About

Justin P. Kline, MD, is a Professor of Medicine at the University of Chicago, specializing in medical oncology with a focus on Hodgkin and non-Hodgkin lymphoma. His clinical expertise includes stem cell transplantation, CAR T cell therapy, and cellular therapy, with a particular interest in developing and utilizing immunotherapy to treat blood cancers. His lab research concentrates on overcoming immune evasion pathways activated in blood cancers and improving the effectiveness of immune-based treatments for lymphoma patients. Dr. Kline's educational background includes an M.D. from the University of Chicago in 2001, followed by training in internal medicine in 2004 and hematology/oncology in 2007 at the same institution. His scholarly work involves integrative genomic analysis of diffuse large B-cell lymphoma (DLBCL), investigating immune environments associated with bispecific antibody response, and exploring mechanisms to enhance CAR T-cell therapy efficacy. He has contributed to research on immune checkpoint receptors such as TIGIT in lymphoma and has been involved in clinical trials related to hematologic malignancies and immunotherapy strategies.

Research topics

• Medicine
• Oncology
• Internal medicine
• Immunology
• Biology
• Gastroenterology
• Cell biology
• Surgery
• Chemistry
• Cancer research
• Biochemistry
• Genetics

Selected publications

• LymphGen-Sig: Integrating genetic and transcriptional states to predict therapeutic response in DLBCL

  medRxiv · 2026-03-02

  article

  Purpose: Genetic classification may advance precision medicine in diffuse large B-cell lymphoma (DLBCL), but existing tools like LymphGen (LG) are limited by complexity, incomplete classification, and do not incorporate non-genetic features that impact disease biology and therapeutic outcomes. To address these limitations, we developed LymphGen-sig (LGsig), a gene expression-based platform that classifies all DLBCLs and harmonizes both genetic and non-genetic dimensions of the disease. Methods: LGsig was built on the distinct subtype-specific gene expression signature of each LG class using paired genomic and transcriptomic data (NCI/BCCA; n=764). Model development was restricted to DLBCLs classified into MCD, BN2, EZB, or ST2. Gene features were selected by differential gene expression, with 294 genes being optimal for classification using a nearest shrunken centroid classifier. LGsig classifications were designated MCDsig, BN2sig, ST2sig, and EZBsig. The final model was applied to RNAseq from archival samples from the POLARIX trial (n=678) to assess outcomes after polatuzumab vedotin-R-CHP (pola-R-CHP) or R-CHOP for each LGsig subtype. Results: LGsig accurately identified LG subtypes using transcriptional data alone, and extended assignments to all previously LG-unclassified cases. Importantly, LG-unclassified DLBCLs reassigned by LGsig, mirrored the transcriptional and clinical features of their corresponding LG counterparts, supporting their reclassification. Additionally, LGsig reassigned LG A53 DLBCLs, characterized by aneuploidy and TP53 alterations, into more biologically and therapeutically-relevant LGsig clusters. Lastly, LGsig improved the performance of LG as a biomarker in the POLARIX study, by identifying distinct DLBCL subtypes exhibiting a survival benefit with pola-R-CHP over R-CHOP in both LG-classified and LG-unclassified cases. Conclusion: LGsig expands molecular classification beyond current genetic classifiers in DLBCL by integrating both genetic and transcriptional dimensions of the disease to better inform subtype-specific therapeutic strategies.

  PublisherDOI

• Targeting BCMA in Plasmablastic Lymphoma With Teclistamab: A Case Study of Three Patients

  Journal of the National Comprehensive Cancer Network · 2026-02-19 · 1 citations

  articleOpen access

  Plasmablastic lymphoma (PBL) is a rare subtype of non-Hodgkin lymphoma (NHL) with limited standard therapeutic options and poor outcomes. PBL typically lacks expression of the B-cell antigens CD20 or CD19 and, accordingly, has not benefited from the incorporation of B-cell-targeted antibodies. However, recent reports demonstrate that B-cell maturation antigen (BCMA) is expressed in most patients with PBL. BCMA is an established therapeutic target in multiple myeloma. Herein, we describe the clinical course of 3 patients with PBL found to express BCMA by immunohistochemistry who were treated with the BCMA×CD3 bispecific antibody teclistamab after developing disease refractory to at least 2 lines of standard therapy. A complete response was observed in 2 patients: 1 patient remains in remission after 2 years of teclistamab treatment, while the second achieved a complete response after 1 cycle of teclistamab, subsequently underwent allogeneic stem cell transplantation, and developed relapsed PBL 3 months post-transplant. The third patient developed a small bowel obstruction and transitioned to hospice care after 1 cycle of teclistamab. This case series adds to the growing evidence that BCMA is expressed in a considerable subset of patients with PBL and suggests that BCMA may serve as a potential molecular biomarker in PBL for further investigation of available BCMA-directed therapies.

  PublisherOA PDFDOI

• Hodgkin Lymphoma, Version 1.2026, NCCN Clinical Practice Guidelines In Oncology

  Journal of the National Comprehensive Cancer Network · 2026-02-01 · 1 citations

  article

  The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Hodgkin lymphoma provide expert, multidisciplinary recommendations for the diagnosis and treatment of Hodgkin lymphoma. The panel convenes annually to update recommendations based on a review of recently published clinical trials. This selection from the NCCN Guidelines for Hodgkin Lymphoma focuses on the management of newly diagnosed and relapsed/refractory classic Hodgkin lymphoma in adults aged 18 to 60 years.

  PublisherDOI

• Supplementary figure S16 from Tumor Cell–Intrinsic <i>Decr2</i> Regulates Ferroptosis and Immunotherapy Efficacy

  2025-08-01

  preprintOpen access

  <p>Supplementary Figure S16. IFN-γ signaling is involved with T cell killing and reprogrammed lipids</p>

  PublisherOA PDFDOI

• Supplementary figure S12 from Tumor Cell–Intrinsic <i>Decr2</i> Regulates Ferroptosis and Immunotherapy Efficacy

  2025-08-01

  preprintOpen access

  <p>Supplementary Figure S12. The gating strategy for flow cytometry analysis of lipid reactive oxygen species (ROS).</p>

  PublisherOA PDFDOI

• Nivolumab plus brentuximab vedotin for relapsed/refractory diffuse large B-cell lymphoma

  Future Oncology · 2025-12-10

  articleOpen access

  AIMS: Up to 40% of patients with diffuse large B-cell lymphoma (DLBCL) have relapsed or refractory (R/R) disease after first-line treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone, and outcomes are poor after hematopoietic stem cell transplantation failure. CheckMate 436 (NCT02581631) was a phase 1/2 study to evaluate the efficacy and safety of nivolumab, a PD-1/PD-L1 inhibitor, plus brentuximab vedotin (BV) for the treatment of R/R non-Hodgkin lymphoma. MATERIALS AND METHODS: Adult patients received nivolumab plus BV in 3-week cycles. The primary endpoint was overall response rate (ORR). Here, we report the results from the R/R DLBCL cohort (n = 42). RESULTS: With a median follow-up of 7.7 months, the ORR was 28.6% (n = 12), and 7.1% (n = 3) of patients achieved a complete response. Median duration of response (95% CI) was 3.6 (1.2-36.5) months. All patients experienced an adverse event (AE), most commonly diarrhea (n = 20, 47.6%). Grade 3/4 and 5 AEs occurred in 24 (57.1%) and 4 (9.5%) patients, respectively. Any-grade treatment-related AEs occurred in 35 (83.3%) patients. No new safety signals were identified. CONCLUSIONS: Overall, the efficacy data from CheckMate 436 do not support the use of nivolumab plus BV for the treatment of R/R DLBCL.

  PublisherOA PDFDOI

• Supplementary figure S11 from Tumor Cell–Intrinsic <i>Decr2</i> Regulates Ferroptosis and Immunotherapy Efficacy

  2025-08-01

  preprintOpen access

  <p>Supplementary Figure S11. Decr2 knockdown tumors are resistant to ferroptosis.</p>

  PublisherOA PDFDOI

• Supplementary figure S8 from Tumor Cell–Intrinsic <i>Decr2</i> Regulates Ferroptosis and Immunotherapy Efficacy

  2025-08-01

  preprintOpen access

  <p>Supplementary Figure S8. Gating strategy for Flow cytometry analysis of B16.SIY tumor microenvironment isolated from B6 mice.</p>

  PublisherOA PDFDOI

• Camidanlumab tesirine for relapsed or refractory classic Hodgkin lymphoma: a phase 2 study

  Blood Advances · 2025-08-14 · 5 citations

  articleOpen access

  ABSTRACT: Outcomes in classic Hodgkin lymphoma (cHL) have steadily improved; however, additional therapies are needed for patients who relapse or do not respond to novel agents. Here, we report the efficacy and safety of camidanlumab tesirine (Cami), an anti-CD25 antibody-drug conjugate, in patients with relapsed/refractory cHL after brentuximab vedotin/programmed cell death protein 1 inhibitor therapies from the phase 2 ADCT-301-201 study. Eligible patients were adults with cHL who had received ≥3 previous lines of systemic therapy (or ≥2 if ineligible for hematopoietic stem cell transplant). Patients received 45 μg/kg Cami (IV, once every 3 weeks) in cycles 1 to 2, followed by 30 μg/kg IV once every 3 weeks for ≤1 year. The primary end point was overall response rate (ORR) per 2014 Lugano classification. Secondary end points included complete response rate (CRR), progression-free survival (PFS), and overall survival (OS). In total, 117 patients were enrolled with a median age of 37.0 years (range, 19-87). The ORR was 70.1% (95% confidence interval [CI], 60.9-78.2), with a CRR of 33.3% (95% CI, 24.9-42.6). The median PFS was 9.13 months (95% CI, 5.3-15.0); median OS was not reached. Thirty-three (28.2%) patients discontinued treatment because of treatment-emergent adverse events; the most common reasons were skin and subcutaneous tissue disorders (n = 10 [8.5%] patients), infections and infestations (n = 5 [4.3%]), and nervous systems disorders (n = 5 [4.3%]). Guillain-Barré-type or polyradiculopathy-type events occurred in 8 (6.8%) patients. Cami was efficacious in this heavily pretreated population; however, the efficacy was overshadowed by substantial issues with the safety profile. This trial was registered at www.clinicaltrials.gov as #NCT04052997.

  PublisherOA PDFDOI

• NCCN Guidelines® Insights: B-Cell Lymphomas 3.2025

  Journal of the National Comprehensive Cancer Network · 2025-10-01 · 9 citations

  article

  The treatment landscape of B-cell lymphomas has significantly evolved in recent years with approval of novel targeted therapies. CD3 × CD20 bispecific antibodies and CD19-directed monoclonal antibodies and antibody-drug conjugates have demonstrated efficacy in relapsed/refractory follicular lymphoma (FL). Bruton tyrosine kinase (BTK) inhibitor-based regimens are emerging as effective treatment options for patients with TP53-mutated classical mantle cell lymphoma (MCL). Results from ongoing clinical trials suggest that the addition of CD3 × CD20 bispecific antibodies to chemoimmunotherapy improves outcomes in patients with relapsed/refractory diffuse large B-cell lymphoma (DLBCL). These NCCN Guideline Insights highlight significant updates to the NCCN Guidelines for B-Cell Lymphomas for the treatment of FL, MCL, and DLBCL.

  PublisherDOI

Recent grants

• NIH Grant K23CA133196

  NIH · $649k · 2013

• NIH Grant R01CA166770

  NIH · $1.6M · 2018

Frequent coauthors

• Sonali M. Smith

  80 shared

• Koen van Besien

  University Hospitals Seidman Cancer Center

  74 shared

• Richard A. Larson

  University of Chicago

  72 shared

• Michael R. Bishop

  University of Illinois Chicago

  72 shared

• Wendy Stock

  University of Chicago

  67 shared

• Xiufen Chen

  University of Chicago

  65 shared

• Andrew Artz

  City of Hope

  64 shared

• Hongtao Liu

  Shanghai Zhangjiang Laboratory

  46 shared

Labs

• Kline LabPI

Education

• M.D.

  University of Chicago

  2001

• Other

  University of Chicago

  2004

• Other

  University of Chicago

  2007