About

Lisa M Rimsza, MD, is the Department Chair and a Professor in the Department of Pathology at the University of Arizona College of Medicine. She is a member of the Graduate Faculty and a Professor at the BIO5 Institute. Dr. Rimsza completed her medical degree at the University of Arizona College of Medicine in 1992 and her fellowship in Hematopathology at the University of New Mexico. She holds certification from the American Board of Pathology in Anatomic and Clinical Pathology. Her professional roles include leadership in pathology and hematopathology, with a focus on diagnostic and research programs within the department.

Research topics

• Biology
• Immunology
• Medicine
• Nuclear medicine
• Oncology
• Radiology
• Cancer research
• Genetics
• Virology
• Internal medicine

Selected publications

• 1184 RNA Sequencing as a Diagnostic Tool in Peripheral T-Cell Lymphoma

  Laboratory Investigation · 2026-03-01

  article
  PublisherDOI

• 1275 BCL2-R-negative, CD23+ Follicle Center Lymphoma (FL): Clinical, Pathologic, and Genetic Evaluation in a Phase III Randomized Clinical Trial Cohort

  Laboratory Investigation · 2026-03-01

  articleSenior author
  PublisherDOI

• High-grade B-cell lymphoma, not otherwise specified: an LLMPP study

  Blood Advances · 2025-07-17 · 9 citations

  articleOpen access

  ABSTRACT: Molecular characterization of high-grade B-cell lymphoma, not otherwise specified (HGBCL-NOS), is hindered by its rarity, evolving definition, and poor diagnostic reproducibility. To address this challenge, we analyzed 92 HGBCL-NOS tumors collected across Lymphoma/Leukemia Molecular Profiling Project sites. Leveraging comparison cohorts of diffuse large B-cell lymphoma, NOS (DLBCL-NOS) and Burkitt lymphoma (BL), and molecular frameworks described in these entities, our analysis revealed a heterogenous molecular landscape, reminiscent of DLBCL-NOS but with an enrichment of BL features. By cell-of-origin classification, 59% were germinal center B-cell-like (GCB), and 25% were activated B-cell-like (ABC). LymphGen, a genetic classifier for DLBCL-NOS, assigned a genetic subtype to 34% of HGBCL-NOS. Although classification rate was lower than in DLBCL-NOS (66%), assigned subtypes spanned the spectrum of LymphGen classes, including 31% of ABCs classified as MCD. Features differentiating HGBCL-NOS from DLBCL-NOS included MYC rearrangement (47% vs 6%); dark zone signature (DZsig) expression (45% vs 7%); and more frequent mutation of ID3, MYC, CCND3, and TP53, all common to BL. A genetic classifier that differentiates DLBCL-NOS from BL classified 53% of DZsig+ tumors as BL-like, and those classified as DLBCL-like were frequently BCL2-rearranged. Among DZsig- GCB tumors, 95% were DLBCL-like. Centralized pathology review reclassified almost half of tumors as DLBCL-NOS but did not identify a more homogenous HGBCL-NOS population, with no difference in features between confirmed and reclassified tumors. In conclusion, molecular testing enables a subset of HGBCL-NOS to be assigned to established categories. Based on rarity and diagnostic challenges, broader inclusion of HGBCL-NOS should be considered in biomarker-driven DLBCL trials.

  PublisherOA PDFDOI

• 81 | REPRESSION OF miR‐29 VIA MYC LEADS TO INCREASED CD40 SIGNALING IN TRANSFORMED FOLLICULAR LYMPHOMA (FL) AND UNFAVOURABLE PROGNOSIS IN FL

  Hematological Oncology · 2025-06-01

  articleOpen access

  Introduction: FL patients are at risk of disease transformation to high-grade lymphoma (tFL). While genetic alterations have been implicated in tFL, the role of microenvironmental interactions and epigenetic regulation by non-coding RNAs remains poorly understood. Results: We performed the first matched profiling of non-coding RNAs (miRNAs) and mRNAs in paired FL and tFL samples (n = 10 pairs). This identified differential expression of 1075 mRNAs and 19 miRNAs, including repression of the miR-29 family in tFL (miR-29a/b/c, Figure A), which we further focused on. We uncovered that MYC activity is uniformly induced in tFL (GSEA, FDR = 0.016) and represses miR-29 by binding to its promotor, and MYC silencing (siRNA) led to miR-29s induction in lymphoma cell lines (p < 0.05). RNAseq in FL-tFL pairs revealed changes in multiple molecular pathways potentially controlled by miR-29s, including CD40 signaling being strongly activated in tFL (GSEA, IPA). CD40 pathway is a major pro-proliferative factor in normal and FL lymph nodes. scRNAseq data reanalysis (Roider et al,2019) revealed that CD40L is amongst the 10 most active ligands in tFL (Figure B). Increased CD40 activation in tFL contrasted with the reduced CD4+ and CD8+ T-cell numbers in tFL niches (IHC in 10 FL-tFL pairs, CIBERSORTx from FL-tFL RNAseq). To directly identify miR-29 targets, we performed RNA profiling in 2 cell lines engineered for miR-29c overexpression, revealing 20 putative miR-29 targets downregulated in both cell lines. This included TRAF4, which has been previously linked to CD40 signaling. miR-29c overexpression leads to ∼50% reduction of TRAF4 levels (Figure C) via miR-29c binding to its 3’UTR. Importantly, cell lines constitutively overexpressing miR-29c or transfected with synthetic miR-29c (1000 nM) were less responsive (↓ pIKKa/b) to recombinant CD40L (Figure C) or HS-5 cells engineered for CD40L expression. Altogether, MYC-mediated miR-29 repression results in increased TRAF4 and CD40 signaling. Importantly, TRAF4 levels were increased in tFL compared to paired FL (n = 11 pairs, Figure D). Ki67 correlated positively with TRAF4 and negatively with miR-29s levels (FL/tFL n = 46), and TRAF4 and MYC were concurrently induced in tFL (R = 0,8, p = 0.004). Lower levels of all miR-29s(a/b/c) were associated with shorter OS and PFS in FL in univariate (n = 185, for miR-29c in Figure E) and multivariate analysis (age, FLIPI, Hgb, LDH, Ann Arbor, B sympt.). Lower miR-29c levels were associated with shorter OS also in a validation FL cohort (n = 92, Figure F) from an R-CHOP arm of a clinical trial (NCT00006721), but not in DLBCL (n = 174). Conclusions: The first whole-genome miRNA profiling in tFL showed that MYC represses miR-29s levels, leading to increased TRAF4 and stronger CD40 signaling propensity (Figure G). This likely represents an adaptive response to reduced CD40L availability from T-cells in the tFL niches. Moreover, low levels of miR-29c can be used as an FFPE-based biomarker of unfavorable FL prognosis. Research funding declaration: Supported by: Czech Science Foundation Grant No.25-15368X; Ministry of Health of the Czech Rep., grant No.NU22-03-00117 and NU23-08-00448; MH CZ-DRO (FNBr, 65269705); MUNI/A/1685/2024; NIH/NCI/NCTN grants U10CA180888, U10CA180819. National Inst. for Cancer Research (programme EXCELES, ID project no.LX22NPO5102)–Funded by the EU–Next Generation EU. Encore Abstract: EHA 2025 Keywords: microenvironment; aggressive B-cell non-Hodgkin lymphoma; indolent non-Hodgkin lymphoma No potential sources of conflict of interest.

  PublisherOA PDFDOI

• Cooperative role of distinctive TP53 and PTEN combined loss in the peripheral T cell lymphoma–GATA3 molecular subgroup

  Science Advances · 2025-10-17 · 1 citations

  articleOpen access

  Peripheral T cell lymphoma (PTCL) is a heterogeneous group of postthymic T cell neoplasms, with ~40% classified as PTCL–not otherwise specified (PTCL-NOS). PTCL-GATA3, a molecularly defined subtype, associated with T helper 2 (T H 2)–like differentiation and poor prognosis, has frequent co-occurrence of TP53 loss/mutation and heterozygous PTEN loss. CD4+ T cell conditional mouse models with Trp53 mutation/deletion and Pten loss demonstrated mature T cell lymphomas (mTCLs) with T H 2-like transcriptomic and immunophenotypic profiles. Molecular studies revealed that codeletion of Trp53/Pten induced T cell receptor and Janus kinase–signal transducer and activator of transcription signaling, promoting T H 2 differentiation while inhibiting T H 1 differentiation. These findings were validated by CRISPR editing of TP53/PTEN loss in human CD4+ T cells and mechanistically evaluated the p53 binding region in intron-3 of GATA3, resulting in transcriptional repression. Transcriptomic profiles of m-TCLs recapitulated human-PTCL-GATA3 transcriptome and distinguished PTCL-NOS subtypes. Preclinical assessment of m-TCLs with PI3Kγ/δ inhibitors significantly improved survival, supporting a therapeutic approach for the p53-aberrant PTCL-GATA3.

  PublisherDOI

• A novel cereblon variant with both exon 8 and 10 deletions in newly diagnosed and relapsed multiple myeloma

  Blood Neoplasia · 2025-04-06 · 1 citations

  articleOpen accessSenior author

  isoform on a gene expression platform and unexpectedly identified a variant with alterations of exon 10 and 8 transcripts in both newly diagnosed and refractory cases. This variant is present at diagnosis and could have separate, yet likely additive, effects on drug resistance.

  PublisherDOI

• Minimal residual disease status predicts outcomes in patients with follicular lymphoma treated with chemo-immunotherapy on the SWOG S0016 trial

  Haematologica · 2025-07-03

  articleOpen access

  Not available.

  PublisherOA PDFDOI

• IBCL-1106: Response-Adapted Therapy With Copanlisib and Rituximab in Untreated Follicular Lymphoma: A Phase 2 Study

  Clinical Lymphoma Myeloma & Leukemia · 2025-08-28

  article
  PublisherDOI

• An immunohistochemical germinal center B-cell dark zone signature identifies Burkitt lymphoma and molecular high-grade B-cell lymphomas

  American Journal of Clinical Pathology · 2025-08-03 · 2 citations

  article

  OBJECTIVE: We hypothesized that a set of immunohistochemistry (IHC) stains could be used to distinguish Burkitt lymphoma (BL), the quintessential B-cell lymphoma with a germinal center B-cell (GCB) dark zone (DZ) expression signature, from diffuse large B-cell lymphoma, not otherwise specified (DLBCL, NOS). This might also be applicable to high-grade B-cell lymphomas (HGBCLs) with MYC and BCL2 rearrangements (double-hit lymphomas [DHLs]) and triple-hit lymphomas (THLs). METHODS: A 5-marker IHC algorithm was designed from gene lists that distinguish physiologic DZ from light zone GCBs. RESULTS: In training and validation cohorts, we distinguished BL from DLBCL, NOS with high sensitivity and specificity. Because DHLs/THLs are enriched for the gene expression DZ signature (DZsig), we evaluated 19 DHLs/THLs and 4 HGBCLs, NOS. Most (83%) cases were IHC DZ. The NanoString DLBCL90 assay was performed on 34 cases to correlate IHC DZ results with the molecular DZsig. The IHC DZ call was significantly associated with the DZsig (P = .0011). The sensitivity and specificity of IHC to recognize DZsig+ cases among DLBCL, NOS and DHLs with BCL2 rearrangements/THLs were 91% and 100%, respectively. CONCLUSIONS: The IHC DZ algorithm can support a diagnosis of BL and identifies MYC-BCL2 DHLs/THLs with a molecular DZsig.

  PublisherDOI

• Gene expression profiling reveals 2 overarching types of ALCL with distinct targetable biology: an LLMPP study

  Blood · 2025-12-02 · 3 citations

  articleOpen access

  ABSTRACT: Anaplastic large cell lymphomas (ALCLs) are CD30+ T-cell lymphomas that share pathologic features but differ in presentation, outcome, and genetics. Current classification incorporates clinical presentation and anaplastic lymphoma kinase (ALK) status but inadequately addresses molecular heterogeneity and therapeutic vulnerabilities. We studied 689 patients with ALCL in the LLMPP (Lymphoma/Leukemia Molecular Profiling Project) and performed expert consensus review, genetic subtyping (ALK, DUSP22, TP63, and triple negative), and immunohistochemistry for phosphorylated STAT3Tyr705. RNA sequencing with unsupervised gene expression profiling in 393 patients identified 2 main molecular types of ALCL that could be predicted with 91% accuracy based on the presence (type I) or absence (type II) of phosphorylated STAT3Y705 expression. Type I ALCLs included ALK+ ALCL and a subset of triple-negative ALCLs (TN-I); type II ALCLs included tumors with DUSP22 and/or TP63 rearrangements and the remaining triple-negative ALCLs (TN-II). Type I ALCLs were enriched for JAK-STAT3, whereas type II ALCLs were enriched for non-tyrosine kinase pathways, particularly epigenetic regulators such as EZH2. Immunohistochemistry showed overexpression of EZH2 and its trimethylated substrate H3K27. Prognosis in systemic ALCL was favorable for DUSP22-rearranged ALCL (5-year overall survival, 95%) and ALK+ ALCL (88%), intermediate for triple-negative ALCL (TN-I, 52% and TN-II, 37%), and poor for TP63-rearranged ALCL (0%). We introduce an integrated molecular classification that preserves currently diagnosed ALCL entities but identifies 4 molecularly distinct ALK- ALCL subtypes (DUSP22-rearranged, TP63-rearranged, TN-I, and TN-II). This classification can be easily implemented on paraffin tissue in routine practice or clinical trials, and stratifies ALCL into diagnostically, prognostically, biologically, and potentially therapeutically relevant subtypes.

  PublisherOA PDFDOI

Recent grants

• Development of Mantle Cell Lymphoma Proliferation Signature Assay

  NIH · $397k · 2017–2019

• Development of Mantle Cell Lymphoma Proliferation Signature Assay

  NIH · $1.0M · 2017–2023

• AIDS and Cancer Specimen Resource (ACSR)

  NIH · $56.7M · 2025–2026

• Molecular Pathogenesis of Two Newly Defined Major Subgroups of PTCL

  NIH · $20.5M · 2018–2024

• Molecular Diagnosis and Prognosis in Aggressive Lymphoma

  NIH · $3.1M · 2011–2018

Frequent coauthors

• Louis M. Staudt

  377 shared

• Elaine S. Jaffe

  National Cancer Institute

  354 shared

• German Ott

  Robert Bosch Hospital

  347 shared

• Andreas Rosenwald

  Comprehensive Cancer Center Mainfranken

  330 shared

• Elı́as Campo

  Università Cattolica del Sacro Cuore

  328 shared

• Wing C. Chan

  City Of Hope National Medical Center

  303 shared

• Rita M. Braziel

  301 shared

• Randy D. Gascoyne

  296 shared

Labs

• Research LabsPI