PIK3CA

Overview

PIK3CA encodes the catalytic p110-alpha subunit of PI3K. In the corpus it appears as a subclonal resistance driver in NSCLC ctDNA, a lineage-conditioned actionable driver in histiocytosis vs germ cell tumors, and a metastasis-differentiating gene in LUAD.

Alterations observed in the corpus

  • Identified as one of eight significantly mutated genes in GBM (7% of cases); contributes to the RTK/RAS/PI3K pathway which is altered in 88% of samples PMID:18772890.
  • Enriched among ctDNA-only alterations (not detected by time-matched tissue) in advanced NSCLC; flagged as a subclonal resistance driver associated with short survival PMID:36357680.
  • Among ten genes differentially altered between ever- and never-metastatic LUAD primary tumors in the 2,532-specimen MSK organotropism cohort; altered less in metastases than primaries PMID:37084736.
  • Mutated in one histiocytosis patient and two ovarian GCT patients in the Make-an-IMPACT rare-cancer program PMID:36862133.
  • PIK3CA was the most frequent PI3K-pathway co-alteration in FGFR2/3-altered urothelial carcinoma (28%, 115/414), but did not predict response to erdafitinib in the MSK bladder_msk_2023 cohort PMID:37682528.
  • PIK3CA mutations (with PIK3R1 and TP53, plus broad CNV load) were used to define “molecular grade-intermediate” in 1p19q codeleted IDH-mutant oligodendrogliomas PMID:37910594.
  • PIK3CA p.E545K was common in breast cancer CSF ctDNA samples; PIK3CA also appeared as an off-target resistance alteration in EGFR-mutant lung cancer CSF ctDNA in the csf_msk_2024 cohort (1,007 CSF samples, 711 patients) PMID:39289779.
  • PIK3CA alterations identified as resistance mechanisms in escape lesions in HER2-positive metastatic esophagogastric cancer (EGC) treated with pembrolizumab + trastuzumab + chemotherapy PMID:37406106.
  • PIK3CA mutations/amplifications in 25% of cervical cancers (N=177); enriched in squamous subtype (38%) vs. gastric type (5%); most common OncoKB level 3B alteration in this cohort PMID:37643132.
  • PIK3CA mutation frequency similar between Black and White endometrial carcinoma patients but with distinct alteration mechanism (more amplification in Black patients) PMID:37651310.
  • PIK3CA oncogenic alterations present in >10% of early-onset esophagogastric cancer patients with no significant differential frequency vs. average-onset PMID:37699004.
  • PIK3CA oncogenic mutations in 5/17 FN-RMS (fusion-negative rhabdomyosarcoma) as part of the RAS/PIK3CA pathway alteration cluster PMID:37730754.
  • PIK3CA oncogenic alterations in 8% of advanced hepatocellular carcinoma (HCC) cases by cfDNA profiling (MSK-ACCESS); actionable at OncoKB level 3b PMID:37769223.
  • PIK3CA co-occurs with BRAF V600E in anaplastic thyroid carcinoma (FDR = 0.034); preferentially mutated in ATCs and co-differentiated thyroid cancers relative to PTC PMID:38412093.
  • PIK3CA mutated in 48% of dMMR/MSI-H gynecologic cancers treated with nivolumab; not associated with clinical benefit or resistance to PD-1 blockade PMID:38653864.
  • PIK3CA plasma detection associated with VTE risk (adjusted HR = 1.47, 95% CI: 1.01–2.13, N=254 patients) in pan-cancer ctDNA liquid biopsy cohort; in multivariate analysis, individual gene-level alterations including PIK3CA were not independently associated with VTE after controlling for ctDNA detection PMID:39147831.
  • PIK3CA hotspot mutation (H1047L — reported as “H1074L” in text) in SARC0117 (USS sarcoma) drove broad PI3K/mTOR pathway sensitivity (alpelisib, apitolisib, copanlisib, BGT226, vistusertib) in PDTO screen. SARC0134 (MPNST) carried the mutation in the primary but lost it in metastasis, predicting non-response. A biomarker-negative osteosarcoma (SARC0069_2) was a top alpelisib responder. PMID:39305899
  • PIK3CA enriched in MAPK-WT PDAC tumors (10% vs 2% in KRAS-mutant, P=0.002) in the MSK 2,336-patient cohort; one of the defining features distinguishing the MAPK-WT subtype. PMID:39753968
  • PIK3CA oncogenic alteration present in 11% of cfDNA samples in a 201-patient metastatic urothelial carcinoma (mUC) cohort (CALGB 90601); associated with significantly shorter OS on multivariable analysis (HR 1.91, 95% CI 1.20–3.04; P=0.006) after adjustment for visceral metastases, performance status, and ctDNA VAF. PMID:40256659
  • PIK3CA was mutated in 18% (13/71) of myxoid/round-cell liposarcomas (MRLS) — first report of PIK3CA mutation in a mesenchymal cancer; mutations clustered in helical (E542K, E545K) and kinase (H1047L, H1047R) domains; mutated tumors had shorter disease-specific survival (log-rank p=0.036, n=65 with outcome data); only helical-domain mutants showed elevated phospho-AKT (Ser473/Thr308), suggesting domain-specific mechanism (sarc_mskcc, n=207) PMID:20601955.
  • Identified as mutated in LUAD (TSP, n=188); part of mTOR pathway altered in >30% of tumours. PMID:18948947
  • Mutated in 13% of a longitudinal African breast cancer cohort PMID:36585450
  • Activating mutations (e.g., E545K) more common in low-grade bladder tumors; 27% discordance rate in primary-metastasis pairs PMID:36543146
  • PIK3CA mutations (E545K/Q, H1047R, P104L, E542K) detected in CRC patient ctDNA at resistance to KRASG12C + EGFR inhibition PMID:36355783
  • PIK3CA E545K hotspot variant observed in metastatic urothelial carcinoma (UC-GENOME cohort) PMID:36333289
  • PIK3CA GOF mutations in 9% of GBC; actionable at OncoKB level 3B (e.g., p.E545K, p.H1047R) PMID:36228155
  • Recurrently amplified and mutated in prostate cancer identified in integrative genomic profiling of 218 tumors PMID:20579941
  • Mutated in pancreatic neuroendocrine tumors (PanNET) identified by exome sequencing PMID:21252315
  • Mutated in high-grade serous ovarian carcinoma (HGSOC) in TCGA integrated genomic analysis PMID:21720365
  • PIK3CA is recurrently mutated in HNSCC (74 tumor-normal pairs, Broad), with hotspot mutations in the helical and kinase domains PMID:21798893
  • PIK3CA mutations identified as recurrent driver events in HNSCC whole-exome sequencing of 32 primary tumors (Johns Hopkins cohort) PMID:21798897
  • PIK3CA mutations co-occur with ARID1A loss in ovarian cancer, and PIK3CA-mutant cells show sensitivity to PI3K pathway inhibition in the context of BET bromodomain inhibition PMID:22037554
  • PIK3CA mutation status was assessed in breast cancer samples undergoing whole-exome sequencing that identified SF3B1 mutations and widespread splicing dysregulation PMID:22158541
  • PIK3CA is one of the most frequently mutated genes in breast cancer; identified by WGS of 65 tumors (BCCRC cohort) PMID:22495314
  • PIK3CA mutations occur in prostate cancer; identified by WES of 112 primary tumors (Broad Institute cohort) PMID:22610119
  • Mutated in >10% of cases in breast cancer WES (100 tumors, Sanger cohort); AKT pathway activation PMID:22722201
  • Missense mutations in helical domain (E542/E545, 40%) and kinase domain (H1047, 47%) in 27% of breast cancer samples (Broad WES, 103 tumors); activates PI3K pathway; mutually exclusive with AKT1 E17K PMID:22722202
  • Activating missense mutations (Q546K, H1047R, N345K) across WNT/SHH/subgroup-4 medulloblastoma (PCGP WGS, 37 tumors); accelerates but does not initiate tumourigenesis via AKT pathway PMID:22722829
  • Mutations in 18% of non-hypermutated colorectal tumors; mutually exclusive with PIK3R1 and PTEN loss in 276-tumor TCGA CRC cohort PMID:22810696
  • Recurrently altered in melanoma (121-tumor Broad WES cohort); listed among recurrently mutated genes PMID:22817889
  • PIK3CA significantly mutated in microsatellite-stable (MSS) colorectal cancer (Genentech WES, 74 tumors) PMID:22895193
  • PIK3CA — no mutations observed in SCLC (CLCGP, 29 tumors); notable negative finding PMID:22941188
  • PIK3CA rare activating hotspot mutations identified in SCLC (JHU WES/WGS, 36 tumors) PMID:22941189
  • PIK3CA mutation and amplification in lung squamous cell carcinoma (TCGA, 178 tumors); part of 47% PI3K pathway alteration rate PMID:22960745
  • PIK3CA activating mutations identified as significant in lung adenocarcinoma (Broad WES, 183 tumors) PMID:22980975
  • E545K hotspot mutation almost exclusively Luminal A (25/27 cases); amplification in 49% of Basal-like tumors; mutations in 45% Luminal A, 39% HER2E, 29% Luminal B, 9% Basal-like across 510 TCGA breast tumors (brca_tcga_pub); statistically significant mutual exclusivity with PIK3R1, PTEN, and AKT1 mutations (P=0.025) PMID:23000897
  • Mutually exclusive with PIK3R1, PTEN, and AKT1 alterations in PDAC (ICGC, 142 tumors); PI3K pathway implicated via GISTIC2.0 copy-number analysis PMID:23103869
  • PI3K pathway activation (elevated pERK, pmTOR, pS6) observed in both near haploid and low hypodiploid ALL; PI3K inhibitor GDC-0941 and dual PI3K/mTOR inhibitor BEZ235 substantially inhibited proliferation of all hypodiploid ALL tumors ex vivo (all_stjude_2013, 124 pediatric cases) PMID:23334668
  • Most frequently mutated actionable gene in EAC (7/145 tumors); hotspot p.E545 cannot be generated by the adenine-to-adenine transversion mutational signature dominant in EAC PMID:23525077
  • Activating mutation and/or 3q copy gain; part of mitogenic pathway altered in 63% of oral squamous cell carcinoma (OSCC) tumors; mutually exclusive with PIK3R1 PMID:23619168
  • Mutated in 71% of POLE-ultramutated and 42% of uterine serous endometrial tumors; mutually exclusive with PIK3R1 across all endometrial subgroups PMID:23636398
  • Three missense mutations at COSMIC hotspots in 5% of ACC cases; functional PI3K/AKT pathway activation confirmed (p-AKT/p-PRAS40 elevated); authors nominate FGF/IGF/PI3K axis as a candidate therapeutic vulnerability in ACC PMID:23685749
  • Canonical activating hotspot p.H1047L detected in ACC exome sequencing (24-case cohort) PMID:23778141
  • Mutation in 18% of high-grade bladder tumors (urothelial carcinoma); PIK3CA/AKT1 mutations confer sensitivity to MK-2206 in cell lines PMID:23897969
  • PI3K-family mutations (PIK3CA/PIK3R1 in p110α/p85α subunits) account for 18.3% of GBM alterations; combined PI3K pathway alterations in 25.1% PMID:24120142
  • Confirmed recurrent driver mutation in transitional cell carcinoma (TCC) of the bladder PMID:24121792
  • PI3K pathway alteration in intrahepatic cholangiocarcinoma (IHCH); part of the 22% PI3K pathway alteration rate in the discovery-screen cohort PMID:24185509
  • Acquired H1047R hotspot mutation detected in a BRAF-inhibitor-resistant melanoma (Patient 48); combined MAPK + PI3K inhibition was synergistic in PTEN-null A2058 cells PMID:24265153
  • TMZ-associated E542K activating mutation acquired in low-grade glioma recurrence (patient 18); activates AKT and induces mTOR-dependent transformation as part of convergent evolution under treatment pressure PMID:24336570
  • Oncogenic Q546 (helical domain) and H1047 (kinase domain) hotspot mutations in rhabdomyosarcoma; frequency 7.4% in PFN tumors; two tumors had concurrent RAS + PIK3CA mutations indicating dual pathway activation PMID:24436047
  • Mutations in 20% of muscle-invasive bladder carcinomas, predominantly in the helical domain near E545; one of the most frequently mutated oncogenes in bladder cancer PMID:24476821
  • PIK3CA activating hotspot mutations (p.Glu545Lys, p.His1047Arg) found in spatially separated regions of ccRCC (EV005), demonstrating parallel evolution; PI3K-mTOR pathway mutation prevalence reaches 60% per case vs much lower per-biopsy estimates PMID:24487277
  • PIK3CA is mutated in ESCC as part of the canonical genomic landscape cited in a review of oral microbiome associations with ESCC PMID:24670651
  • PIK3CA harbors activating mutations and amplification in ESCC, contributing to PI3K pathway activation PMID:24686850
  • PIK3CA is a PI3K/AKT pathway driver in HCC identified by integrated genomic analysis PMID:24735922
  • PI3K/AKT pathway activation implicated in HCC; PIK3CA mutations contribute to the oncogenic signaling landscape, and the pathway is reactivated downstream of MET in the context of EGFR/MET resistance mechanisms PMID:24798001
  • PIK3CA mutations in 80% of EBV-positive gastric tumors (mostly non-exon-20, dispersed) and 12% across the whole gastric cancer cohort; targetable via PI3-kinase inhibition PMID:25079317
  • PIK3CA mutations in 7% of LUAD (TCGA, n=230); enriched in transversion-low tumors; drives mTOR pathway activation via p-AKT in subset PMID:25079552
  • PIK3CA recurrent activating helical-domain missense mutations in 21% of muscle-invasive bladder cancer (BLCA, n=47 TURBT); associated with favorable recurrence-free and cancer-specific survival after radical cystectomy PMID:25092538
  • Convergent evolution with independent E542K and E545K hotspot mutations in primary vs metastasis; three additional private events including primary-specific E545K (x2) and metastasis-specific N107 in-frame deletion; subclonal PI3K heterogeneity is clinically relevant given active PI3K inhibitor development PMID:25164765
  • Hotspot activating mutations in 9/22 (41%) uterine/ovarian carcinosarcoma cases; mutually exclusive with PIK3R1; co-occurs with PTEN; PI3K pathway hits in >50% of cases support trials of PI3K/mTOR/AKT inhibitors PMID:25233892
  • Mutated in 10% (4/39) of aggressive cSCC cases with 5 total mutations; no canonical E545/H1047 hotspot; 2 inactivating; not reaching significance as a driver in this cohort PMID:25303977
  • PIK3CA mutations overlap with BRAFV600E in the HotNet2 MAPK subnetwork in papillary thyroid carcinoma (PTC); PI3K/PPARγ pathway alterations (including PIK3CA) found in ~4.5% of PTCs. PMID:25417114
  • PIK3CA mutations in ~6% of intrahepatic cholangiocarcinoma (iCCA) and 3–7% of extrahepatic CCA (eCCA); approximately 6.8% in advanced cfDNA cohorts. PMID:25526346
  • PIK3CA p.E542K mutation detected in a multi-clonal gastric cancer (GC) case alongside KRAS p.G13D and BRCA2 mutations in separate clones, illustrating intratumor heterogeneity of PI3K-ERBB pathway alterations. PMID:25583476
  • Classic CRC driver included in comparison analysis in an African American vs. Caucasian CRC cohort; mutation frequency not highlighted as AA-specific PMID:25583493
  • P471L activating mutation observed in cutaneous SCC (cSCC); recurrence between this cohort and a prior 11-tumor cSCC NGS cohort suggests a functional role; high-level amplification absent in cSCC (unlike lung SCC) PMID:25589618
  • Mutated in 21% of HNSCC (56% in HPV(+), 34% in HPV(−)); 73% of mutations at hotspots E542K/E545K/H1047R/L; helical-domain enriched in HPV(+); often co-amplified; component of RTK/RAS/PI(3)K pathway altered in 61–62% of tumours PMID:25631445
  • In HCC, PIK3CA is a component of the PI3K/AKT/mTOR pathway altered in 51% of cases. PMID:25822088
  • In PAAD, PIK3CA activating mutations occur in 4% of cases, mutually exclusive with KRAS; found in KRAS-wildtype cases alongside BRAF V600E; nominate PI3K inhibitors (buparlisib, GDC-0941). PMID:25855536
  • In mCRPC, PIK3CA harbors hotspot mutations, focal amplifications, and novel activating fusions; part of the PI3K pathway altered in 49% (73/150) of cases in the SU2C–PCF cohort; activating fusions result in PIK3CA overexpression. PMID:26000489
  • In cutaneous melanoma (SKCM), PIK3CA mutations (E545K, H1047L) were identified as recurrent events and nominated as biomarkers for combination MEK + PI3K/AKT/mTOR therapy. PMID:26091043
  • Absent in 12 breast adenoid cystic carcinomas (AdCC); sharp contrast to ~10% mutation rate in common-type basal-like/TNBC, highlighting distinct mutational landscape of breast AdCC. PMID:26095796
  • Rare oncogenic kinase mutation (along with BRAF and KIT) in SCLC; found in only 4 tumors total, suggesting genotyping SCLC patients may identify rare candidates for targeted therapy. PMID:26168399
  • Mutated in 10.2% of upper tract urothelial carcinoma (UTUC) vs 21.6% of urothelial carcinoma of the bladder (UCB) (p=0.084 trend); E542K hotspot in 1 tumor. PMID:26278805
  • E542K hotspot mutation in 1 desmoplastic melanoma tumor. PMID:26343386
  • Mutated in 48% of ILC vs 33% of IDC; not associated with pAKT levels in this dataset despite driving PI3K pathway activation — CDH1 loss and upstream RTK alterations (ERBB2, EGFR) proposed as context-permissive factors PMID:26451490
  • HDR-based introduction of H1047R into rat Pik3ca yielded predominantly benign fibroadenomas (8/10); combined Pik3caH1047R + Tp53Indel produced moderately differentiated invasive ductal carcinoma at 42-day median latency in a CRISPR rat mammary tumor platform PMID:26437033
  • Hotspot mutations (E545K, Q546K, N345I, C420R, E542A) in 6 prostate adenocarcinoma tumors; focal amplification with overexpression in ~1% in the TCGA cohort (n=333) PMID:26544944
  • PIK3CA mutated as part of the PI3K/AKT/mTOR pathway (disrupted in 39% ATC vs 11% PDTC, P=1×10⁻³); PIK3CA helical-domain mutations restricted to ATC in a targeted-sequencing study of advanced thyroid cancers. PMID:26878173
  • PIK3CA recurrently altered in plasmacytoid-variant bladder cancer; flagged by the authors as a clinically actionable target supporting early use of PI3K-pathway inhibitors. PMID:26901067
  • Significantly more frequently mutated in lung SqCC than lung ADC (p < 0.01, Fisher’s exact); one of only six genes significantly mutated in both NSCLC histologies (alongside TP53, RB1, ARID1A, CDKN2A, NF1). PIK3CA p.E542K is a recurrent predicted neoepitope candidate for off-the-shelf vaccine design. PMID:27158780
  • Most frequently mutated gene in the METABRIC 2,433-tumor breast cancer cohort (40.1% coding-mutation frequency); ER+ ONC=94%, ER- ONC=81%. Helical-domain (codons 542/545) and codon 345 hotspots enriched in ER+; kinase-domain codon 1047 enriched in ER-. Mutually exclusive with AKT1, PIK3R1, and FOXO3. Prognostic in ER- disease (HR=1.4); prognostic in ER+ only within IntClusts 1, 2, and 9 (defined by 17q23, 11q13-14, and 8q24 amplifications). 45.2% of all tumors had a mutation in at least one Akt-pathway member. PMID:27161491
  • PIK3CA E542K mutations (n=4) identified in cisplatin-resistant germ cell tumor patients; classified as actionable PI3K-pathway alteration in a targeted sequencing cohort PMID:27646943.
  • PIK3CA mutated in 10% of recurrent/metastatic HPV-positive HNSCC (down from 36% in primary HPV+ tumors); 4 HNSCC and 1 NPC and 1 ACYC patients enrolled on PI3K-inhibitor trials based on this alteration PMID:27442865.
  • Canonical UC driver with heterogeneous clonal sharing between primary and post-chemotherapy urothelial carcinoma samples in a 32-patient WES cohort; present in both truncal and sub-clonal compartments PMID:27749842
  • N345K activating mutation in nephroblastomatosis (related to Wilms tumor, WT); PI3K/AKT/mTOR-inhibitor target; variant also supported diagnostic clarification in a pediatric precision-oncology cohort PMID:28007021
  • PI3K-pathway activating alterations (alongside PTEN and PIK3R1) in 24% of ESCCs; all 4 ESCC3 tumours had PI3K-activating alterations in a multi-platform GEA genomic study PMID:28052061
  • 17 LUAD patients with PIK3CA as highest-level driver; 25 EGFR+PIK3CA co-mutations across the 860-patient MSK cohort; matched therapy uptake and benefit not specifically reported for PIK3CA-alone group PMID:28336552
  • Recurrent low-VAF hotspot mutations in endometrial polyps (WGS, 23 polyps); part of a canonical UCEC driver landscape that includes PIK3R1, PTEN, ERBB2, PPP2R1A, and FBXW7; supports treating polyps as potential precursor lesions PMID:28445112
  • E365K and H1047R hotspot mutations in 2/19 (10.5%) of 1p/19q-codeleted anaplastic oligodendroglioma; OncoKB Level 3B; each hotspot observed in >20 principal tumor types in the MSK-IMPACT pan-cancer cohort, reflecting cross-lineage selection PMID:28472509
  • H1047 and E545 hotspots each observed in >20 principal tumor types across 10,336 MSK-IMPACT cases, exemplifying cross-lineage oncogenic selection; part of the 36.7% of patients with an OncoKB-actionable alteration PMID:28481359
  • Mutated in 23.8% of clear-cell endometrial carcinoma (CCEC; n=63); part of the 34.9% of CCECs with PI3K-pathway alterations (PIK3CA/PIK3R1/PTEN), suggesting potential vulnerability to PI3K/AKT/mTOR-axis inhibitors PMID:28485815
  • Altered in 26% of non-muscle-invasive bladder cancer (NMIBC; n=105); part of the broadly altered RTK/PI3K pathway present in 79% of tumors PMID:28583311
  • Most frequently altered oncogene in the MET500 pan-cancer metastatic cohort (67/500, 13.4%) PMID:28783718
  • Predominantly known activating hotspots in advanced prostate cancer; one patient acquired a PIK3CA E545K hotspot ~3 years post-prostatectomy, illustrating late-emergent actionable PI3K-pathway events PMID:28825054
  • PIK3CA mutated in 22% of MIBC (n=100); helical-domain E542/E545 (n=54) more common than kinase M1043/H1047 (n=10); APOBEC-attributable mutagenesis PMID:28988769
  • PIK3CA oncogenic alterations in 7% of CIN gastroesophageal tumors; activating co-mutations enriched post-trastuzumab progression (2% pre vs 8.6% post); newly acquired E545K mutation observed in one post-progression sample PMID:29122777
  • Mutated in 18% of mCRC overall; enriched in MSI-H (41% vs 16% MSS, p<0.01); right-sided enrichment observed PMID:29316426
  • PI3K/AKT/mTOR pathway activation (including PIK3CA) did NOT adversely affect benefit from neratinib in HER2-mutant solid tumors (p=0.753), contrasting with its negative-predictor role in HER2-amplified disease PMID:29420467
  • Altered in 40% of vulvar SCC cases overall; first description in HPV(+) vulvar SCC; authors propose PI3K-pathway inhibition as a tractable hypothesis in this disease PMID:29422544
  • Called as a KIRC SMG uniquely by MutSig2CV (not MuSiC2) in the MC3 pan-cancer open-access MAF, illustrating how caller choice and filtering stringency affect gene discovery PMID:29596782.
  • SOX2, PIK3CA, and TERC are chr_3q oncogenes invoked to explain the squamous chr_3q-gain signature; in the AALE experimental model, chr_3p-deleted clones rescued their proliferation defect by duplicating chromosome 3, thereby co-gaining the 3q arm containing PIK3CA PMID:29622463.

Cancer types (linked)

Co-occurrence and mutual exclusivity

Therapeutic relevance

  • One PIK3CA-mutant histiocytosis patient had a durable response to alpelisib; two PIK3CA-mutant ovarian GCT patients had no durable response, suggesting lineage-specific conditioning of PI3K inhibitor response PMID:36862133.

Open questions

Sources

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