JCO Precision Oncology

Our medical research library holds 6 studies published in JCO Precision Oncology (2017–2026). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 4 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: American Society of Clinical Oncology
• Published: 2017 to the present, United States
• Language: English
• ISSN: 2473-4284 (electronic)
• Its record in the NLM Catalog

2020s

• Diffuse Pleural Mesothelioma in Young (Age ≤50 Years) and Very Young (Age ≤35 Years) Patients: Clinical Characteristics, Genomics, and Survival. H. Ollila, A. Tidjani, J.L. Sauter, et al. 2026;10(3):e2501171. PubMed · Publisher · Free full text

  Abstract

  Purpose: Although we typically consider diffuse pleural mesothelioma (DPM) as a disease of elderly males with a history of asbestos exposure, young individuals are also affected. Given the increasing incidence of cancer in young individuals, we investigated the characteristics and underlying biology of young patients with DPM.

  Methods: We identified patients with DPM age ≤50 years from Memorial Sloan Kettering Cancer Center (1990-2023). Clinicopathologic and genetic characteristics were compared between very young (≤35 years) and young (36-50 years) patients.

  Results: We identified 273 patients with DPM age ≤50 years; 39% were female, 40% had a history of self-reported occupational asbestos exposure (very young, 16% v young, 45%; P < .01), 16% had a personal history of cancer (very young, 7% v young, 18%; P = .07), and 70% had a family history of cancer (most commonly breast, lung, and colon). Most frequently altered somatic genes (51/273 tested; 46/51 positive) included BAP1 (22/47, 47%), NF2(18/47, 38%), CDKN2A/B (12/48, 25%), and TP53 (10/48, 21%). Very young patients had less somatic alterations in BAP1 (13% v 63%, P < .01) and a lower tumor mutational burden (0.9 v 1.8 mut/mB, P < .01); they were less frequently carriers of germline alterations (0% [0/8] v 43% [6/14], P = .05). Somatic alterations in CDKN2B were more frequent among females (females 42% v males 12%, P = .03).

  Conclusion: Young patients with DPM have strong personal and family histories of cancer, and heterogeneous somatic and germline alterations, indicating divergent underlying biology. With the increasing prevalence of young adults with cancers, mesotheliomas, although uncommon, should be on the differential for patients even without asbestos exposure history in this age group.

• Genomics of MTAP Loss in >500,000 Solid Tumor Specimens Profiled Using Comprehensive Genomic Profiling Platforms. D.C. Pavlick, S. Rengarajan, J.K. Lee, et al. 2026;10(5):e2600037. PubMed · Publisher · Free full text

  Abstract

  Purpose: Methylthioadenosine phosphorylase (MTAP) genomic loss is an emerging biomarker for PRMT5 and MAT2A inhibitors based on synthetic lethality. The MTAP gene is located on chromosome 9p21.3 near CDKN2A/B. MTAP homozygous loss across tumor types, specific exons lost, MTAP expression, and the landscape of coalterations were assessed.

  Methods: 409,755 tissue biopsies (TBx) and 85,801 liquid biopsies (LBx) were sequenced using hybrid capture-based NGS (FoundationOne CDx or FoundationOne Liquid CDx), evaluating all classes of genomic alterations and circulating tumor DNA (ctDNA) tumor fraction (TF). Additionally, 6,740 TBx were subjected to both RNA and DNA sequencing to compare MTAP gene expression with genomic MTAPloss.

  Results: The prevalence of pan-tumor MTAPloss was 11.4% using TBx, with the highest prevalence observed in mesothelioma (32.8%), glioma (32.7%), pancreatic (28.9%), and bladder cancers (26.4%). Prevalence of MTAPloss on LBx approximated that of TBx when ctDNA TF ≥20% (positive percent agreement [PPA] = 86.2%). CDKN2Aloss was not a reliable proxy for MTAPloss; 33.7% of CDKN2Aloss cases did not have MTAPloss. MTAPloss was enriched with CDKN2A/B losses pan-tumor, EGFR in NSCLC, ERBB2 in colorectal cancer, and PTEN in prostate cancer, while MTAPno_loss was enriched for RB1 pan-tumor, APC in colorectal cancer, CCNE1 in breast and ovarian cancer, and SPOP in prostate cancer. Complete loss (exons 1-8) was observed in 82.9%, multiple exons in 16.5% and exon 8 alone in <1%. MTAPloss, specifically the number of exons lost, was correlated with reduced RNA expression.

  Conclusion: MTAPloss is a frequent pan-tumor alteration that predicts potential sensitivity to PRMT5 or MAT2A inhibitors. Although most tumors exhibit complete MTAPloss, 16.5% are characterized by partial MTAPloss where clinical benefit remains uncertain. The genomic coalteration landscape reported here may inform future PRMT5 or MAT2A clinical trials, potentially in combination with other agents.

• STRN-ALK Fusion in a Case of Malignant Peritoneal Mesothelioma: Mixed Response to Crizotinib, Mode of Resistance, and Brigatinib Sequential Therapy. V. Gerthofer, A. Scheiter, F. Lüke, et al. 2021;5. Case report PubMed · Publisher · Free full text

2010s

• STRN -ALK Rearranged Malignant Peritoneal Mesothelioma With Dramatic Response Following Ceritinib Treatment. J.H. Rüschoff, E. Gradhand, A. Kahraman, et al. 2019;3. Case report PubMed · Publisher · Free full text

• Megakaryocyte Potentiating Factor as a Predictive Biomarker for Therapies Against Malignant Mesothelioma. L. Cao, Y. Yu, A. Thomas, et al. 2018;2018. PubMed · Publisher · Free full text

  Abstract

  Purpose: Effective biomarkers for malignant mesothelioma (MM) are needed for clinical management and the development of mesothelin-targeted therapies. We evaluated serum megakaryocyte potentiating factor (MPF) as a biomarker predictive of treatment outcome in patients with MM and for developing mesothelin-targeted therapies.

  Materials And Methods: Serial serum samples from patients with MM in two clinical trials of an antimesothelin immunotoxin were tested with our clinically validated MPF assay. Correlative studies were performed to determine the test effectiveness in treatment monitoring and outcome prediction. MPF was further evaluated for an association with response to an antimesothelin therapy and for disease monitoring.

  Results: There was a significant reduction of serum MPF in patients with elevated baseline and radiologic response, with an average change from -52% to -78% after one to six cycles. Using a -50% change as the cutoff, patients with MM with positive MPF response had significantly improved progression-free survival (P < .001), with the median extended from 1.9 to 11.3 months. These patients with MPF response further exhibited improved overall survival (P = .004), with the median extended from 8.8 to 22.3 months. In patients with refractory MM, there was an association between elevated pretreatment serum MPF and radiologic response to an antimesothelin therapy (P = .033). Furthermore, in these response patients, serum MPF was monitored between 32.2 and 63.8 months and was found to reflect treatment response and disease progression.

  Conclusion: At a cutoff of -50% change after receiving systemic therapies, a reduction in MPF was associated with improved clinical outcome, both progression-free survival and overall survival. An elevated baseline serum MPF was associated with a response to an antimesothelin therapy in patients with refractory MM; however, this finding needs to be confirmed in another study.

• Landscape of Microsatellite Instability Across 39 Cancer Types. R. Bonneville, M.A. Krook, E.A. Kautto, et al. 2017;2017. PubMed · Publisher · Free full text

  Abstract

  Purpose: Microsatellite instability (MSI) is a pattern of hypermutation that occurs at genomic microsatellites and is caused by defects in the mismatch repair system. Mismatch repair deficiency that leads to MSI has been well described in several types of human cancer, most frequently in colorectal, endometrial, and gastric adenocarcinomas. MSI is known to be both predictive and prognostic, especially in colorectal cancer; however, current clinical guidelines only recommend MSI testing for colorectal and endometrial cancers. Therefore, less is known about the prevalence and extent of MSI among other types of cancer.

  Methods: Using our recently published MSI-calling software, MANTIS, we analyzed whole-exome data from 11,139 tumor-normal pairs from The Cancer Genome Atlas and Therapeutically Applicable Research to Generate Effective Treatments projects and external data sources across 39 cancer types. Within a subset of these cancer types, we assessed mutation burden, mutational signatures, and somatic variants associated with MSI.

  Results: We identified MSI in 3.8% of all cancers assessed-present in 27 of tumor types-most notably adrenocortical carcinoma (ACC), cervical cancer (CESC), and mesothelioma, in which MSI has not yet been well described. In addition, MSI-high ACC and CESC tumors were observed to have a higher average mutational burden than microsatellite-stable ACC and CESC tumors.

  Conclusion: We provide evidence of as-yet-unappreciated MSI in several types of cancer. These findings support an expanded role for clinical MSI testing across multiple cancer types as patients with MSI-positive tumors are predicted to benefit from novel immunotherapies in clinical trials.

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