Stefan K. Barta
· MD, MSVerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 1999–2026
About
Stefan K. Barta, MD, MS, is an Associate Professor of Medicine (Hematology-Oncology) at the Hospital of the University of Pennsylvania and serves as the Director of the T-cell Lymphoma Program at UPenn. His clinical expertise includes T-cell lymphomas, HIV-associated lymphomas, and cutaneous lymphomas. His research focuses on HIV-related lymphomas, T-cell lymphomas, and cutaneous lymphomas, contributing to the understanding and treatment of these hematologic malignancies. Dr. Barta's work involves both clinical practice and research, aiming to improve outcomes for patients with lymphoma through innovative therapies and comprehensive studies.
Research topics
- Internal medicine
- Medicine
- Pathology
- Cancer research
- Immunology
- Oncology
Selected publications
Leukemia & lymphoma/Leukemia and lymphoma · 2026-03-14
articleSenior authorBlood Cancer Journal · 2026-03-23 · 1 citations
articleOpen accessSenior authorPlasmablastic lymphoma (PBL) is a rare, aggressive AIDS-related lymphoma observed in patients with immunosuppressed states as well as in immunocompetent individuals. We sought to determine survival outcomes, prognostic factors, and optimal treatment regimens in a large, contemporary cohort of patients with PBL in the United States. We performed a multicenter, retrospective cohort study, including 344 patients diagnosed with PBL between 2005 and 2022. Patients were stratified into cohorts according to underlying immune status. Survival outcomes were calculated using Kaplan-Meier statistics, with cohort-specific survival outcomes adjusted using propensity score-based weighting. Factors associated with outcomes were assessed via multivariable models using multiple imputation. The median age at diagnosis was 53 years, most patients were male (n = 270), and many had HIV (n = 164). The median OS was 5.0 years, with a median PFS of 1.4 years. Patients living with HIV had the best outcomes, whereas patients with prior organ transplantation had the worst outcomes. Use of higher intensity chemotherapy regimens and use of a proteasome inhibitor in the frontline setting did not show survival benefit. While there was no clear optimal treatment approach in the frontline setting, the median OS of 5.0 years is dramatically improved compared with historical controls.
2026-03-16
articleOpen access<p>All Supplementary Data</p>
Practical Radiation Oncology · 2026-04-01
articleOpen accessPURPOSE: Low-dose total skin electron therapy (TSET) is an established treatment for diffuse cutaneous T-cell lymphoma. Although traditionally delivered using standard fractionation (STD-fx) schedules, hypofractionated (H-fx) regimens offer a practical, time-efficient alternative; however, comparative data remain limited. This study evaluated clinical responses, toxicity, and hematologic effects of H-fx versus STD-fx low-dose TSET. METHODS AND MATERIALS: We retrospectively analyzed 121 courses of low-dose TSET (12 Gy total) delivered to 111 patients with cutaneous T-cell lymphoma from 2015 to 2023. STD-fx was defined as 12 Gy in 6 fractions; H-fx included regimens of 12 Gy in 3 or 4 fractions. Acute toxicities were graded per the Common Terminology Criteria for Adverse Events v5.0 and categorized as "new or worsened" from baseline. Hematologic toxicity was assessed through serial complete blood counts. Overall survival and progression-free survival were measured from TSET completion to event or last follow-up; survival comparisons between regimens were exploratory. RESULTS: Of 121 TSET courses, 104 (86%) were STD-fx and 17 (14%) were H-fx. Median follow-up was 21 months overall and was shorter in H-fx (8 vs 22 months; P < .01). Eastern Cooperative Oncology Group 2 to 4 status was more frequent in H-fx (35% vs 13%; P = .03). Overall response rate (complete response + partial response) was 94% in both groups. At 24 months, overall survival was 87% for STD-fx versus 66.7% for H-fx (P = .13), and progression-free survival was 19% versus 17%, respectively (P = .59). New or worsened acute toxicities were common (98.1% vs 94.1%; P = .37) but mostly low-grade, with no grade 4 events. Rates of dermatitis were similar in STD-fx and H-fx groups (76.9% vs 76.5%), including high-grade events (12.5% vs 23.5%; P = .26). Cytopenias were prevalent at baseline and remained similar posttreatment, with no significant differences between regimens. CONCLUSIONS: H-fx low-dose TSET was feasible and demonstrated similar short-term response, acute toxicity, and hematologic effects as STD-fx, although long-term and comparative inferences are limited by the small H-fx cohort and short follow-up duration. In appropriately selected patients, abbreviated TSET regimens may be considered when shorter treatment courses are clinically indicated.
Cancer · 2026-04-09
articleThe Bridging the Gaps (BTG) in Leukemia, Lymphoma and Multiple Myeloma Consensus Conference 2025 brought together a multidisciplinary group of oncology experts to address the complexities of lymphoma management, focusing on mantle cell lymphoma (MCL), chronic lymphocytic leukemia (CLL), and diffuse large B-cell lymphoma (DLBCL). This article presents consensus recommendations developed through a modified Delphi process, which emphasize the need for tailored therapeutic strategies in light of recent advancements in treatment options. Key recommendations include the screening for high-risk features in MCL, use of the BOVen regimen (zanubrutinib, obinutuzumab, and venetoclax) for TP53-aberrant cases, and integration of chimeric antigen receptor T-cell therapy for patients with mantle cell lymphoma that is refractory to covalent Bruton tyrosine kinase inhibitors. For CLL, recommendations include consideration of time-limited therapies for younger patients and a "watch and wait" strategy for asymptomatic patients despite the improved activity and safety of current treatment regimens. For DLBCL, this article highlights the challenges in treatment sequencing and the role of circulating tumor DNA and minimal residual disease testing in monitoring disease progression. Overall, the conference describes the importance of ongoing research to refine management strategies and improve patient outcomes in lymphoma care, addressing the gaps in clinical practice where high-level evidence is lacking.
Blood Cancer Journal · 2026-04-25
articleOpen accessAddition of Bruton's tyrosine kinase inhibitor (BTKi) to first-line (1 L) bendamustine-rituximab (BR) improved progression-free survival (PFS) in patients with mantle cell lymphoma (MCL) in the SHINE and ECHO trials. We investigated whether sequential treatment with 1 L BR and second-line (2 L) BTKi can result in similar cumulative PFS compared to BR-BTKi combination therapy, using a multicenter cohort of 755 patients treated with 1 L BR between 2014 and 2020. Event-free survival (EFS), EFS2, and overall survival (OS) were analyzed. By intention-to-treat (ITT), EFS2 was defined as time from 1 L BR start to progression/relapse or retreatment following 2 L BTKi or death. After a median follow-up of 61.4 (95% CI 56.4-65.9) months, the median EFS after 1 L BR was 34.2 (95% CI 31.5-38.4) months. The median EFS2 following 1 L BR and 2 L BTKi by ITT analysis was 64.8 (95% CI 56.7-82.8) months, and the 5-year OS rate after 1 L BR was 57.9% (95% CI 54.1-62.0%), close to SHINE and ECHO results. Patients without high-risk features (high simplified MIPI, high Ki-67, blastoid/pleomorphic morphology, TP53 mutation, or complex karyotype) had more favorable survival outcomes. These results suggest that sequential treatment with 1 L BR and 2 L BTKi remains reasonable for select patients with MCL, particularly those without high-risk features.
Blood · 2025-11-03
articleAbstract INTRODUCTION We and others have demonstrated that patients with refractory nodal mature T-Cell lymphomas (nMTCL) have worse overall survival (OS) versus relapsed disease.1–3 Among patients who relapse, responses and OS in (nMTCL) remain poor with little data to tailor decision-making based on disease kinetics.1–9 Time-to-relapse (TTR) is a significant predictor of survival and decision-making tool among many other lymphomas,10–18 however a majority of nMTCL patients will relapse prior to 24 months.14 We aimed to characterize how TTR may affect survival and explore differential second-line (2L) therapy effects based on TTR subgroups. METHODS This was a global retrospective cohort study using multiple international cohorts: PETAL (n=1414) and GELL (n=487).1,3,19–21 Two separate independent cohorts validated TTR12 as an OS predictor: an observational U.S. multicenter cohort (n=138) and the phase 3 randomized trial of romidepsin-CHOP versus CHOP.22 Patients with PTCL-NOS, AITL/TFHL, or ALCL with a CR to 1L were included. Patients without progression or 2L within the study period were included as not having TTR12 per landmark methods,11,23–25 and were removed for sensitivity analyses. The primary objective was OS among nMTCL who relapsed or started 2L26 within 12m from 1L (TTR12) versus without TTR12 because nearly half of patients in our cohort and previous studies of nMTCL relapsed within 12m.6,14 The secondary objective was to compare OS among 2L novel agents (NA) versus chemotherapy (CC) in those with and without TTR12. Kaplan-Meier and Cox PH methods were used adjusting for a priori covariates.1,3 The primary analysis was a modified-landmark analysis (m-LM) with OS measured from relapse or 2L start (TTR12 group) or from 12m from 1L start (without TTR12 group) to death. Sensitivity analyses used standard 12m landmark (s-LM; excluded patients who died or lost-to-follow &lt;12m),11,25 and time-dependent Cox (td-Cox; OS 1L start to death). For 2L analyses, OS was measured from 2L start to death. RESULTS A total 452 were included in the final cohort and for td-Cox, 428 in m-LM, and 388 in s-LM. Of the 452 total, 165 (36.5%) had TTR12, 181 (40%) relapsed ≥12m, and 106 (23.5%) never relapsed (total without TTR12: 287 [63.5%]). The median (range) age was 58 (18-89) and 60 (15-92), PTCL-NOS included 47.3% and 43.2%, AITL/TFHL included 35.8% and 32.1%, and ALCL included 16.4% and 24.7% of patients with TTR12 and without TTR12 respectively. Patients received similar frontline regimens and HSCT utilization was comparable. Demographics in the validation cohorts largely mirrored the primary cohort. Using m-LM, TTR12 conferred worse OS (aHR 2.14, 95%CI: 1.58-2.90; p&lt;0.001) overall, irrespective of 1L HSCT or PIT score, and across prespecified subgroups (PTCL-NOS: aHR 2.32, 95%CI: 1.51-3.55; p&lt;0.001, AITL/TFHL: aHR 1.92, 95%CI: 1.15-3.21; p=0.013, ALCL: aHR 3.34, 95%CI: 1.18-9.50; p=0.023, no 2L HSCT: aHR 2.27, 95%CI: 1.63-3.15; p&lt;0.001). TTR12 patients who received any 2L HSCT had similar OS than those without TTR12 (aHR 1.85, 95%CI: 0.73-4.65; p=0.194). When excluding patients that did not relapse, TTR12 still showed poorer OS (aHR 1.60, 95%CI: 1.18-2.18; p=0.003). In the observational validation cohort, TTR12 patients had worse OS across all analyses in both univariate (HR 3.72, 95%CI 1.85-7.46; p&lt;0.001) and multivariate models adjusting for covariates (aHR 3.60, 95%CI 1.77-7.34; p&lt;0.001). In the phase 3 validation cohort, TTR12 patients also had worse OS (aHR 3.71, 95%CI 2.17-6.32; p&lt;0.001). All results were consistent across s-LM and td-Cox sensitivity analyses. TTR12 predicted worse OS in parallel to, and compounding with, PIT score, with patients who had TTR12 and PIT≥2 exhibiting the worst OS. Patients with PIT score of 4 were at a significantly higher odds of developing TTR12 (OR 3.64, 95%CI 1.07-12.38; p=0.038). In TTR12 patients, 2L NA significantly improved OS versus CC (aHR 0.60, 95%CI: 0.37-0.97; p=0.038). In those without TTR12 who received 2L, there were no significant differences in OS with NA versus CC (aHR 0.82, 95%CI 0.51-1.32; p=0.407 CONCLUSION TTR12 consistently exhibited worse OS in nMTCL and highlighted differential responses to 2L, defining a unique risk group after 1L. TTR12 may be a novel endpoint for clinical trials and may better inform treatment decisions upon progression. Prospective validation and correlation with molecular alterations has been initiated and is the focus of the PETAL consortium.
Haematologica · 2025-11-27
articleOpen accessNot available.
Blood · 2025-11-03
articleAbstract Introduction: Mantle cell lymphoma (MCL) is usually an incurable lymphoma with no standard frontline therapy. Increasingly, Bruton tyrosine kinase inhibitors are utilized in frontline therapy, especially in older patients, but data remain limited in younger patients. We report our experience with a cohort of patients with MCL who received frontline second-generation BTKi +/- rituximab. Methods: We reviewed all patients treated at our institution with either acalabrutinib or zanubrutinib (BTKi) +/- maintenance rituximab who had therapy initiated by July 10, 2024. Adverse events (AEs) were graded based on CTCAE v5. We defined patients as either younger or older: patients &lt;65 years old were considered younger unless noted to be autologous hematopoietic stem cell transplant (ASCT) ineligible. Patients ≥70 years were considered older. Patients aged 65-70 were assessed for ASCT eligibility; ASCT-ineligible patients were considered older. A cohort of patients who had frontline standard-of-care chemotherapy (R-HyperCVAD or R-CHOP/R-DHAP) was also collected for comparison to the younger BTKi-treated cohort. Results: Thirty patients received frontline second-generation BTKi. Eleven (37%) were younger and 19 (63%) were older. Twenty-three patients (77%) received acalabrutinib (10 with rituximab maintenance) and 7 patients (23%) received zanubrutinib (4 with rituximab maintenance). Twenty (67%) were male, 27 (90%) were white, and 3 (10%) were black. Median age was 70.9 years (range 44.8-93.4). Twenty-five (83%) had ECOG performance status (PS) 0-1. Twenty-seven patients had advanced stage disease (90%). MIPIb was high risk in 21 (70%); Ki-67 was ≥ 50% in 6/26 (23%) and ≥ 30% in 12/26 (46%). Three (10%) patients had blastoid MCL. Five of 26 (19%) patients had a TP53 aberration. Between younger and older cohorts, there were no significant differences in sex, ECOG PS, blastoid MCL, or presence of TP53 aberrations. MIPIb was significantly higher in older patients (6.3 vs. 7.2, p=0.003). Overall, 24 patients (80%) had an AE related to BTKi, with 7 (23%) experiencing a serious AE (SAE). The most common AEs were bleeding/bruising (33%), infections (n=8, 27%; 1 URI, 4 pneumonia, 1 bacteremia, 1 urinary tract infection, 1 cellulitis; 3 were SAEs), and rash (20.0%). There was no significant difference between rate of any AE or SAE between older and younger patients. Five patients discontinued BTKi due to toxicity (recurrent neutropenia, rash, cellulitis, pneumonitis, dysgeusia) and one due to patient preference. Thirty-two patients were included in the frontline chemotherapy cohort. Twenty-five patients (78.1%) were male, 29 (90.6%) were white, two (6.3%) were black, and one (3.1%) was Hispanic. Median age was 60.3 years (range 27.3-74.5 years). Twenty-eight (87.5%) patients had an ECOG PS 0-1. Median stage was 4 (range 2-4) and median MIPIb was 6.8 (range 5.4-9.6). Nineteen (59.4%) of patients had classical MCL and 13 (40.6%) had blastoid/pleomorphic MCL. Five of 28 (18%) patients had a TP53 aberration. Comparing younger patients who received frontline BTKi and younger patients who received frontline chemotherapy, there were no significant differences in sex, ECOG PS, MIPIb, or presence of TP53 aberrations or proportion of patients who received maintenance rituximab; however, the younger BTKi cohort did have a significantly lower incidence of blastoid MCL (10% vs. 37%, p=0.02). Median follow-up for the entire cohort (n=62) was 58 months; estimated 3-year PFS for the BTKi (n=30) and chemotherapy cohorts (n=32) was 57% (95%CI 34-74%) vs. 43% (95%CI 26-60%). Median follow-up for the younger BTKi and younger chemotherapy cohorts was 35 and 102 months, respectively. Estimated 3-year PFS for the younger BTKi cohort (n=11) vs. younger chemotherapy cohort (n=27) was 52% (95%CI 20-77%) vs. 48% (95%CI 25-61%). Conclusions: Second-generation BTKi with and without rituximab appear safe and effective frontline therapy for MCL regardless of patient age. We also observed excellent BTKi outcomes in younger patients comparable to standard-of-care chemotherapy. Limitations include a higher proportion of patients in the frontline chemotherapy group with blastoid MCL as well as relatively short follow-up in the BTKi cohort. Nevertheless, second generation BTKi may represent an effective frontline therapeutic approach for patients with MCL. Further studies are needed to determine the role of chemotherapy with BTKi vs chemotherapy-free regimens in this setting.
Blood · 2025-11-03
article1st authorCorrespondingAbstract Background: Despite a decreasing incidence, NHL remains the leading cause of cancer-attributable deaths in PWH (Horner MJ, et al. Clin Infect Dis 2021). Nevertheless, PWH were excluded based on their HIV status alone from trials leading to the FDA approval of the currently available CD19-directed CAR-T cell (CART19) products for relapsed or refractory B-cell lymphomas. Thus, information on safety and effectiveness of this potentially curative treatment has been largely limited to few published case reports. In this collaborative effort between the AMC and the CIBMTR, we determined outcomes of PWH who received CART19 therapy and compared them with a matched cohort of people without HIV. Methods: We prospectively collected data on 35 patients (pts) diagnosed with HIV who received CART19 therapy between 8/30/2017 and 11/05/2024 for B-cell lymphoid malignancies. Data on patient, HIV, and disease characteristics, treatment, treatment-related outcomes and toxicities were collected. We next created a matched cohort of 135 pts without HIV (HIV-) who underwent CART19 therapy during the same period matched on key clinical factors (age, performance score, NHL subtype, CART19 product, and disease status pre-CART). Outcomes compared included Cytokine Release Syndrome (CRS), Neurologic Toxicity Associated with Immune Effector Cells (ICANS), disease response, hematologic recovery, progression-free survival (PFS), and overall survival (OS). To account for matching, a marginal univariable Cox model (OS, PFS) and a marginal univariable Fine-Gray model (CRS, ICANS, hematological recovery, complete and overall response) were used for calculating and comparing survival probabilities and cumulative incidences, respectively, between both cohorts. Results: A total of 170 pts were included in this analysis (35 HIV+, 135 HIV-). The cohorts were matched for age (median age: HIV+ 56 years (y) (range 29-69); HIV- 57y (24-73)); disease subtype (DLBCL: 91%; FL: 6%; and MCL: 3%, each); CART19 product (axi-cel 97%; brexu-cel 3%, each); and response prior to CART19 (CR 3% each; PR 14% each; relapse/resistant 62.9% vs 60.7%; relapse untreated 2.9% vs 4.4%; relapse chemosensitive 8.6% vs 13.3%; relapse sensitivity unknown 8.6% vs 4.4%). The HIV+ cohort included more men (88.6% vs. 55.6%, p&lt;0.01), more Blacks (25.7% vs 8.1%, p&lt;0.01), and more people seropositive for HepB (17.1% vs 0%, p&lt;0.01) or HepC (8.6% vs 0%, p&lt;0.01). In addition, there were differences that did not achieve statistical significance: bendamustine lymphodepletion (17.1% vs 8.9%, p=0.22) and bridging therapy (62.9% vs 48.1%, p=0.15) were more common in the HIV+ cohort. For PWH, the median time from HIV diagnosis to CART19 was 132 months (1.6-490.0). Median pre-CART19 CD4 count was 191 cells/mm3 (0-252) and median pre-CART HIV viral load (VL) 20 copies/ml (0-10x106); only 11.4% had a HIV VL &gt;400 copies/ml. CRS occurred less commonly in the HIV+ cohort (any grade 68.6% vs 82.2%, p=0.04). ICANS was comparable (any grade 22.9% vs 44.4%, p=0.17). Bacterial infections at 100 days were more common in PWH (28.6% vs. 10.4%, p&lt;0.01). Median follow-up for survivors was 14.5 mo for the entire cohort. At 100 days, neutrophil recovery was similar (91.7% vs 94.8%; p=0.33) with delayed platelet recovery in PWH (71.1% vs 80.4% p=0.06). Cumulative incidence at 6 months of overall response (42.6% vs. 65.8%, p=0.013) and complete response (34.6% vs. 57.4%, p=0.021) was lower in PWH. PFS was not significantly different between cohorts (1-and 2-year PFS: 36.1%/28.3% (HIV+) vs 51.1%/43.6% (HIV-); p=0.103), but OS was lower in PWH (1- and 2-year OS 45.7%/37.3% (HIV+) vs 65.9%/59.7% (HIV-); p=0.016). There was no difference in treatment-related mortality (TRM; p=0.197). The primary cause of death was PD (94.7% (HIV+) vs 73.9% (HIV-) followed by infections (5.3% vs 6.5%) in both cohorts.Conclusion: CART19therapywas safely administered in this large prospective cohort of PWH with 28.3% alive and in remission at 2 years from therapy. Compared to a matched HIV- cohort, toxicities were mostly similar except for more infections in PWH. The lower OS and responses for PWH was driven by lymphoma-related features rather than TRM. Notably, the HIV+ cohort contained a larger proportion of Black patients who are commonly underrepresented in clinical trials and may represent a clinically distinct entity with worse outcomes (Lee MJ, et al. Cancer 2020). AMC-112 is currently enrolling onto a prospective CART19 study.
Frequent coauthors
- 235 shared
Daniel J. Landsburg
- 227 shared
Jakub Svoboda
University of Pennsylvania
- 225 shared
Stephen J. Schuster
University of Pennsylvania
- 210 shared
Sunita D. Nasta
University of Pennsylvania
- 197 shared
Elise A. Chong
Hospital of the University of Pennsylvania
- 172 shared
James N. Gerson
University of Pennsylvania
- 127 shared
Marco Ruella
University of Pennsylvania
- 101 shared
Narendranath Epperla
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute
Labs
T-cell Lymphoma Program, UPennPI
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