bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure S1 from Granulocyte colony stimulating factor is a novel mediator of T cell suppression and an immunotherapeutic target for women with colon cancer
Authors: Ray Anita L. , Saunders Apryl S. , Nofchissey Robert A. , Reidy Megan A. , Kamal Maria , Lerner Megan R. , Fung Kar-Ming , Lang Mark L. , Hanson Joshua A. , Guo Shaoxuan , Urdaneta-Perez Maria G. , Lewis Samara E. , Cloyde Michael , Morris Katherine T.
Published: September 2024

Supplementary Figure S1
Supplemental Figure 8 from Myosin light chain kinase inhibition potentiates the anti-tumor effects of avapritinib in PDGFRA D842V-mutant gastrointestinal stromal tumor
Authors: Rossi Ferdinand , Liu Mengyuan , Tieniber Andrew , Etherington Mark S. , Hanna Andrew , Vitiello Gerardo A. , Param Nesteene J. , Do Kevin , Wang Laura , Antonescu Cristina R. , Zeng Shan , Zhang Jennifer Q. , DeMatteo Ronald P.
Published: September 2024

Supplemental Figure 8.
Relative MYLK mRNA expression by qPCR in GIST PDGFRA D842V PDXs treated with vehicle
(Veh) or imatinib (IM) for 2 weeks.
Supplementary Table S2 from Early on-treatment changes in circulating tumor DNA fraction and response to enzalutamide or abiraterone in metastatic castration-resistant prostate cancer
Authors: Tolmeijer Sofie H. , Boerrigter Emmy , Sumiyoshi Takayuki , Kwan Edmond M. , Ng Sarah , Annala Matti , Donnellan Grainne , Herberts Cameron , Benoist Guillemette E. , Hamberg Paul , Somford Diederik M. , van Oort Inge M. , Schalken Jack A. , Mehra Niven , van Erp Nielka P. , Wyatt Alexander W.
Published: September 2024

Evidence for ctDNA estimates per patient per timepoint
Supplementary Figure S2 from Early on-treatment changes in circulating tumor DNA fraction and response to enzalutamide or abiraterone in metastatic castration-resistant prostate cancer
Authors: Tolmeijer Sofie H. , Boerrigter Emmy , Sumiyoshi Takayuki , Kwan Edmond M. , Ng Sarah , Annala Matti , Donnellan Grainne , Herberts Cameron , Benoist Guillemette E. , Hamberg Paul , Somford Diederik M. , van Oort Inge M. , Schalken Jack A. , Mehra Niven , van Erp Nielka P. , Wyatt Alexander W.
Published: September 2024

On-treatment ctDNA fraction, PSA and LDH changes and durability of treatment response
Supplementary Figure S10 from Early on-treatment changes in circulating tumor DNA fraction and response to enzalutamide or abiraterone in metastatic castration-resistant prostate cancer
Authors: Tolmeijer Sofie H. , Boerrigter Emmy , Sumiyoshi Takayuki , Kwan Edmond M. , Ng Sarah , Annala Matti , Donnellan Grainne , Herberts Cameron , Benoist Guillemette E. , Hamberg Paul , Somford Diederik M. , van Oort Inge M. , Schalken Jack A. , Mehra Niven , van Erp Nielka P. , Wyatt Alexander W.
Published: September 2024

Changes in ctDNA fraction and PSA levels between baseline and 4 weeks on-treatment in relation to the durability of response
Supplemental Table 2 from Multi-center phase I trial of Ivosidenib as Maintenance Treatment following Allogeneic Hematopoietic Cell Transplantation for IDH1-Mutated Acute Myeloid Leukemia
Authors: Fathi Amir T. , Kim Haesook T. , Soiffer Robert J. , Levis Mark J. , Li Shuli , Kim Annette S. , DeFilipp Zachariah , El-Jawahri Areej , McAfee Steve L. , Brunner Andrew M. , Amrein Philip C. , Mims Alice S. , Knight Laura W. , Kelley Devon , Bottoms AJ S. , Perry Lindsey H. , Wahl Jonathan L. , Brock Jennifer , Breton Elayne , Marchione Dylan M. , Ho Vincent T. , Chen Yi-Bin
Published: September 2024

Marrow IDH1 VAF prior to Transplant and Maintenance
Figure S6 from Proteostasis modulation in germline missense von Hippel Lindau disease
Authors: Chittiboina Prashant , Mandal Debjani , Bugarini Alejandro , Asuzu David T. , Mullaney Dustin , Mastorakos Panagiotis , Stoica Stefan , Alvarez Reinier , Scott Gretchen , Maric Dragan , Elkahloun Abdel , Zhuang Zhengping , Chew Emily Y. , Yang Chunzhang , Linehan Marston , Lonser Russell R.
Published: September 2024

Figure S6
Supplementary Figure S3 from An immune-related gene expression signature predicts benefit from adding atezolizumab to FOLFOXIRI plus bevacizumab in metastatic colorectal cancer
Authors: Antoniotti Carlotta , Boccaccino Alessandra , Seitz Robert , Giordano Mirella , Catteau Aurélie , Rossini Daniele , Pietrantonio Filippo , Salvatore Lisa , McGregor Kimberly , Bergamo Francesca , Conca Veronica , Leonetti Simone , Morano Federica , Papiani Giorgio , Tamburini Emiliano , Bensi Maria , Murgioni Sabina , Ross Douglas Teller. , Passardi Alessandro , Boquet Isabelle , Nielsen Tyler J. , Galon Jerome , Varga Matthew Gordon. , Schweitzer Brock L. , Cremolini Chiara
Published: September 2024

Kaplan Meier estimates of progression-free survival in the pMMR population (optimized cut-point), according to IO status (a) and to both IO status and treatment arm (b).
Legend: HR: hazard ratio, NR: not reached. Control arm indicates FOLFOXIRI plus bevacizumab. Atezo arm indicates FOLFOXIRI plus bevacizumab and atezolizumab.
Supplementary Figure S2 from An immune-related gene expression signature predicts benefit from adding atezolizumab to FOLFOXIRI plus bevacizumab in metastatic colorectal cancer
Authors: Antoniotti Carlotta , Boccaccino Alessandra , Seitz Robert , Giordano Mirella , Catteau Aurélie , Rossini Daniele , Pietrantonio Filippo , Salvatore Lisa , McGregor Kimberly , Bergamo Francesca , Conca Veronica , Leonetti Simone , Morano Federica , Papiani Giorgio , Tamburini Emiliano , Bensi Maria , Murgioni Sabina , Ross Douglas Teller. , Passardi Alessandro , Boquet Isabelle , Nielsen Tyler J. , Galon Jerome , Varga Matthew Gordon. , Schweitzer Brock L. , Cremolini Chiara
Published: September 2024

Kaplan Meier estimates of progression-free survival in the overall population (optimized cut-point), according to IO status (a) and to both IO status and treatment arm (b).
Legend: HR: hazard ratio, NR: not reached. Control arm indicates FOLFOXIRI plus bevacizumab. Atezo arm indicates FOLFOXIRI plus bevacizumab and atezolizumab.
Table S2 from Clinical importance of the lncRNA NEAT1 in cancer patients treated with immune checkpoint inhibitors.
Authors: Toker Joseph , Iorgulescu J. Bryan. , Ling Alexander L. , Villa Genaro R. , Gadet Josephina A.M.A. , Parida Laxmi , Getz Gad , Wu Catherine J. , Reardon David A. , Chiocca E. Antonio , Mineo Marco
Published: September 2024

Melanoma patient characteristics (GSE78220)
Supplementary Fig. 2 from Clinical importance of the lncRNA NEAT1 in cancer patients treated with immune checkpoint inhibitors.
Authors: Toker Joseph , Iorgulescu J. Bryan. , Ling Alexander L. , Villa Genaro R. , Gadet Josephina A.M.A. , Parida Laxmi , Getz Gad , Wu Catherine J. , Reardon David A. , Chiocca E. Antonio , Mineo Marco
Published: September 2024

Supplementary Fig. 2 NEAT1 expression is associated with the interferon-gamma response in melanoma.
Supplementary Tables
S1-S14 from Proinflammatory macrophage activation by the polysialic acid-Siglec-16 axis is linked to increased survival of glioblastoma patients
Authors: Thiesler Hauke , Gretenkort Lina , Hoffmeister Leonie , Albers Iris , Ohlmeier Luisa , Röckle Iris , Verhagen Andrea , Banan Rouzbeh , Köpcke Nora , Krönke Nicole , Feuerhake Friedrich , Behling Felix , Barrantes-Freer Alonso , Mielke Dorothee , Rohde Veit , Hong Bujung , Varki Ajit , Schwabe Kerstin , Krauss Joachim K. , Stadelmann Christine , Hartmann Christian , Hildebrandt Herbert
Published: September 2024

Supplementary Table S1.
Demographic and clinical parameters of GB patient cohorts.
Supplementary Table S2.
Characteristics of the two cohorts of n = 70 (MHH) and n = 100 (UMG) GB patients stratified for the
presence of a functional SIGLEC16 allele (A) or for the occurrence of polySia on tumor cells (B).
Supplementary Table S3.
Cox proportional hazards regression analysis of covariates for SIGLEC16 and polySia status in relation to OS (MHH and UMG cohorts combined).
Supplementary Table S4.
Median age of GB cases stratified for SIGLEC16 genotype and polySia on tumor cells.
Supplementary Table S5.
OS analysis of GB cases receiving (A) or not receiving gross total resection (B) stratified for SIGLEC16 genotype and polySia on tumor cells (MHH and UMG cohorts combined).
Supplementary Table S6.
OS analysis of GB cases receiving (A) or not receiving chemotherapy (B) stratified for SIGLEC16 genotype and polySia on tumor cells (MHH cohort only).
Supplementary Table S7.
OS analysis of GB cases receiving gross total resection and chemotherapy stratified for SIGLEC16 genotype and polySia on tumor cells (MHH and UMG cohorts combined, n=101).
Supplementary Table S8.
OS analysis of IDH-wildtype GB cases (UMG cohort) stratified for SIGLEC16 genotype and polySia on tumor cells.
Supplementary Table S9.
OS analysis of UMG cohort stratified for MGMT gene promoter methylation and SIGLEC16 genotype, polySia on tumor cells, CD163 and CD74 status.
Supplementary Table S10.
Characteristics of the two cohorts of n = 70 (MHH) and n = 100 (UMG) GB patients stratified for CD74low and CD74high.
Supplementary Table S11. Median age at resection of GB cases stratified for CD163 to CD68 (A) or CD74 to IBA1 ratios (B) alone or in combination with the SIGLEC16 genotype.
Supplementary Table S12. OS analysis of GB cases receiving (A) or not receiving gross total resection (B) stratified for CD163 to CD68 or CD74 to IBA1 ratios alone or in combination with the SIGLEC16 genotype (MHH and UMG cohorts combined).
Supplementary Table S13. OS analysis of GB cases receiving (A) or not receiving chemotherapy (B) stratified for CD163 to CD68 or CD74 to IBA1 ratios alone or in combination with the SIGLEC16 genotype (MHH cohort only).
Supplementary Table S14.
OS analysis of GB cases receiving both gross total resection and chemotherapy stratified for CD163 to CD68 or CD74 to IBA1 ratios alone or in combination with the SIGLEC16 genotype (MHH and UMG cohorts combined, n=101).
Supplementary Fig. 1 from Combination Treatment with Sipuleucel-T and Abiraterone Acetate or Enzalutamide for Metastatic Castration-Resistant Prostate Cancer: STAMP and STRIDE Trials
Authors: Antonarakis Emmanuel S. , Subudhi Sumit K. , Pieczonka Christopher M. , Karsh Lawrence I. , Quinn David I. , Hafron Jason M. , Wilfehrt Helen M. , Harmon Matthew , Sheikh Nadeem A. , Shore Neal D. , Petrylak Daniel P.
Published: September 2024

Supplementary Fig 1 Analysis of Survival by Baseline Median PSA across the two studies using the study-specific median and quartiles.
Supplementary Table S2 from Clinical relevance of BRCA1 promoter methylation testing in ovarian cancer patients.
Authors: Blanc-Durand Félix , Tang Roseline , Pommier Margaux , Nashvi Marzieh , Cotteret Sophie , Genestie Catherine , Le Formal Audrey , Pautier Patricia , Michels Judith , Kfoury Maria , Hervé Robert , Mengue Sylvie , Wafo Estelle , Elies Antoine , Miailhe Gregoire , Uzan Jennifer , Rouleau Etienne , Leary Alexandra
Published: September 2024

Clinical data and outcomes of patients included
Supplementary Data File 2 from Phase II Investigation of TVB-2640 (denifanstat) with Bevacizumab in Patients with First Relapse High-Grade Astrocytoma
Authors: Kelly William , Diaz Duque Adolfo Enrique , Michalek Joel , Konkel Brandon , Caflisch Laura , Chen Yidong , Pathuri Sarath Chand. , Madhusudanannair Kunnuparampil Vinu , Floyd John , Brenner Andrew
Published: September 2024

RNA Analysis Summary
Supplemental Figure S3 from Phase II Investigation of TVB-2640 (denifanstat) with Bevacizumab in Patients with First Relapse High-Grade Astrocytoma
Authors: Kelly William , Diaz Duque Adolfo Enrique , Michalek Joel , Konkel Brandon , Caflisch Laura , Chen Yidong , Pathuri Sarath Chand. , Madhusudanannair Kunnuparampil Vinu , Floyd John , Brenner Andrew
Published: September 2024

Overall Survival by Exosome (50-120nm N=24) Concentration Relative Change (< -0.01, > -0.01): p=0.57 [<-0.01: median=8.9, 95% CI 5.1 to 17.5, >-0.01: median=8.3 95% CI 4.0, 14.1]
Supplementary Table S1 from A Phase I/II trial of HER-2/neu vaccine primed autologous T-cell infusions in patients with treatment refractory HER-2/neu overexpressing breast cancer
Authors: Disis Mary L. , Dang Yushe , Coveler Andrew L. , Childs Jennifer S. , Higgins Doreen M. , Liu Ying , Zhou Jing , Mackay Sean , Salazar Lupe G.
Published: September 2024

Representativeness of study participants.
Supplementary Data 3 from Uncoupling CD4+ TIL-mediated tumor killing from JAK-signaling in melanoma
Authors: Draghi Arianna , Presti Mario , Jensen Agnete W.P. , Chamberlain Christopher A. , Albieri Benedetta , Rasmussen Anne-Christine K. , Andersen Mads H. , Crowther Michael D. , Svane Inge Marie , Donia Marco
Published: September 2024

CD4+ TILs can exert cytotoxicity against JAK1KO MHCIIConst+ tumors even in absence of IFNγ stimulation (TCL#17)
Figure S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
Authors: Rastegar Bahar , Andersson Natalie , Petersson Alexandra , Karlsson Jenny , Chattopadhyay Subhayan , Valind Anders , Jansson Caroline , Durand Geoffroy , Romerius Patrik , Jirstrom Karin , Holmquist Mengelbier Linda , Gisselsson David
Published: September 2024

Supplementary Figure 1 Geographic overview of histological and genetic features.
Supplementary Figure S5 from TIGIT expression delineates T cell populations with distinct functional and prognostic impact in pancreatic cancer
Authors: Heiduk Max , Klimova Anna , Reiche Charlotte , Digomann David , Beer Carolin , Aust Daniela E. , Distler Marius , Weitz Jürgen , Seifert Adrian M. , Seifert Lena
Published: September 2024

Representative flow plots of cytokine expression.
Supplementary Figure S11 from TIGIT expression delineates T cell populations with distinct functional and prognostic impact in pancreatic cancer
Authors: Heiduk Max , Klimova Anna , Reiche Charlotte , Digomann David , Beer Carolin , Aust Daniela E. , Distler Marius , Weitz Jürgen , Seifert Adrian M. , Seifert Lena
Published: September 2024

Survival analyses for PD-1 and TIGIT co-expression in blood.
Supplementary Table S1 from Phase I study of SYNB1891, an engineered E coli Nissle strain expressing STING agonist, with and without atezolizumab in advanced malignancies
Authors: Luke Jason J. , Piha-Paul Sarina A. , Medina Theresa , Verschraegen Claire F. , Varterasian Mary , Brennan Aoife M. , Riese Richard J. , Sokolovska Anna , Strauss James F. , Hava David L. , Janku Filip
Published: September 2024

Supplemental Table 1. Representativeness of Study Participants
Supplementary Data S1 from Targeting BET proteins downregulates miR-33a to promote synergy with PIM inhibitors in CMML
Authors: Letson Christopher T. , Balasis Maria E. , Newman Hannah , Binder Moritz , Vedder Alexis , Kinose Fumi , Ball Markus , Kruer Traci , Quintana Ariel , Lasho Terra L. , Finke Christy M. , Almada Luciana L. , Grants Jennifer M. , Zhang Guolin , Fernandez-Zapico Martin E. , Gaspar-Maia Alexandre , Lancet Jeffrey , Komrokji Rami , Haura Eric , Sallman David A. , Reuther Gary W. , Karsan Aly , Rix Uwe , Patnaik Mrinal M. , Padron Eric
Published: September 2024

Raw data associated with miRNA Array performed for Supplemental Figure 4F
Supplementary Table S2 from Phase II study of docetaxel and trametinib in patients with KRAS mutation positive recurrent non-small cell lung cancer (NSCLC) (SWOG S1507, NCT-02642042)
Authors: Gadgeel Shirish M. , Miao Jieling , Riess Jonathan W. , Moon James , Mack Philip C. , Gerstner Gregory J. , Burns Timothy F. , Taj Asma , Akerley Wallace L. , Dragnev Konstantin H. , Laudi Noel , Redman Mary W. , Gray Jhanelle E. , Gandara David R. , Kelly Karen
Published: September 2024

Supplementary Table 2. Representativeness of Study Participants
Supplementary Table S2 from Association of Antifolate Response Signature Status and Clinical Activity of Pemetrexed-Platinum Chemotherapy in Non-Small Cell Lung Cancer - The Piedmont Study
Authors: Eisner Joel R. , Mayhew Gregory M. , Davison James M. , Beebe Kirk D. , Shibata Yoichiro , Guo Yuelong , Farhangfar Carol , Farhangfar Farhang , Uronis Joshua M. , Conroy Jeffrey M. , Milburn Michael V. , Hayes David Neil. , Mileham Kathryn F.
Published: September 2024

Expression Matrix of Patient Tumor Sample RNAseq
Supplementary Table S1 from A bi-functional PARP-HDAC inhibitor with activity in Ewing sarcoma
Authors: Ramos Louise , Truong Sarah , Zhai Beibei , Joshi Jay , Ghaidi Fariba , Lizardo Michael M. , Shyp Taras , Kung Sonia H.Y. , Rezakhanlou Alireza M. , Oo Htoo Zarni , Adomat Hans , Le Bihan Stephane , Collins Colin , Bacha Jeffrey , Brown Dennis , Langlands John , Shen Wang , Lallous Nada , Sorensen Poul H. , Daugaard Mads
Published: September 2024

Blood cell panel counts and weight loss percentage of in vivo toxicity study
Supplemental Figure 4 from Transcriptomic Signatures of MSI-high Metastatic Colorectal Cancer Predict Efficacy of Immune Checkpoint Inhibitors
Authors: Gallois Claire , Landi Matteo , Taieb Julien , Sroussi Marine , Saberzadeh-Ardestani Bahar , Cazelles Antoine , Lonardi Sara , Bergamo Francesca , Intini Rossana , Maddalena Giulia , Pietrantonio Filippo , Corti Francesca , Ambrosini Margherita , Martinetti Antonia , Germani Marco Maria. , Boccaccio Chiara , Vetere Guglielmo , Mouillet-Richard Sophie , de Reynies Aurelien , Sinicrope Frank A. , Cremolini Chiara , Laurent-Puig Pierre
Published: September 2024

Heatmap with unsupervised clustering in the validation cohort
Supplementary Figure S3 from Novel Genomic Risk Stratification Model for Primary Gastrointestinal Stromal Tumors (GIST) in the Imatinib and Adjuvant Therapy Era
Authors: Dermawan Josephine K. , Kelly Ciara , Gao Zhidong , Smith Shaleigh , Jadeja Bhumika , Singer Samuel , Tap William D. , Chi Ping , Antonescu Cristina R.
Published: September 2024

Supplementary Figure 3. Genomic risk groups versus tumor size and mitotic rate.
Supplementary Table S5 from Baseline mutations and ctDNA dynamics as prognostic and predictive factors in ER-positive/HER2-negative metastatic breast cancer patients
Authors: Pascual Javier , Gil-Gil Miguel , Proszek Paula , Zielinski Christoph , Reay Alistair , Ruiz-Borrego Manuel , Cutts Rosalind , Ciruelos Gil Eva M. , Feber Andrew , Muñoz-Mateu Montserrat , Swift Claire , Bermejo Begoña , Herranz Jesus , Margeli Vila Mireia , Antón Antonio , Kahan Zsuzsanna , Csöszi Tibor , Liu Yuan , Fernandez Garcia Daniel , Garcia-Murillas Isaac , Hubank Michael , Turner Nicholas C. , Martín Miguel
Published: September 2024

Supplementary Table 5. Baseline characteristics comparison between treatment arms in the selected study population
Supplementary Figure S5 from Baseline mutations and ctDNA dynamics as prognostic and predictive factors in ER-positive/HER2-negative metastatic breast cancer patients
Authors: Pascual Javier , Gil-Gil Miguel , Proszek Paula , Zielinski Christoph , Reay Alistair , Ruiz-Borrego Manuel , Cutts Rosalind , Ciruelos Gil Eva M. , Feber Andrew , Muñoz-Mateu Montserrat , Swift Claire , Bermejo Begoña , Herranz Jesus , Margeli Vila Mireia , Antón Antonio , Kahan Zsuzsanna , Csöszi Tibor , Liu Yuan , Fernandez Garcia Daniel , Garcia-Murillas Isaac , Hubank Michael , Turner Nicholas C. , Martín Miguel
Published: September 2024

Supplementary Figure 5. CDR and clinical benefit rate
within the longitudinal predictive ctDNA analysis.
Supplementary Data 1 from Preclinical efficacy of LP-184, a tumor site activated synthetic lethal therapeutic, in glioblastoma
Authors: Lal Bachchu , Kulkarni Aditya , McDermott Joseph , Rais Rana , Alt Jesse , Wu Ying , Lopez-Bertoni Hernando , Sall Sophie , Kathad Umesh , Zhou Jianli , Slusher Barbara S. , Bhatia Kishor , Laterra John
Published: September 2024

Supplemental Materials
Figures 1 from Preclinical efficacy of LP-184, a tumor site activated synthetic lethal therapeutic, in glioblastoma
Authors: Lal Bachchu , Kulkarni Aditya , McDermott Joseph , Rais Rana , Alt Jesse , Wu Ying , Lopez-Bertoni Hernando , Sall Sophie , Kathad Umesh , Zhou Jianli , Slusher Barbara S. , Bhatia Kishor , Laterra John
Published: September 2024

Supplemental Figures
Tables 3 from Tumor microenvironment modifications induced by afatinib in squamous cell carcinoma of the head and neck - a window-of-opportunity study (EORTC90111-24111)
Authors: Beyaert Simon P. , Loriot Axelle E. , Huyghe Nicolas D. , Goebbels Rose M. , Mendola Antonella , Govaerts Anne-Sophie , Fortpied Catherine , Baldin Pamela , Licitra Lisa F. , Lalami Yassine , Clement Paul M. , Machiels Jean-Pascal H. , Schmitz Sandra
Published: September 2024

Lists of expressed hallmark genesets in GSEA
Supplementary Figure S8 from Integrating Multisector Molecular Characterization into Personalized Peptide Vaccine Design for Patients with Newly Diagnosed Glioblastoma
Authors: Johanns Tanner M. , Garfinkle Elizabeth A.R. , Miller Katherine E. , Livingstone Alexandra J. , Roberts Kaleigh F. , Rao Venkata Lakshmi P. , Dowling Joshua L. , Chicoine Michael R. , Dacey Ralph G. , Zipfel Gregory J. , Kim Albert H. , Mardis Elaine R. , Dunn Gavin P.
Published: September 2024

CDR3beta sequences ranked by ratio
Data from A phase 2 study of epacadostat and pembrolizumab in patients with advanced sarcoma
Authors: Kelly Ciara M. , Qin Li-Xuan , Whiting Karissa A. , Richards Allison L. , Avutu Viswatej , Chan Jason E. , Chi Ping , Dickson Mark A. , Gounder Mrinal M. , Keohan Mary Louise. , Movva Sujana , Nacev Benjamin A. , Rosenbaum Evan , Adamson Travis , Singer Samuel , Bartlett Edmund K. , Crago Aimee M. , Yoon Sam S. , Hwang Sinchun , Erinjeri Joseph P. , Antonescu Cristina R. , Tap William D. , D'Angelo Sandra P.
Published: September 2024

Abstract
Purpose: Epacadostat, an indole 2,3 dioxygenase 1 (IDO1) inhibitor proposed to shift the tumor microenvironment toward an immune-stimulated state, showed early promise in melanoma but has not been studied in sarcoma. This study combined epacadostat with pembrolizumab, which has modest activity in select sarcoma subtypes. Experimental Design: This phase 2 study enrolled patients with advanced sarcoma into five cohorts including i) undifferentiated pleomorphic sarcoma (UPS)/myxofibrosarcoma, ii) liposarcoma (LPS), iii) leiomyosarcoma (LMS), iv) vascular sarcoma, including angiosarcoma and epithelioid hemangioendothelioma (EHE), and v) other subtypes. Patients received epacadostat 100 mg twice daily plus pembrolizumab at 200 mg/dose every 3 weeks. The primary endpoint was best objective response rate (ORR), defined as complete response (CR) and partial response (PR), at 24 weeks by Response Evaluation Criteria In Solid Tumors (RECIST v.1.1). Results: Thirty patients were enrolled (60% male; median age 54 years [range, 24–78]). The best ORR at 24 weeks was 3.3% (PR, n=1 [leiomyosarcoma]; two-sided 95% CI, 0.1%–17.2%). The median PFS was 7.6 weeks (two-sided 95% CI: 6.9–26.7). Treatment was well tolerated. Grade 3 treatment-related adverse events occurred in 23% (n=7) of patients. In paired pre- and post-treatment tumor samples, no association was found between treatment and PD-L1 or IDO1 tumor expression or IDO-pathway–related gene expression by RNA sequencing. No significant changes in serum tryptophan or kynurenine levels were observed after baseline. Conclusions: Combination epacadostat and pembrolizumab was well tolerated and showed limited antitumor activity in sarcoma. Correlative analyses suggested that inadequate IDO1 inhibition was achieved.
Data from Collagen-anchored interleukin-2 and interleukin-12 safely reprogram the tumor microenvironment in canine soft tissue sarcomas
Authors: Stinson Jordan A. , Sheen Allison , Momin Noor , Hampel Jordan , Bernstein Rebecca , Kamerer Rebecca , Fadl-Alla Bahaa , Samuelson Jonathan , Fink Elizabeth , Fan Timothy M. , Wittrup K. Dane
Published: September 2024

Abstract
Purpose: Cytokine therapies such as interleukin-2 and -12 suffer from impractically small therapeutic windows driven by their on-target, off-tumor activity, limiting their clinical potential despite potent antitumor effects. We previously engineered cytokines that bind and anchor to tumor collagen following intratumoral injection, and sought to test their safety and biomarker activity in spontaneous canine soft tissue sarcomas (STS). Methods: Collagen-binding cytokines were canine-ized to minimize immunogenicity and were used in a rapid dose-escalation study in healthy beagles to identify a maximum tolerated dose. Ten client-owned pet dogs with STS were then enrolled into trial, receiving cytokines at different intervals prior to surgical tumor excision. Tumor tissue was analyzed through immunohistochemistry (IHC) and Nanostring RNA profiling for dynamic changes within treated tumors. Archived, untreated STS samples were analyzed in parallel as controls. Results: Intratumorally administered collagen-binding IL-2 and IL-12 were well-tolerated by STS-bearing dogs, with only Grade 1/2 adverse events observed (mild fever, thrombocytopenia, neutropenia). IHC revealed enhanced T cell infiltrates, corroborated by an enhancement in gene expression associated with cytotoxic immune function. We found concordant increases in expression of counterregulatory genes that we hypothesize would contribute to a transient antitumor effect, and confirmed in mouse models that combination therapy to inhibit this counterregulation can improve responses to cytokine therapy. Conclusions: These results support the safety and activity of intratumorally-delivered, collagen-anchoring cytokines for inflammatory polarization of the canine soft tissue sarcoma tumor microenvironment. We are further evaluating the efficacy of this approach in additional canine cancers, including oral malignant melanoma.
Data from Osimertinib and selpercatinib efficacy, safety, and resistance in a multicenter, prospectively treated cohort of EGFR-mutant and RET fusion-positive lung cancers
Authors: Rotow Julia , Patel Jyoti D. , Hanley Matthew P. , Yu Helena , Awad Mark , Goldman Jonathan W. , Nechushtan Hovav , Scheffler Matthias , Kuo Chih-Hsi S. , Rajappa Senthil , Harada Guilherme , Clifford Sarah , Santucci Alison , Silva Laura , Tupper Rebecca , Oxnard Geoffrey R. , Kherani Jennifer , Drilon Alexander
Published: September 2024

Abstract
Purpose: Acquired RET fusions have been reported at resistance to treatment with EGFR inhibitors in EGFR-mutant non-small cell lung cancer (NSCLC), however, a multicenter cohort of patients with EGFR-mutant lung cancers treated with osimertinib and selpercatinib for RET fusion-mediated osimertinib resistance has not previously been published. Patients and methods: Patients who received selpercatinib in combination with osimertinib on a prospective expanded access clinical trial (NCT03906331) and single-patient compassionate use programs across five countries were centrally analyzed. All patients had advanced EGFR-mutant NSCLC with a RET fusion detected from tissue or plasma following osimertinib therapy. Clinicopathologic and outcomes data were collected. Results: Fourteen patients with EGFR-mutant and RET fusion-positive lung cancers who experienced prior progression on osimertinib received osimertinib and selpercatinib. EGFR exon 19 deletions (±T790M, 86%) and non-KIF5B fusions (CCDC6-RET 50%, NCOA4-RET 36%) predominated. Osimertinib 80mg daily and selpercatinib 80mg twice daily were the most commonly administered dosages. The response rate, disease control rate, and median treatment duration were 50% (95%CI 25%-75%, n=12), 83% (95%CI 55%-95%%), and 7.9 months (range 0.8-25+), respectively. Resistance was complex, involving EGFR on-target (EGFR C797S), RET on-target (RET G810S), and off-target (EML4-ALK/STRN-ALK, KRAS G12S, BRAF V600E) mechanisms, RET fusion loss, or polyclonal mechanisms. Conclusions: For patients with EGFR-mutant NSCLC with an acquired RET fusion as a mechanism of EGFR inhibitor resistance, the addition of selpercatinib to osimertinib was feasible, safe, and offered clinical benefit, supporting the prospective evaluation of this combination.
Data from Frequent overexpression of HER3 in brain metastases from breast and lung cancer
Authors: Tomasich Erwin , Steindl Ariane , Paiato Christina , Hatziioannou Teresa , Kleinberger Markus , Berchtold Luzia , Puhr Rainer , Hainfellner Johannes A. , Müllauer Leonhard , Widhalm Georg , Eckert Franziska , Bartsch Rupert , Heller Gerwin , Preusser Matthias , Berghoff Anna Sophie.
Published: September 2024

Abstract
Purpose: HER3 belongs to a family of receptor tyrosine kinases with oncogenic properties and is targeted by a variety of novel anticancer agents. There is a huge unmet medical need for systemic treatment options in patients with brain metastases (BM). Therefore, we aimed to investigate HER3 expression in BM of breast (BCa) and non-small cell lung (NSCLC) cancer as the basis for future clinical trial design. Experimental Design: We analyzed 180 BM samples of BCa or NSCLC and 47 corresponding NSCLC extracranial tissue. Immunohistochemistry was performed to evaluate protein expression of HER3, and immune cells based on CD3, CD8, and CD68. To identify dysregulated pathways based on differential DNA methylation patterns we used Infinium MethylationEPIC microarrays. Results: 99/132 (75.0%) of BCa-BM and 35/48 (72.9%) of NSCLC-BM presented with HER3 expression. Among BCa, HER2-positive and HER2-low BM showed significantly higher rates of HER3 co-expression than HER2-negative BM (87.1%/85.7% vs. 61.0%, p=0.004). Among NSCLC, HER3 was more abundantly expressed in BM than in matched extracranial samples (72.9% vs. 41.3%, p=0.003). No correlation of HER3 expression and intratumoral immune cell density was observed. HER3 expression did not correlate with overall survival from BM diagnosis. Methylation signatures differed according to HER3 status in BCa-BM samples. Pathway analysis revealed subtype specific differences, such as TrkB and Wnt signaling pathways dysregulated in HER2-positive and TNBC BM, respectively. Conclusions: HER3 is highly abundant in BM of BCa and NSCLC. Given the promising results of antibody-drug conjugates in extracranial disease, BM specific trials that target HER3 are warranted.
Data from Phase II Investigation of TVB-2640 (denifanstat) with Bevacizumab in Patients with First Relapse High-Grade Astrocytoma
Authors: Kelly William , Diaz Duque Adolfo Enrique , Michalek Joel , Konkel Brandon , Caflisch Laura , Chen Yidong , Pathuri Sarath Chand. , Madhusudanannair Kunnuparampil Vinu , Floyd John , Brenner Andrew
Published: September 2024

Abstract
Purpose: Glioblastoma (GBM) represents the most common primary brain tumor. Although anti-angiogenics are employed in the recurrent setting, they do not prolong survival. GBM is known to upregulate fatty acid synthase (FASN) to facilitate lipid biosynthesis. TVB-2640, a FASN inhibitor, impairs this activity. Patients and Methods: We conducted a prospective, single-center, open-label, unblinded, phase II study of TVB-2640 plus bevacizumab in patients with recurrent high-grade astrocytoma. Patients were randomized to TVB-2640 (100mg/m2 oral daily) plus bevacizumab (10mg/kg IV, D1 and D15) or bevacizumab monotherapy for cycle 1 only (28 days) for biomarker analysis. Thereafter, all patients received TVB-2640 plus bevacizumab until treatment-related toxicity or progressive disease. The primary endpoint was progression-free survival. Results: A total of 25 patients were enrolled. The most frequently reported AEs were palmar-plantar erythrodysesthesia, hypertension, mucositis, dry eye, fatigue and skin infection. Most were Grade 1 or 2 in intensity. The ORR for TVB-2640 plus bevacizumab was 56% (CR 17%, PR 39%). PFS6 for TVB-2640 plus bevacizumab was 31.4%. This represented a statistically significant improvement in PFS6 over historical bevacizumab monotherapy (BELOB 16%, p=0.008) and met the primary study endpoint. The observed OS6 was 68%, with survival not reaching significance by log rank test (p=0.56). Conclusions: In this phase II study of relapsed high-grade astrocytoma, TVB-2640 was found to be a well-tolerated oral drug that could be safely combined with bevacizumab. The favorable safety profile and response signals support the initiation of a larger multicenter trial of TVB-2640 plus bevacizumab in astrocytoma.
Data from PI3K Inhibition Restores and Amplifies Response to Ruxolitinib in Patients with Myelofibrosis
Authors: Moyo Tamara K. , Kishtagari Ashwin , Villaume Matthew T. , McMahon Brandon , Mohan Sanjay R. , Stopczynski Tess , Chen Sheau-Chiann , Fan Run , Huo Yuankai , Moon Hyeonsoo , Tang Yucheng , Bejan Cosmin A. , Childress Merrida , Anderson Ingrid , Rawling Kyle , Simons Rhea M. , Moncrief Ashley , Caza Rebekah , Dugger Laura , Collins Aunshka , Dudley Channing V. , Ferrell P. Brent , Byrne Michael , Strickland Stephen A. , Ayers Gregory D. , Landman Bennett A. , Mason Emily F. , Mesa Ruben A. , Palmer Jeanne M. , Michaelis Laura C. , Savona Michael R.
Published: September 2024

AbstractPurpose:
Treatment options are limited beyond JAK inhibitors for patients with primary myelofibrosis (MF) or secondary MF. Preclinical studies have revealed that PI3Kδ inhibition cooperates with ruxolitinib, a JAK1/2 inhibitor, to reduce proliferation and induce apoptosis of JAK2V617F-mutant cell lines.
Patients and Methods:
In a phase I dose-escalation and -expansion study, we evaluated the safety and efficacy of a selective PI3Kδ inhibitor, umbralisib, in combination with ruxolitinib in patients with MF who had a suboptimal response or lost response to ruxolitinib. Enrolled subjects were required to be on a stable dose of ruxolitinib for ≥8 weeks and continue that MTD at study enrollment. The recommended dose of umbralisib in combination with ruxolitinib was determined using a modified 3+3 dose-escalation design. Safety, pharmacokinetics, and efficacy outcomes were evaluated, and spleen size was measured with a novel automated digital atlas.
Results:
Thirty-seven patients with MF (median age, 67 years) with prior exposure to ruxolitinib were enrolled. A total of 2 patients treated with 800 mg umbralisib experienced reversible grade 3 asymptomatic pancreatic enzyme elevation, but no dose-limiting toxicities were seen at lower umbralisib doses. Two patients (5%) achieved a durable complete response, and 12 patients (32%) met the International Working Group-Myeloproliferative Neoplasms Research and Treatment response criteria of clinical improvement. With a median follow-up of 50.3 months for censored patients, overall survival was greater than 70% after 3 years of follow-up.
Conclusions:
Adding umbralisib to ruxolitinib in patients was well tolerated and may resensitize patients with MF to ruxolitinib without unacceptable rates of adverse events seen with earlier generation PI3Kδ inhibitors. Randomized trials testing umbralisib in the treatment of MF should be pursued.
Data from A Phase I/II trial of HER-2/neu vaccine primed autologous T-cell infusions in patients with treatment refractory HER-2/neu overexpressing breast cancer
Authors: Disis Mary L. , Dang Yushe , Coveler Andrew L. , Childs Jennifer S. , Higgins Doreen M. , Liu Ying , Zhou Jing , Mackay Sean , Salazar Lupe G.
Published: September 2024

Abstract
Purpose: High levels of Type I T-cells are needed for tumor eradication. We evaluated whether the HER2 specific vaccine primed T-cells are readily expanded ex vivo to achieve levels needed for therapeutic infusion. Patients and Methods: Phase I/II non-randomized trial of escalating doses of ex-vivo expanded HER2 specific T-cells after in vivo priming with a multiple peptide-based HER2 intracellular domain vaccine. Vaccines were given weekly for a total of 3 immunizations. Two weeks after the third vaccine, patients underwent leukapheresis for T-cell expansion, then received 3 escalating cell doses over 7-10-day intervals. Booster vaccines were administered after the T-cell infusions. The primary objective was safety. The secondary objectives included extent and persistence of HER2 specific T-cells, development of epitope spreading, and clinical response. Patients received a CT scan prior to enrollment and 1 month after the last T-cell infusion. Results: Nineteen patients received T-cell infusions. Treatment was well tolerated. One month after the last T-cell infusion, 82% of patients had significantly augmented T-cells to at least one of the immunizing epitopes and 81% of patients demonstrated enhanced intramolecular epitope spreading compared to baseline (p<0.05). There were no complete responses, one partial response (6%) and eight patients with stable disease (47%) for a disease control rate of 53%. The median survival for those with progressive disease was 20.5 months and for responders (PR+SD) was 45.0 months. Conclusions: Adoptive transfer of HER2 vaccine primed T-cells was feasible, associated with minimal toxicity, and resulted in an increased overall survival in responding patients.
Data from Cytochrome P450 oxidoreductase, POR, associated with severe paclitaxel-induced peripheral neuropathy in patients of European ancestry from ECOG-ACRIN E5103
Authors: Shen Fei , Jiang Guanglong , Philips Santosh , Gardner Laura , Xue Gloria , Cantor Erica , Ly Reynold C. , Osei Wilberforce , Wu Xi , Dang Chau , Northfelt Donald , Skaar Todd , Miller Kathy D. , Sledge George W. , Schneider Bryan P.
Published: September 2024

Abstract
Purpose: Paclitaxel is a widely used anti-cancer therapeutic. Peripheral neuropathy is the dose-limiting toxicity and negatively impacts quality of life. Rare germline gene markers were evaluated for predicting severe taxane induced peripheral neuropathy (TIPN) in the patients of European ancestry. In addition, the impact of Cytochrome P450 (CYP) 2C8, CYP3A4, and CYP3A5 metabolizer status on likelihood of severe TIPN was also assessed. Experimental design: Whole exome sequencing (WES) analyses were performed in 340 patients of European ancestry who received a standard dose and schedule of paclitaxel in the adjuvant, randomized phase III breast cancer trial, E5103. Patients who experienced grade 3-4 (n=168) TIPN were compared to controls (n=172) who did not experience TIPN. For the analyses, rare variants with a minor allele frequency ≤3% and predicted to be deleterious by protein prediction programs were retained. A gene-based, case-control analysis using SKAT was performed to identify genes that harbored an imbalance of deleterious variants associated with increased risk of severe TIPN. CYP star alleles for CYP2C8, CYP3A4, and CYP3A5 were called. An additive logistic regression model was performed to test the association of CYP2C8, CYP3A4, and CYP3A5 metabolizer status with severe TIPN. Results: Cytochrome P450 oxidoreductase, POR, was significantly associated with severe TIPN (p-value=1.8 ×10-6). Six variants were predicted to be deleterious in POR. There were no associations between CYP2C8, CYP3A4 or CYP3A5 metabolizer status with severe TIPN. Conclusions: Rare variants in POR, predict an increased risk of severe TIPN in patients of European ancestry who receive paclitaxel.
Data from Clinicopathologic, genomic, and immunophenotypic landscape of ATM mutations in non-small cell lung cancer
Authors: Ricciuti Biagio , Elkrief Arielle , Alessi Joao , Wang Xinan , Li Yvonne , Gupta Hersh , Muldoon Daniel M. , Bertram Arrien A. , Pecci Federica , Lamberti Giuseppe , Di Federico Alessandro , Barrichello Adriana , Vaz Victor R. , Gandhi Malini , Lee Elinton , Shapiro Geoffrey I. , Park Hyesun , Nishino Mizuki , Lindsay James , Felt Kristen D. , Sharma Bijaya , Cherniack Andrew D. , Rodig Scott , Gomez Daniel R. , Shaverdian Narek , Rakaee Mehrdad , Bandlamudi Chaitanya , Ladanyi Marc , Janne Pasi A. , Schoenfeld Adam J. , Sholl Lynette M. , Awad Mark M. , Cheng Michael L.
Published: September 2024

Abstract
Introduction: ATM is the most commonly mutated DNA damage and repair gene in non-small cell lung cancer (NSCLC), however limited characterization has been pursued. Methods: Clinicopathologic, genomic, and treatment data were collected for 5172 patients with NSCLC tumors which underwent genomic profiling. ATM immunohistochemistry (IHC) was performed on 182 NSCLCs with ATM mutations. Multiplexed immunofluorescence was performed on a subset of 535 samples to examine tumor-infiltrating immune cell subsets. Results: A total of 562 deleterious ATM mutations were identified in 9.7% of NSCLC samples. ATMMUT NSCLC was significantly associated with female sex (P=0.02), ever smoking status (P<0.001), non-squamous histology (P=0.004) and higher tumor mutational burden (DFCI: P<0.0001; MSK: P<0.0001) compared to ATMWT cases. Among 3687 NSCLCs with comprehensive genomic profiling, co-occurring KRAS, STK11, and ARID2 oncogenic mutations were significantly enriched among ATMMUT NSCLCs (Q<0.05), while TP53 and EGFR mutations were enriched in ATMWT NSCLCs. Among 182 ATMMUT samples with ATM IHC, tumors with nonsense, insertions/deletions, or splice site mutations were significantly more likely to display ATM loss by IHC (71.4% vs 28.6%, P<0.0001) compared to tumors with only predicted pathogenic missense mutations. Clinical outcomes to PD-(L)1 monotherapy (N=1522) and chemo-immunotherapy (N=951) were similar between ATMMUT and ATMWT NSCLCs. Patients with concurrent ATM/TP53 mutations had significantly improved response rate and progression-free survival with PD-(L)1 monotherapy. Conclusion: Deleterious ATM mutations defined a subset of NSCLC with unique clinicopathologic, genomic, and immunophenotypic features. Our data may serve as resource to guide interpretation of specific ATM mutations in NSCLC.
Data from CD49d expression identifies a biologically distinct subtype of chronic lymphocytic leukemia with inferior progression-free survival on BTK inhibitor therapy.
Authors: Alsadhan Anfal , Chen Jonathan , Gaglione Erika M. , Underbayev Chingiz , Tuma Pamela L. , Tian Xin , Freeman Lita A. , Baskar Sivasubramanian , Nierman Pia , Soto Susan , Itsara Andy , Ahn Inhye E. , Sun Clare , Bibikova Elena , Hartmann Tanja Nicole. , Mhibik Maissa , Wiestner Adrian
Published: September 2024

Abstract
Purpose: To determine the role of CD49d for response to Bruton’s tyrosine kinase inhibitors (BTKis) in patients with chronic lymphocytic leukemia (CLL). Methods: In patients treated with acalabrutinib (n=48), CD49d expression, VLA-4 integrin activation, and tumor transcriptomes of CLL cells were assessed. Clinical responses to BTKis were investigated in acalabrutinib (n=48; NCT02337829), and ibrutinib (n=73; NCT01500733) treated patients. Results: In patients treated with acalabrutinib, treatment induced lymphocytosis was comparable for both subgroups but resolved more rapidly for CD49d+ cases. Acalabrutinib inhibited constitutive VLA-4 activation but was insufficient to block BCR and CXCR4 mediated inside-out activation. Transcriptomes of CD49d+ and CD49d− cases were compared using RNA sequencing at baseline and at 1 and 6 months on treatment. Gene set enrichment analysis revealed increased constitutive NF-кB and JAK-STAT signaling, enhanced survival, adhesion, and migratory capacity in CD49d+ over CD49d− CLL that was maintained during therapy. In the combined cohorts of 121 BTKi treated patients, 48 (39.7%) progressed on treatment with BTK and/or PLCG2 mutations detected in 87% of CLL progressions. Consistent with a recent report, homogeneous and bimodal CD49d positive cases (the latter having concurrent CD49d+ and CD49d- CLL subpopulations, irrespective of the traditional 30% cutoff), had a shorter time to progression of 6.6 years, while 90% of cases homogenously CD49d negative were estimated progression-free at 8 years (P = .0004). Conclusions: CD49d/VLA-4 emerges as a microenvironmental factor that contributes to BTKi resistance in CLL. The prognostic value of CD49d is improved by considering bimodal CD49d expression.
Data from Targeting Replication Stress and Chemotherapy Resistance with a Combination of Sacituzumab Govitecan and Berzosertib: A Phase I Clinical Trial
Authors: Abel Melissa L. , Takahashi Nobuyuki , Peer Cody , Redon Christophe E. , Nichols Samantha , Vilimas Rasa , Lee Min-Jung , Lee Sunmin , Shelat Meenakshi , Kattapuram Robbie , Sciuto Linda , Pinkiert Danielle , Graham Chante , Butcher Donna , Karim Baktiar , Sharma Ajit Kumar. , Malin Justin , Kumar Rajesh , Schultz Christopher W. , Goyal Shubhank , Del Rivero Jaydira , Krishnamurthy Manan , Upadhyay Deep , Schroeder Brett , Sissung Tristan , Tyagi Manoj , Kim Jung , Pommier Yves , Aladjem Mirit , Raffeld Mark , Figg William Douglas. , Trepel Jane , Xi Liqiang , Desai Parth , Thomas Anish
Published: September 2024

Abstract
Purpose: Despite promising preclinical studies, toxicities have precluded combinations of chemotherapy and DNA damage response (DDR) inhibitors. We hypothesized that tumor-targeted chemotherapy delivery might enable clinical translation of such combinations. Patients and Methods: In a phase I trial, we combined sacituzumab govitecan, antibody-drug conjugate (ADC) that delivers topoisomerase-1 inhibitor SN-38 to tumors expressing Trop-2, with ataxia telangiectasia and Rad3-related (ATR) inhibitor berzosertib. Twelve patients were enrolled across three dose levels. Results: Treatment was well tolerated, with improved safety over conventional chemotherapy-based combinations, allowing escalation to the highest dose. No dose-limiting toxicities or clinically relevant ≥ grade 4 adverse events occurred. Tumor regressions were observed in two patients with neuroendocrine prostate cancer and a patient with small cell lung cancer transformed from EGFR-mutant non-small cell lung cancer. Conclusions: ADC-based delivery of cytotoxic payloads represents a new paradigm to increase efficacy of DDR inhibitors.
Data from Clonal Hematopoiesis in Young Women Treated for Breast Cancer
Authors: Gibson Christopher J. , Fell Geoffrey G. , Sella Tal , Sperling Adam S. , Snow Craig , Rosenberg Shoshana M. , Kirkner Gregory , Patel Ashka , Dillon Deborah , Bick Alexander G. , Neuberg Donna , Partridge Ann H. , Miller Peter G.
Published: September 2024

Abstract
Background: Young women treated for breast cancer with cytotoxic therapies are at risk for clonal hematopoiesis of indeterminate potential (CHIP), a condition in which blood cells carrying a somatic mutation associated with hematologic malignancy comprise at least 4% of the total blood system. CHIP has primarily been studied in older patient cohorts with limited clinical phenotyping. Materials and Methods: We performed targeted sequencing on longitudinal blood samples to characterize the clonal hematopoietic landscape of 878 women treated for breast cancer enrolled in the prospective Young Women’s Breast Cancer Study. Results: We identified somatic driver mutations in 252 study subjects (28.7%), but only 24 (2.7%) had clones large enough to meet criteria for CHIP. The most commonly mutated genes were DNMT3A and TET2, similar to mutations observed in non-cancer cohorts. At nine years median follow up, we found no association between the presence of a somatic blood mutation (regardless of clone size) and adverse breast cancer (distant relapse-free survival) or non-breast cancer-related outcomes in this cohort. A subset of paired blood samples obtained over four years showed no evidence of mutant clonal expansion, regardless of genotype. Finally, we identified a subset of patients with likely germline mutations in genes known to contribute to inherited cancer risk, such as TP53 and ATM. Conclusions: Our data show that for young women with early-stage breast cancer, CHIP is uncommon after cytotoxic exposure, is unlikely to contribute to adverse outcomes over the decade-long follow up and may not require additional monitoring if discovered incidentally.