tbuckley/cabot-search huggingface dataset:
Nilotinib with or without cytarabine for Philadelphia-positive acute lymphoblastic leukemia
Authors: Yves Chalandon, Philippe Rousselot, Sylvie Chevret, Jean-Michel Cayuela, Rathana Kim, Françoise Huguet, Patrice Chevallier, Carlos Graux, Anne Thiebaut-Bertrand, Sylvain Chantepie, Xavier Thomas, Laure Vincent, Céline Berthon, Yosr Hicheri, Emmanuel Raffoux, Martine Escoffre-Barbe, Isabelle Plantier, Magalie Joris, Pascal Turlure, Florence Pasquier, Amine Belhabri, Gabrielle Roth Guepin, Sabine Blum, Michael Gregor, Marina Lafage-Pochitaloff, Julie Quessada, Véronique Lhéritier, Emmanuelle Clappier, Nicolas Boissel, Hervé Dombret
Journal: Blood (2024)
18F-FDG PET/CT in Pediatric Immunoglobulin G4–Related Disease
Authors: Karan Singh, Olivia Bennett, Eva Alina Wegner, Amanda Marsden, Davinder Singh Grewal
Journal: Clinical Nuclear Medicine (2024)

A 14-year-old boy presented with severe, nonintentional weight loss, fatigue, and cough. Investigations were notable for raised inflammatory markers and significantly elevated serum immunoglobulin G4 (IgG4). 18 F-FDG PET/CT was obtained for assessment of disease involvement and extent, to exclude differential diagnoses and to guide biopsy. The study demonstrated extensive FDG-avid nodal disease and multisystem organ involvement. Excisional biopsy of a right inguinal lymph node demonstrated reactive changes with numerous IgG4-positive plasma cells consistent with IgG4-related disease. He was commenced on immunosuppressive therapy with consequent weight restoration and symptom resolution.
Intravitreal aflibercept 8 mg in neovascular age-related macular degeneration (PULSAR): 48-week results from a randomised, double-masked, non-inferiority, phase 3 trial
Authors: Paolo Lanzetta, Jean-François Korobelnik, Jeffrey S Heier, Sergio Leal, Frank G Holz, W Lloyd Clark, David Eichenbaum, Tomohiro Iida, Sun Xiaodong, Alyson J Berliner, Andrea Schulze, Thomas Schmelter, Ursula Schmidt-Ott, Xin Zhang, Robert Vitti, Karen W Chu, Kimberly Reed, Rohini Rao, Rafia Bhore, Yenchieh Cheng, Wei Sun, Boaz Hirshberg, George D Yancopoulos, Tien Y Wong
Journal: The Lancet (2024)
System-wide approaches to antimicrobial therapy and antimicrobial resistance in the UK: the AMR-X framework
Authors: Kathryn Abel, Emily Agnew, James Amos, Natalie Armstrong, Darius Armstrong-James, Thomas Ashfield, Stephen Aston, J Kenneth Baillie, Steven Baldwin, Gavin Barlow, Victoria Bartle, Julia Bielicki, Colin Brown, Enitan Carrol, Michelle Clements, Graham Cooke, Aaron Dane, Paul Dark, Jeremy Day, Anthony de-Soyza, Andrew Dowsey, Stephanie Evans, David Eyre, Timothy Felton, Tom Fowler, Robbie Foy, Karen Gannon, Alessandro Gerada, Anna Goodman, Tracy Harman, Gail Hayward, Alison Holmes, Susan Hopkins, Philip Howard, Alexander Howard, Yingfen Hsia, Gwen Knight, Nick Lemoine, James Koh, Alasdair Macgowan, Charis Marwick, Catrin Moore, Seamus O’Brien, Raymond Oppong, Sharon Peacock, Sarah Pett, Koen Pouwels, Chris Queree, Najib Rahman, Mark Sculpher, Laura Shallcross, Michael Sharland, Jasvinder Singh, Karen Stoddart, Emma Thomas-Jones, Andrew Townsend, Andrew Ustianowski, Tjeerd Van Staa, Sarah Walker, Peter White, Paul Wilson, Iain Buchan, Beth Woods, Peter Bower, Martin Llewelyn, William Hope
Journal: The Lancet Microbe (2024)

<h2>Summary</h2> Antimicrobial resistance (AMR) threatens human, animal, and environmental health. Acknowledging the urgency of addressing AMR, an opportunity exists to extend AMR action-focused research beyond the confines of an isolated biomedical paradigm. An AMR learning system, AMR-X, envisions a national network of health systems creating and applying optimal use of antimicrobials on the basis of their data collected from the delivery of routine clinical care. AMR-X integrates traditional AMR discovery, experimental research, and applied research with continuous analysis of pathogens, antimicrobial uses, and clinical outcomes that are routinely disseminated to practitioners, policy makers, patients, and the public to drive changes in practice and outcomes. AMR-X uses connected data-to-action systems to underpin an evaluation framework embedded in routine care, continuously driving implementation of improvements in patient and population health, targeting investment, and incentivising innovation. All stakeholders co-create AMR-X, protecting the public from AMR by adapting to continuously evolving AMR threats and generating the information needed for precision patient and population care.
SMARCA4 is a haploinsufficient B cell lymphoma tumor suppressor that fine-tunes centrocyte cell fate decisions
Authors: Qing Deng, Priya Lakra, Panhong Gou, Haopeng Yang, Cem Meydan, Matthew Teater, Christopher Chin, Wenchao Zhang, Tommy Dinh, Usama Hussein, Xubin Li, Estela Rojas, Weiguang Liu, Patrick K Reville, Atish Kizhakeyil, Darko Barisic, Sydney Parsons, Ashley Wilson, Jared Henderson, Brooks Scull, Channabasavaiah Gurumurthy, Francisco Vega, Amy Chadburn, Branko Cuglievan, Nader Kim El-Mallawany, Carl Allen, Christopher Mason, Ari Melnick, Michael R Green
Journal: Cancer Cell (2024)

SMARCA4 encodes one of two mutually exclusive ATPase subunits in the BRG/BRM associated factor (BAF) complex that is recruited by transcription factors (TFs) to drive chromatin accessibility and transcriptional activation. SMARCA4 is among the most recurrently mutated genes in human cancer, including ∼30% of germinal center (GC)-derived Burkitt lymphomas. In mice, GC-specific Smarca4 haploinsufficiency cooperated with MYC over-expression to drive lymphomagenesis. Furthermore, monoallelic Smarca4 deletion drove GC hyperplasia with centroblast polarization via significantly increased rates of centrocyte recycling to the dark zone. Mechanistically, Smarca4 loss reduced the activity of TFs that are activated in centrocytes to drive GC-exit, including SPI1 (PU.1), IRF family, and NF-κB. Loss of activity for these factors phenocopied aberrant BCL6 activity within murine centrocytes and human Burkitt lymphoma cells. SMARCA4 therefore facilitates chromatin accessibility for TFs that shape centrocyte trajectories, and loss of fine-control of these programs biases toward centroblast cell-fate, GC hyperplasia and lymphoma.
Cosmetic directors on ACGME program requirements: A cross-sectional survey
Authors: Kira Minkis, Erik J. Stratman, Victoria J. Shi, Tanya Greywal, Jenny C. Hu, Kathleen C. Suozzi, Sami K. Saikaly, Arisa Ortiz, Bianca Y. Kang, Murad Alam, A. Shadi Kourosh, Alison Boucher, Amanda K. Suggs, Anna Bar, Brian Cahn, Carolyn A. Robinson, Cynthia A. Schlick, Deirdre Hooper, Diana Antonovich, Diana Bolotin, Elika Hoss, Erica Ghareeb, Farhana Ikmal Hisham, Gabriella Alvarez, Helena Kuhn, Janiene Luke, Jared E. Roberts, Jayne Joo, Jeffrey S. Orringer, Jessica G. Labadie, Kalee Shah, Kimberley H.M. Ward, Kristen M. Kelly, Ladan Shahabi, Lauren C.S. Kole, Leila Tolaymat, Loma Dave, M. Laurin Council, Maggie L. Chow, Michael D. Yi, Michelle V. Pearlstein, Milad Eshaq, Min Deng, Naomi Lawrence, Neelam A. Vashi, Nour Kibbi, Olivia L. Schenck, Rachel Elsanadi, Ronda S. Farah, Saranya P. Wyles, Simon S. Yoo, Umer Nadir, Vesna Petronic-Rosic, Yakir S. Levin, Zeena Y. Nawas
Journal: Journal of the American Academy of Dermatology (2024)
Functional characterization of cooperating MGA mutations in RUNX1::RUNX1T1 acute myeloid leukemia
Authors: Melvin E. Thomas, Wenqing Qi, Michael P. Walsh, Jing Ma, Tamara Westover, Sherif Abdelhamed, Lauren J. Ezzell, Chandra Rolle, Emily Xiong, Wojciech Rosikiewicz, Beisi Xu, Allister J. Loughran, Shondra M. Pruett-Miller, Laura J. Janke, Jeffery M. Klco
Journal: Leukemia (2024)

MGA (Max-gene associated) is a dual-specificity transcription factor that negatively regulates MYC-target genes to inhibit proliferation and promote differentiation. Loss-of-function mutations in MGA have been commonly identified in several hematological neoplasms, including acute myeloid leukemia (AML) with RUNX1::RUNX1T1, however, very little is known about the impact of these MGA alterations on normal hematopoiesis or disease progression. We show that representative MGA mutations identified in patient samples abolish protein-protein interactions and transcriptional activity. Using a series of human and mouse model systems, including a newly developed conditional knock-out mouse strain, we demonstrate that loss of MGA results in upregulation of MYC and E2F targets, cell cycle genes, mTOR signaling, and oxidative phosphorylation in normal hematopoietic cells, leading to enhanced proliferation. The loss of MGA induces an open chromatin state at promoters of genes involved in cell cycle and proliferation. RUNX1::RUNX1T1 expression in Mga-deficient murine hematopoietic cells leads to a more aggressive AML with a significantly shortened latency. These data show that MGA regulates multiple pro-proliferative pathways in hematopoietic cells and cooperates with the RUNX1::RUNX1T1 fusion oncoprotein to enhance leukemogenesis.
Early skin inflammatory biomarker is predictive of development and persistence of atopic dermatitis in infants
Authors: Georgios N. Stamatas, Takahiro Sato, Carol Ní Chaoimh, Thierry Oddos, Richard Insel, Jonathan O’B. Hourihane, Alan D. Irvine
Journal: Journal of Allergy and Clinical Immunology (2024)

Background The STOP AD study, a randomized, open-label trial evaluating the effect of short-term (first four postnatal days to 8 weeks) skin barrier protection using AVEENO® Dermexa Fast & Long-Lasting Balm in infants with a parent with allergic disease, demonstrated decreased cumulative incidence and decreased prevalence of AD at 12 months of age. Objective We aimed to identify skin biomarkers in the STOP AD study that are associated with risk of development of AD. Methods Skin swabs were collected from the cheek and antecubital fossa (AF) at baseline, 8 weeks, and 12 months from subsets of study participants from each of the intervention arm (43 of 119) and control arm (43 of 138) and were analyzed for specific cytokines (CCL27, CXCL2, hBD1, IL18, IL8, IL1α, IL1RA, IL1β, S100A8/9, IL36γ) by ELISA. Results Higher titers of S100A8/9 at the AF at 8 weeks in infants with filaggrin wild type genotype (FLGwt), but not in those with filaggrin loss-of-function mutations (FLGmut), predicted: 1) Development of AD in the first year of life (p=0.033); 2) Presence of AD at 6 months or 12 months of age (p=0.009 and 0.035, respectively); 3) Persistence of AD between 6 and 12 months of age (p<0.001); 4) Development of AD with the emollient intervention. Conclusion Increased titers of S100A8/9 from skin swabs of the AF in high-risk infants at 8 weeks with FLGwt was predictive of AD developing in the first year of life and of other AD features. These findings suggest that there are different molecular pathways leading to AD in FLGmut individuals and in FLGwt individuals. Early identification of infants who are likely to develop AD will allow more targeted interventions.
Neoadjuvant-Adjuvant vs Neoadjuvant-Only PD-1 and PD-L1 Inhibitors for Patients With Resectable NSCLC
Authors: Yixin Zhou, Anlin Li, Hui Yu, Yuhong Wang, Xuanye Zhang, Huijuan Qiu, Wei Du, Linfeng Luo, Sha Fu, Li Zhang, Shaodong Hong
Journal: JAMA Network Open (2024)

Neoadjuvant therapy combining programmed cell death 1 (PD-1) and programmed death ligand 1 (PD-L1) inhibitors with platinum-based chemotherapy has demonstrated significant improvement in pathologic response and survival rates among patients with resectable non-small cell lung cancer (NSCLC). However, it remains controversial whether PD-1 blockade therapy given before and after surgery (neoadjuvant-adjuvant treatment) is associated with better outcomes than when given only before surgery (neoadjuvant-only treatment).
Immunotherapy or Chemoimmunotherapy in Older Adults With Advanced Non–Small Cell Lung Cancer
Authors: Yoko Tsukita, Takehiro Tozuka, Kohei Kushiro, Shinobu Hosokawa, Toshiyuki Sumi, Mao Uematsu, Osamu Honjo, Ou Yamaguchi, Tetsuhiko Asao, Jun Sugisaka, Go Saito, Jun Shiihara, Ryo Morita, Seigo Katakura, Takehiro Yasuda, Kakeru Hisakane, Eisaku Miyauchi, Satoshi Morita, Kunihiko Kobayashi, Hajime Asahina
Journal: JAMA Oncology (2024)

Immune checkpoint inhibitor (ICI) plus chemotherapy combination treatment (ICI-chemotherapy) is now a standard treatment for non-small cell lung cancer (NSCLC) without targetable oncogene alterations, but there are few data on ICI-chemotherapy for patients 75 years and older.
Association between high levels of nitrogen dioxide and increased cumulative incidence of lung cancer in patients with idiopathic pulmonary fibrosis
Authors: Hee-Young Yoon, Sun-Young Kim, Jin Woo Song
Journal: European Respiratory Journal (2024)

Background Lung cancer is a fatal complication of idiopathic pulmonary fibrosis (IPF) with a poor prognosis. However, the association between individual exposure to air pollutants and lung cancer development in patients with IPF is unknown. This study aimed to assess the effect of individual exposure to nitrogen dioxide (NO 2 ) on lung cancer development in patients with IPF. Methods We enrolled 1085 patients from an IPF cohort in the Republic of Korea (mean age 65.6 years, males 80.6%). We estimated individual-level long-term exposures to NO 2 at the patients' residential addresses using a national-scale exposure prediction model based on data from air quality regulatory monitoring stations. To evaluate the association between NO 2 levels and lung cancer development in IPF, we used an individual- and area-level covariates adjusted model as our primary model. Results The estimated average annual NO 2 concentration was 23.1 ppb. During a median follow-up of 4.3 years, 86 patients (7.9%) developed lung cancer. NO 2 concentration was associated with lung cancer development in an unadjusted model (HR 1.219; p=0.042), while a marginal association was found in the primary model (HR 1.280; p=0.084). When NO 2 concentration was stratified by the median value (21.0 ppb), exposure to high NO 2 levels (≥21.0 ppb) was associated with a 2.0-fold increase in the risk of lung cancer development (HR 2.023; p=0.047) in the primary model. Conclusion Individual exposure to high NO 2 levels may increase the risk of lung cancer development in patients with IPF.
Drug Efficacy in the Treatment of Antipsychotic-Induced Akathisia
Authors: Cyril Gerolymos, Romain Barazer, Dong Keon Yon, Anderson Loundou, Laurent Boyer, Guillaume Fond
Journal: JAMA Network Open (2024)

Antipsychotic-induced akathisia (AIA) occurs in 14% to 35% of patients treated with antipsychotics and is associated with increased suicide and decreased adherence in patients with schizophrenia. However, no comprehensive review and network meta-analysis has been conducted to compare the efficacy of treatments for AIA.
P2Y12 Inhibitor Monotherapy vs Dual Antiplatelet Therapy After Deployment of a Drug-Eluting Stent
Authors: Pil-Ki Min, Tae Soo Kang, Yun-Hyeong Cho, Sang-Sig Cheong, Byeong-Keuk Kim, Sung Woo Kwon, Woo Jung Park, Jung-Hee Lee, Wonho Kim, Wang-Soo Lee, Young Won Yoon, Byoung Kwon Lee, Hyuck Moon Kwon, Bum-Kee Hong, Bum-Kee Hong, Pil-Ki Min, Tae Soo Kang, Yun-Hyeong Cho, Sang-Sig Cheong, Byeong-Keuk Kim, Sung Woo Kwon, Woo Jung Park, Jung-Hee Lee, Wonho Kim, Wang-Soo Lee, Young Won Yoon, Byoung Kwon Lee, Hyuck Moon Kwon, Jin-Ok Jeong, Byung Jin Kim, Sang-Ho Park, Seung Hwan Lee, Namho Lee, Ae-Young Her, Jinman Cho, Jun Hee Lee, Jin Yong Hwang, Sung Uk Kwon
Journal: JAMA Network Open (2024)

P2Y12 inhibitor monotherapy after dual antiplatelet therapy (DAPT; a P2Y12 inhibitor plus aspirin) for a brief duration has recently emerged as an attractive alternative for patients undergoing percutaneous coronary intervention (PCI) with a drug-eluting stent.
Prospective Data on Stereotactic Ablative Radiotherapy Provides Guidance in an Unusual Clinical Scenario
Authors: Ashley A. Weiner, Lawrence B. Marks
Journal: JAMA Oncology (2024)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2024 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
Stereotactic Radiation Therapy in Early Non–Small Cell Lung Cancer and Interstitial Lung Disease
Authors: David A. Palma, Houda Bahig, Andrew Hope, Stephen Harrow, Brock J. Debenham, Alexander V. Louie, Thi Trinh Thuc (Toni) Vu, Edith Filion, Andrea Bezjak, Marie-Pierre Campeau, Adele Duimering, Meredith E. Giuliani, Joanna M. Laba, Pencilla Lang, Benjamin H. Lok, X. Melody Qu, Srinivas Raman, George B. Rodrigues, Christopher D. Goodman, Stewart Gaede, Julie Morisset, Andrew Warner, Inderdeep Dhaliwal, Christopher J. Ryerson
Journal: JAMA Oncology (2024)

Patients with interstitial lung disease (ILD) and early-stage non-small cell lung cancer (NSCLC) have been reported to be at high risk of toxic effects after stereotactic ablative radiotherapy (SABR), but for many patients, there are limited alternative treatment options.
Network Meta-Analyses—Better Than Nothing?
Authors: Massimo Di Maio
Journal: JAMA Network Open (2024)

Yixin Zhou, MD; Anlin Li, MD; Hui Yu, MD; Yuhong Wang, MD; Xuanye Zhang, MD; Huijuan Qiu, MD; Wei Du, MD; Linfeng Luo, MD; Sha Fu, MD; Li Zhang, MD; Shaodong Hong, MD
The dual HCK/BTK inhibitor KIN-8194 impairs growth and integrin-mediated adhesion of BTKi-resistant mantle cell lymphoma
Authors: Hildo C Lantermans, Fangxue Ma, Annemieke Kuil, Sanne van Kesteren, Sevtap Yasinoglu, Guang Yang, Sara J Buhrlage, Jinhua Wang, Nathanael S Gray, Marie José Kersten, Steven P Treon, Steven T Pals, Marcel Spaargaren
Journal: Leukemia (2024)

Although Bruton's tyrosine kinase (BTK) inhibitors (BTKi) have significantly improved patient prognosis, mantle cell lymphoma (MCL) is still considered incurable due to primary and acquired resistance. We have recently shown that aberrant expression of the Src-family tyrosine kinase hematopoietic cell kinase (HCK) in MCL correlates with poor prognosis, and that genetic HCK perturbation impairs growth and integrin-mediated adhesion of MCL cells. Here, we show that KIN-8194, a dual inhibitor of BTK and HCK with in vivo activity against Myd88-L265P-driven diffuse large B-cell lymphoma and Waldenström Macroglobulinemia, has a potent growth inhibitory effect in MCL cell lines and primary MCL cells, irrespective of their sensitivity to BTKi (ibrutinib and acalabrutinib). In BTKi-resistant cells this is mediated by inhibition of HCK, which results in repression of AKT-S6 signaling. In addition, KIN-8194 inhibits integrin-mediated adhesion of BTKi-sensitive and insensitive MCL cells to fibronectin and stromal cells in an HCK-dependent manner. Finally, we show that MCL cells with acquired BTKi resistance retain their sensitivity to KIN-8194. Taken together, our data demonstrate that KIN-8194 inhibits growth and integrin-mediated adhesion of BTKi-sensitive MCL cells, as well as MCL cells with primary or acquired BTKi resistance. This renders KIN-8194 a promising novel treatment for MCL patients.
Functional ultrasound imaging of the human spinal cord
Authors: K.A. Agyeman, D.J. Lee, J. Russin, E.I. Kreydin, W. Choi, A. Abedi, Y.T. Lo, J. Cavaleri, K. Wu, V.R. Edgerton, C. Liu, V.N. Christopoulos
Journal: Neuron (2024)

Utilizing the first in-human functional ultrasound imaging (fUSI) of the spinal cord, we demonstrate the integration of spinal functional responses to electrical stimulation. We record and characterize the hemodynamic responses of the spinal cord to a neuromodulatory intervention commonly used for treating pain and increasingly used for the restoration of sensorimotor and autonomic function. We found that the hemodynamic response to stimulation reflects a spatiotemporal modulation of the spinal cord circuitry not previously recognized. Our analytical capability offers a mechanism to assess blood flow changes with a new level of spatial and temporal precision in vivo and demonstrates that fUSI can decode the functional state of spinal networks in a single trial, which is of fundamental importance for developing real-time closed-loop neuromodulation systems. This work is a critical step toward developing a vital technique to study spinal cord function and effects of clinical neuromodulation.
Therapeutic Targeting of TIM-4-L with Engineered T Cells for Acute Myeloid Leukemia
Authors: Brandon Cieniewicz, Edson Oliveira, Mike Saxton, Damoun Torabi, Ankit Bhatta, Phanidhar Kukutla, Alexander Arballo, Zhuo Yang, Bi Yu, Maria Fate, Hongxiu Ning, Lawrence Corey, Abhishek Maiti, Daniel Corey
Journal: Clinical Cancer Research (2024)

Abstract Purpose: Disruption of lipid bilayer asymmetry is a common feature observed in cancer cells and offers novel routes for therapeutic targeting. We used the natural immune receptor TIM-4 to interrogate for loss of plasma membrane phospholipid polarity in primary acute myelogenous leukemia (AML) samples and evaluated the anti-leukemic activity of TIM-4-L–directed T-cell therapy in preclinical AML models. Experimental Design: We performed FACS analysis on 33 primary AML bone marrow specimens and correlated TIM-4-L expression frequency and intensity with molecular disease characteristics. Using Kasumi-1 and MV-4–11 AML cell lines, we further tested the anti-leukemic effects of TIM-4-L–directed engineered T cells in vitro and in vivo. Results: We found that 86% of untreated AML blasts displayed upregulation of cell surface TIM-4-L. These observations were agnostic to AML genetic classification, as samples with mutations in TP53, ASXL1, and RUNX1 displayed TIM-4-L upregulation similar to that seen in favorable and intermediate subtypes. TIM-4-L dysregulation was also stably present in AML cell lines. To evaluate the potential of targeting upregulated TIM-4-L with adoptive T-cell therapy, we constructed TIM-4-L–directed engineered T cells, which demonstrated potent anti-leukemic effects, effectively eliminating AML cell lines with a range of endogenous TIM-4-L expression levels both in vitro and in vivo. Conclusions: These results highlight TIM-4-L as a highly prevalent target on AML across a range of genetic classifications and novel target for T-cell–based therapy in AML. Further investigations into the role of TIM-4-L in AML pathogenesis and its potential as an anti-leukemic target for clinical development are warranted.