positive | HER2+ early breast cancer with residual invasive disease after neoadjuvant therapy: T-DM1 vs trastuzumab for 14 cycles | iDFS HR 0.50; OS HR 0.66. | |
KRISTINE NCT02131064 | 3 | Negative | Stage II to III HER2-positive breast cancer: neoadjuvant trastuzumab emtansine plus pertuzumab vs docetaxel, carboplatin, trastuzumab and pertuzumab | Pathological complete response 44.4% (T-DM1 + pertuzumab) vs 55.7% (TCHP); more locoregional progression before surgery with T-DM1. | |
TRAIN-2 NCT01996267 | 3 | Positive | Stage II to III HER2-positive breast cancer: neoadjuvant carboplatin and paclitaxel with trastuzumab and pertuzumab, with or without three cycles of anthracycline first | Pathological complete response 67% without anthracycline vs 68% with; 3-year event-free survival 93.5% vs 92.7%. | |
APHINITY NCT01358877 | 3 | Positive | Adjuvant HER2+ early breast cancer: pertuzumab + trastuzumab + chemotherapy vs placebo + trastuzumab + chemotherapy | 8-year iDFS HR 0.78; node-positive absolute +4.9%. | |
LUX-Lung 3 NCT00949650 | 3 | Positive | Untreated stage IIIB or IV lung adenocarcinoma with an EGFR mutation: afatinib 40 mg daily versus up to six cycles of cisplatin with pemetrexed, with progression-free survival by independent review as the primary endpoint | Median progression-free survival 11.1 against 6.9 months (hazard ratio 0.58); 13.6 against 6.9 months in exon 19 deletion or L858R disease. | |
CLEOPATRA NCT00567190 | 3 | Positive | First-line HER2+ metastatic breast cancer: pertuzumab + trastuzumab + docetaxel vs placebo + trastuzumab + docetaxel | OS 57.1 vs 40.8 months, HR 0.69. | |
ToGA NCT01041404 | 3 | Positive | First-line HER2-positive advanced gastric/GEJ adenocarcinoma: trastuzumab + cisplatin/fluoropyrimidine vs chemotherapy | OS 13.8 vs 11.1 months, HR 0.74. |
TOP1 mutations (e.g., E418K) or reduced expression prevent trapping of the cleavage complex.
Schlafen-11 is required for replication-stress-induced death; its epigenetic silencing confers resistance to TOP1 (and platinum) agents.
SN-38 is an ABCG2 substrate; DXd and MMAE are ABCB1 substrates; mesenchymal states upregulate both.
Reduced HER2 or TROP2 surface expression after treatment; less frequent than payload resistance for HER2-low disease.
Defective endocytosis or lysosomal cathepsin activity limits payload release.
Without RB, CDK4/6 inhibition cannot arrest the cell cycle.
KEGG's bladder cancer map shows two routes: low-grade papillary tumours driven by FGFR3 or HRAS activating the MAPK relay, and high-grade invasive tumours that lose TP53 and RB1. Erdafitinib targets the first route; antibody-drug conjugates and PD-1 antibodies now anchor treatment of the second.
Which nodes have drugs →KEGG's breast cancer map lays out the three clinical subtypes as signalling routes: oestrogen receptor driving cyclin D and CDK4/6 in hormone-receptor-positive disease, HER2 driving PI3K/AKT and MAPK in HER2-positive disease, and EGFR, Notch, Wnt and BRCA defects in triple-negative disease. Each route has its own drug class.
Which nodes have drugs →KEGG's endometrial cancer map shows oestrogen-related type I tumours with PTEN loss, KRAS and beta-catenin mutations and faulty mismatch repair, and type II tumours with TP53 mutation and HER2 amplification. Immunotherapy for mismatch-repair-deficient tumours and HER2-directed therapy follow directly from this split.
Which nodes have drugs →This KEGG map splits stomach cancer into two routes: the intestinal type that accumulates TP53, APC and HER2 changes step by step, and the diffuse type driven by loss of the cell glue E-cadherin plus MET or FGFR2 amplification. It matters because HER2, FGFR2, claudin 18.2 and PD-1 status now decide first-line treatment.
Which nodes have drugs →When a cell divides, a scaffold of microtubules (the spindle) pulls one copy of each chromosome to each side. A checkpoint holds the split until every chromosome is hooked on. Taxanes and vinca alkaloids freeze the spindle so the cell is stuck at this checkpoint until it dies.
Which nodes have drugs →Natural killer cells patrol for cells that have lost their identity papers (MHC-I) or that display stress flags. Cancers that hide from T cells by dropping MHC-I become visible to NK cells, unless they also shed the stress flags, wrap themselves in a second inhibitory badge (HLA-E), or soak the neighbourhood in TGF-β.
Which nodes have drugs →This KEGG map shows the order of genetic hits that turn normal pancreatic duct cells into ductal adenocarcinoma: KRAS mutation first, then loss of the p16 brake, then loss of TP53, SMAD4 and BRCA2. It matters because nearly every pancreatic cancer is driven by KRAS, which until recently had no drug.
Which nodes have drugs →The cell's 'grow and survive' circuit. Growth signals from the surface switch on PI3K, which switches on AKT, which switches on mTOR, which builds proteins and blocks self-destruction.
Which nodes have drugs →The brain's blood vessels are sealed tight and fitted with pumps that eject most drugs. That protects the brain from poisons but also from chemotherapy and antibodies. Cancer cells that do squeeze through recruit the brain's own support cells, astrocytes, to feed and shield them.
Which nodes have drugs →| Assay | Platform | Cut-off | Gates |
|---|---|---|---|
| HercepTest Agilent (Dako) · FDA CDx 1998 | IHC | IHC 3+ (or 2+ confirmed by ISH) for trastuzumab; IHC 1+ or 2+/ISH-negative (HER2-low) for trastuzumab deruxtecan; IHC 0 with faint membrane staining (HER2-ultralow) for trastuzumab deruxtecan in HR-positive breast cancer | |
| PATHWAY anti-HER2/neu (4B5) Roche Diagnostics · FDA CDx | IHC | IHC 3+ (HER2-positive); IHC 1+ or 2+/ISH-negative (HER2-low) for trastuzumab deruxtecan; IHC 3+ solid tumours for tumour-agnostic trastuzumab deruxtecan | |
| HER2 IQFISH pharmDx and INFORM HER2 Dual ISH Agilent; Roche Diagnostics · FDA CDx | FISH/ISH | HER2/CEP17 ratio at least 2.0, or ratio below 2.0 with average HER2 copy number at least 6.0 (ASCO/CAP 2018) | |
| FoundationOne CDx Foundation Medicine (Roche) · FDA CDx 2017 | NGS tissue | Per companion claim: EGFR, ALK, BRAF V600, ERBB2 amplification, KRAS wild-type, BRCA1/2 and HRR genes, PIK3CA, MET exon 14, RET, FGFR2 fusions, IDH1, NTRK fusions; MSI-high; TMB at least 10 mutations per megabase | |
| Guardant360 CDx Guardant Health · FDA CDx 2020 | NGS plasma | Per companion claim: EGFR (osimertinib), EGFR exon 20 insertions (amivantamab), KRAS G12C (sotorasib), ESR1 mutations (elacestrant), ERBB2 mutations (zongertinib); negative plasma reflexes to tissue |
| Cell line | Identifiers | Why it is used |
|---|---|---|
| SK-BR-3 | CVCL_0033 · ACH-000017 | Breast, HER2-amplified. |
| BT-474 | CVCL_0179 · ACH-000927 | Breast, HER2-amplified, ER-positive; ADC xenograft standard. |
| HCC1954 | CVCL_1259 · ACH-000859 | Breast, HER2-amplified, trastuzumab-resistant. |
| NCI-N87 | CVCL_1603 · ACH-000427 | Gastric, HER2-amplified. |
| OE19 | CVCL_1622 · ACH-000679 | Oesophagogastric junction, HER2-amplified. |
| MDA-MB-453 | CVCL_0418 · ACH-000910 | Breast, HER2-low (IHC 1+ to 2+); used for HER2-low ADC bystander studies. |
| MCF-7 | CVCL_0031 · ACH-000019 | HER2-low breast line used as the HER2-low or negative comparator. |
| Ba/F3 ERBB2 exon 20 | not resolved | Engineered YVMA insertion lines for zongertinib- and sevabertinib-type TKIs. |
Why unresolved. DESTINY-Breast04 and 06 made IHC 1+ and faint IHC 0 staining actionable, yet inter-observer agreement at the low end is poor and the antibodies, controls and cut-offs were validated for amplification.
What would answer it. Ring studies with reference materials at the low end, AI-assisted scoring validated against trial outcomes, and label language tied to a reproducible assay.
Why unresolved. Resistance to topoisomerase-I payloads (TOP1 mutation, SLFN11 loss, efflux) is target-independent, so a second TOP1 ADC often fails; whether switching payload class restores benefit has not been tested prospectively.
What would answer it. Randomised or well-controlled sequencing studies with pre-treatment biopsies characterising TOP1, SLFN11 and HER2 status.
Query for this target: (TITLE:"HER2" OR ABSTRACT:"HER2" OR TITLE:"ERBB2" OR ABSTRACT:"ERBB2") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about HER2, not a curated reading list.
The dossier as machine-readable JSON, at /api/v1/dossiers/her2.json: identifiers from HGNC, Ensembl, UniProt and ChEMBL, products with status, trials, pathways, hotspots, open questions and assays. The full entity record is in the open API at /api/v1/entities/her2.json. Licence CC BY-NC 4.0.