bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from CD59-Regulated Ras Compartmentalization Orchestrates Antitumor T-cell Immunity
Authors: Li Luying , Ding Peipei , Lv Xinyue , Xie Suhong , Li Ling , Chen Jianfeng , Zhou Danlei , Wang Xiaochao , Wang Qi , Zhang Wei , Xu Yanqing , Lu Renquan , Hu Weiguo
Published: April 2023

Abstract
T cell–mediated immunotherapy represents a promising strategy for cancer treatment; however, it has achieved satisfactory clinical responses in only a limited population. Thus, a broader view of the T-cell immune response is required. The Ras/MAPK pathway operates in many important signaling cascades and regulates multiple cellular activities, including T-cell development, proliferation, and function. Herein, we found that the typical membrane-bound complement regulatory protein CD59 is located intracellularly in T cells and that the intracellular form is increased in the T cells of patients with cancer. When intracellular CD59 is abundant, it facilitates Ras transport to the inner plasma membrane via direct interaction; in contrast, when CD59 is insufficient or deficient, Ras is arrested in the Golgi, thus enhancing Ras/MAPK signaling and T-cell activation, proliferation, and function. mCd59ab deficiency almost completely abolished tumor growth and metastasis in tumor-bearing mice, in which CD4+ and CD8+ T cells were significantly increased compared with their proportions in wild-type littermates, and their proportions were inversely correlated with tumor growth. Using bone marrow transplantation and CD4+ and CD8+ T-cell depletion assays, we further demonstrated the critical roles of these cells in the potent antitumor activity induced by mCd59ab deficiency. Reducing CD59 expression also enhanced MAPK signaling and T-cell activation in human T cells. Therefore, the subcellular compartmentalization of Ras regulated by intracellular CD59 provides spatial selectivity for T-cell activation and a potential T cell–mediated immunotherapeutic strategy.
Data from The Conventional Dendritic Cell 1 Subset Primes CD8+ T Cells and Traffics Tumor Antigen to Drive Antitumor Immunity in the Brain
Authors: Bowman-Kirigin Jay A. , Desai Rupen , Saunders Brian T. , Wang Anthony Z. , Schaettler Maximilian O. , Liu Connor J. , Livingstone Alexandra J. , Kobayashi Dale K. , Durai Vivek , Kretzer Nicole M. , Zipfel Gregory J. , Leuthardt Eric C. , Osbun Joshua W. , Chicoine Michael R. , Kim Albert H. , Murphy Kenneth M. , Johanns Tanner M. , Zinselmeyer Bernd H. , Dunn Gavin P.
Published: April 2023

Abstract
The central nervous system (CNS) antigen-presenting cell (APC) that primes antitumor CD8+ T-cell responses remains undefined. Elsewhere in the body, the conventional dendritic cell 1 (cDC1) performs this role. However, steady-state brain parenchyma cDC1 are extremely rare; cDCs localize to the choroid plexus and dura. Thus, whether the cDC1 play a function in presenting antigen derived from parenchymal sources in the tumor setting remains unknown. Using preclinical glioblastoma (GBM) models and cDC1-deficient mice, we explored the presently unknown role of cDC1 in CNS antitumor immunity. We determined that, in addition to infiltrating the brain tumor parenchyma itself, cDC1 prime neoantigen-specific CD8+ T cells against brain tumors and mediate checkpoint blockade-induced survival benefit. We observed that cDC, including cDC1, isolated from the tumor, the dura, and the CNS-draining cervical lymph nodes harbored a traceable fluorescent tumor antigen. In patient samples, we observed several APC subsets (including the CD141+ cDC1 equivalent) infiltrating glioblastomas, meningiomas, and dura. In these same APC subsets, we identified a tumor-specific fluorescent metabolite of 5-aminolevulinic acid, which fluorescently labeled tumor cells during fluorescence-guided GBM resection. Together, these data elucidate the specialized behavior of cDC1 and suggest that cDC1 play a significant role in CNS antitumor immunity.
Data from CD161 Characterizes an Inflamed Subset of Cytotoxic T Lymphocytes Associated with Prolonged Survival in Human Papillomavirus–Driven Oropharyngeal Cancer
Authors: Wei Ye , Xu Tingting , Li Chong , Zhou Xin , Qian Wei , Shen Chunying , Wang Qifeng , Xing Xing , Ou Xiaomin , He Xiayun , Yin Hongmei , Hu Chaosu , Wang Yu , Ji Qinghai , Su Fengtao , Lu Xueguan
Published: April 2023

Abstract
Human papillomavirus (HPV)–driven oropharyngeal carcinoma (OPSCC) is distinct from tobacco- or alcohol-associated OPSCC and has a unique immune landscape. Studies have supported the heterogeneity of T cells, accompanied by a broad repertoire of T-cell responses, within tumors driven by HPV infection. However, the phenotype and function of these HPV-related T cells remain unclear. Using a combination of single-cell RNA sequencing, flow cytometry, pharmacologic inhibition, and immunofluorescence staining, we explored the prognostic implication of HPV-related T cells and further validated our findings in two independent cohorts. Cytotoxic T lymphocytes (CTL) within OPSCC displayed a spectrum of transcriptional signatures. Among which, we identified CD161 receptor, encoded by KLRB1, as a potential marker to distinguish the CTL subsets in HPV-positive OPSCC with a divergent evolutionary trajectory. In-depth analysis revealed that CD161+ CTLs exhibited a more robust immune response over the CD161− counterparts and a T cell–inflamed phenotype that could be further reinvigorated by immune-checkpoint blockade. Despite the high expression of exhaustion markers, reinforcement of CD161+ CTL reactivity was expected to boost immune responses, considering their functional reversibility. We further confirmed that the high level of intratumoral CD161+ CTLs associated with a favorable treatment response and prolonged overall survival. Therefore, our research not only provides an insight into the immune landscape of HPV-driven OPSCC but also sheds light on a special subset of CTLs with prognostic and therapeutic significance.
Data from Cancer Cell Resistance to IFNγ Can Occur via Enhanced Double-Strand Break Repair Pathway Activity
Authors: Han Tong , Wang Xujun , Shi Sailing , Zhang Wubing , Wang Jue , Wu Qiu , Li Ziyi , Fu Jingxin , Zheng Rongbin , Zhang Jiamin , Tang Qin , Zhang Peng , Wang Chenfei
Published: April 2023

Abstract
The pleiotropic cytokine interferon-gamma (IFNγ) is associated with cytostatic, antiproliferation, and proapoptotic functions in cancer cells. However, resistance to IFNγ occurs in many cancer cells, and the underlying mechanism is not fully understood. To investigate potential IFNγ-resistance mechanisms, we performed IFNγ-sensitivity screens in more than 40 cancer cell lines and characterized the sensitive and resistant cell lines. By applying CRISPR screening and transcriptomic profiling in both IFNγ-sensitive and IFNγ-resistant cells, we discovered that activation of double-strand break (DSB) repair genes could result in IFNγ resistance in cancer cells. Suppression of single-strand break (SSB) repair genes increased the dependency on DSB repair genes after IFNγ treatment. Furthermore, inhibition of the DSB repair pathway exhibited a synergistic effect with IFNγ treatment both in vitro and in vivo. The relationship between the activation of DSB repair genes and IFNγ resistance was further confirmed in clinical tumor profiles from The Cancer Genome Atlas (TCGA) and immune checkpoint blockade (ICB) cohorts. Our study provides comprehensive resources and evidence to elucidate a mechanism of IFNγ resistance in cancer and has the potential to inform combination therapies to overcome immunotherapy resistance.
Data from Reverse Translation Identifies the Synergistic Role of Immune Checkpoint Blockade and IL15 to Enhance Immunotherapy of Ovarian Cancer
Authors: Felices Martin , Wesley Erin , Bendzick Laura E. , Kodal Behiye , Hopps Rachel , Grzywacz Bartosz , Hinderlie Peter , Miller Jeffrey S. , Geller Melissa A.
Published: April 2023

Abstract
Immune checkpoint blockade (ICB) has changed the standard of care for many patients with cancer, yet no ICB is approved for ovarian cancer. We hypothesized that maintenance therapy with an IL15 “superagonist” (N-803) and ICB in combination could induce potent immune activation in ovarian cancer. Using flow cytometry, cytometry by time of flight analysis, and cytotoxicity assays, we analyzed patient samples from women with advanced epithelial ovarian cancer treated with N-803 for indications of PD-1/PD-L1 upregulation with this treatment. In addition, ICB and N-803 were evaluated in preclinical studies to determine the functional impact of combination therapy on natural killer (NK) cells in vitro and in vivo. We observed that N-803 stimulated initial NK-cell expansion in patient samples; however, proliferation was not sustained beyond 2 weeks despite continued treatment. This result was reverse translated back to the laboratory to determine the functional relevance of this finding. The addition of ICB with an antibody-dependent cellular cytotoxicity IgG1 antibody against PD-L1 (avelumab) or an IgG4 antibody against PD-1 (pembrolizumab) enhanced N-803 induced NK-cell function in vitro. Using models of human ovarian cancer and NK-cell adoptive transfer in mice, we showed enhanced antitumor control with N-803 and ICB, as well as a combination effect that enhanced NK-cell persistence and expansion in vivo. This work suggests that PD-1/PD-L1 blockade combined with IL15 signaling may overcome resistance to cytokine therapy in ovarian cancer.
Supplementary Figures 1-15, Supplementary Table 1 from ROBO1 Promotes Homing, Dissemination, and Survival of Multiple Myeloma within the Bone Marrow Microenvironment
Authors: Bianchi Giada , Czarnecki Peter G. , Ho Matthew , Roccaro Aldo M. , Sacco Antonio , Kawano Yawara , Gullà Annamaria , Samur Anil Aktas , Chen Tianzeng , Wen Kenneth , Tai Yu-Tzu , Moscvin Maria , Wu Xinchen , Camci-Unal Gulden , Da Vià Matteo C. , Bolli Niccolo' , Sewastianik Tomasz , Carrasco Ruben D. , Ghobrial Irene M. , Anderson Kenneth C.
Published: April 2023

Supplementary Figure 1 showing ROBO1 expression in primary MM cells versus normal donor bone marrow plasma cells via gene expression profiling and immunohistochemistry. Supplementary Figure 2 showing distribution of ROBO1 expression in the CoMMpass database; ROBO1 expression in CoMMpass database according to cytogenetics; ROBO1 expression in IFM170 database according to cytogenetics; ROBO1 expression in t(4;14) cell lines WT or KO for MMSET. Supplementary Figure 3 showing ROBO1 protein down regulation after ROBO1 knock down via shRNA. Supplementary Figure 4 showing effects of shRNA4- and shRNA-5 mediated ROBO1 KD on cell viability across a panel of MM cell lines with western confirming proper protein down regulation. Supplementary Figure 5 showing successful ROBO1 KO across several KMS11 monoclones, but not H929 monoclones. Supplementary Figure 6 showing expression of ROBO1 FL construct in polyclonally and monoclonally-transduced OPM2 cells. Supplementary Figure 7 showing expression of FL ROBO1 addback in distinct KMS11 ROBO1 KO monoclones. Supplementary Figure 8 showing radiographic images of WT versus KO ROBO1 mu-SCID mice. Supplementary Figure 9 showing adhesion defect in ROBO1 KO KMS11 cells that is fully rescued by FL ROBO1 addback. Supplementary Figure 10 showing Kaplan-Meier survival curve of disseminated mouse model injected with ROBO1 KO versus FL OPM2 cells. Supplementary Figure 11 showing cleaved cytosolic ROBO1 fragments in 293T cells transduced with FL ROBO1 tagged with C-LAP tag and in WT MM.1S cells. Supplementary Figure 12 showing interacting partners of ROBO1 cytosolic domain as deconvoluted via STRING database. Supplementary Figure 13 showing differentially expressed genes in ROBO1 WT versus KO plasmacytoma represented via Volcano plot. Supplementary Figure 14 showing gene set enrichment analysis of differentially expressed genes in ROBO1 WT versus KO plasmacytoma. Supplementary Figure 15 showing schema of patient-derived ROBO1 mutation and expression of G674 truncation in WT and KO ROBO1 OPM2 cells. Supplementary Table 1 showing clinical annotation of newly diagnosed MM parents used in Supplementary figure 1.
Supplementary Figure from Identification and Targeting of the Developmental Blockade in Extranodal Natural Killer/T-cell Lymphoma
Authors: Mundy-Bosse Bethany L. , Weigel Christoph , Wu Yue-Zhong , Abdelbaky Salma , Youssef Youssef , Casas Susana Beceiro , Polley Nicholas , Ernst Gabrielle , Young Karen A. , McConnell Kathleen K. , Nalin Ansel P. , Wu Kevin G. , Broughton Megan , Lordo Matthew R. , Altynova Ekaterina , Hegewisch-Solloa Everardo , Enriquez-Vera Daniel Y. , Dueñas Daniela , Barrionuevo Carlos , Yu Shan-Chi , Saleem Atif , Suarez Carlos J. , Briercheck Edward L. , Molina-Kirsch Hernan , Loughran Thomas P. , Weichenhan Dieter , Plass Christoph , Reneau John C. , Mace Emily M. , Gamboa Fabiola Valvert , Weinstock David M. , Natkunam Yasodha , Caligiuri Michael A. , Mishra Anjali , Porcu Pierluigi , Baiocchi Robert A. , Brammer Jonathan E. , Freud Aharon G. , Oakes Christopher C.
Published: April 2023

Supplementary Figure from Identification and Targeting of the Developmental Blockade in Extranodal Natural Killer/T-cell Lymphoma
Supplementary Data from Identification and Targeting of the Developmental Blockade in Extranodal Natural Killer/T-cell Lymphoma
Authors: Mundy-Bosse Bethany L. , Weigel Christoph , Wu Yue-Zhong , Abdelbaky Salma , Youssef Youssef , Casas Susana Beceiro , Polley Nicholas , Ernst Gabrielle , Young Karen A. , McConnell Kathleen K. , Nalin Ansel P. , Wu Kevin G. , Broughton Megan , Lordo Matthew R. , Altynova Ekaterina , Hegewisch-Solloa Everardo , Enriquez-Vera Daniel Y. , Dueñas Daniela , Barrionuevo Carlos , Yu Shan-Chi , Saleem Atif , Suarez Carlos J. , Briercheck Edward L. , Molina-Kirsch Hernan , Loughran Thomas P. , Weichenhan Dieter , Plass Christoph , Reneau John C. , Mace Emily M. , Gamboa Fabiola Valvert , Weinstock David M. , Natkunam Yasodha , Caligiuri Michael A. , Mishra Anjali , Porcu Pierluigi , Baiocchi Robert A. , Brammer Jonathan E. , Freud Aharon G. , Oakes Christopher C.
Published: April 2023

Supplementary Data from Identification and Targeting of the Developmental Blockade in Extranodal Natural Killer/T-cell Lymphoma
Supplementary Data from ZNF384 Fusion Oncoproteins Drive Lineage Aberrancy in Acute Leukemia
Authors: Dickerson Kirsten M. , Qu Chunxu , Gao Qingsong , Iacobucci Ilaria , Gu Zhaohui , Yoshihara Hiroki , Backhaus Emily A. , Chang Yunchao , Janke Laura J. , Xu Beisi , Wu Gang , Papachristou Evangelia K. , D'Santos Clive S. , Roberts Kathryn G. , Mullighan Charles G.
Published: April 2023

Supplementary Data from ZNF384 Fusion Oncoproteins Drive Lineage Aberrancy in Acute Leukemia
Supplementary Table from Genetic and Transcriptional Contributions to Relapse in Normal Karyotype Acute Myeloid Leukemia
Authors: Petti Allegra A. , Khan Saad M. , Xu Ziheng , Helton Nichole , Fronick Catrina C. , Fulton Robert , Ramakrishnan Sai M. , Nonavinkere Srivatsan Sridhar , Heath Sharon E. , Westervelt Peter , Payton Jacqueline E. , Walter Matthew J. , Link Daniel C. , DiPersio John , Miller Christopher , Ley Timothy J.
Published: April 2023

Supplementary Table from Genetic and Transcriptional Contributions to Relapse in Normal Karyotype Acute Myeloid Leukemia
Supplementary Data from Genetic and Transcriptional Contributions to Relapse in Normal Karyotype Acute Myeloid Leukemia
Authors: Petti Allegra A. , Khan Saad M. , Xu Ziheng , Helton Nichole , Fronick Catrina C. , Fulton Robert , Ramakrishnan Sai M. , Nonavinkere Srivatsan Sridhar , Heath Sharon E. , Westervelt Peter , Payton Jacqueline E. , Walter Matthew J. , Link Daniel C. , DiPersio John , Miller Christopher , Ley Timothy J.
Published: April 2023

Supplementary Data from Genetic and Transcriptional Contributions to Relapse in Normal Karyotype Acute Myeloid Leukemia
Supplementary Table from Convergent Clonal Evolution of Signaling Gene Mutations Is a Hallmark of Myelodysplastic Syndrome Progression
Authors: Menssen Andrew J. , Khanna Ajay , Miller Christopher A. , Nonavinkere Srivatsan Sridhar , Chang Gue Su , Shao Jin , Robinson Joshua , O'Laughlin Michele , Fronick Catrina C. , Fulton Robert S. , Brendel Kimberly , Heath Sharon E. , Saba Raya , Welch John S. , Spencer David H. , Payton Jacqueline E. , Westervelt Peter , DiPersio John F. , Link Daniel C. , Schuelke Matthew J. , Jacoby Meagan A. , Duncavage Eric J. , Ley Timothy J. , Walter Matthew J.
Published: April 2023

Supplementary Table from Convergent Clonal Evolution of Signaling Gene Mutations Is a Hallmark of Myelodysplastic Syndrome Progression
Supplementary Data from Transcriptional Plasticity Drives Leukemia Immune Escape
Authors: Eagle Kenneth , Harada Taku , Kalfon Jérémie , Perez Monika W. , Heshmati Yaser , Ewers Jazmin , Koren Jošt Vrabič , Dempster Joshua M. , Kugener Guillaume , Paralkar Vikram R. , Lin Charles Y. , Dharia Neekesh V. , Stegmaier Kimberly , Orkin Stuart H. , Pimkin Maxim
Published: April 2023

Supplementary Data from Transcriptional Plasticity Drives Leukemia Immune Escape
Supplementary Data from RETRACTED: In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
Authors: Murakami Shohei , Barroca Vilma , Perié Leïla , Bravard Anne , Bernardino-Sgherri Jacqueline , Tisserand Amandine , Devanand Caroline , Edmond Valérie , Magniez Aurélie , Tenreira Bento Sabrina , Torres Claire , Pasquier Florence , Plo Isabelle , Vainchenker William , Villeval Jean-Luc , Roméo Paul-Henri , Lewandowski Daniel
Published: April 2023

Supplementary Data from RETRACTED: In Vivo Monitoring of Polycythemia Vera Development Reveals Carbonic Anhydrase 1 as a Potent Therapeutic Target
Supplementary Data from Follicular Lymphoma Microenvironment Characteristics Associated with Tumor Cell Mutations and MHC Class II Expression
Authors: Han Guangchun , Deng Qing , Marques-Piubelli Mario L. , Dai Enyu , Dang Minghao , Ma Man Chun John , Li Xubin , Yang Haopeng , Henderson Jared , Kudryashova Olga , Meerson Mark , Isaev Sergey , Kotlov Nikita , Nomie Krystle J. , Bagaev Alexander , Parra Edwin R. , Solis Soto Luisa M. , Parmar Simrit , Hagemeister Fredrick B. , Ahmed Sairah , Iyer Swaminathan P. , Samaniego Felipe , Steiner Raphael , Fayad Luis , Lee Hun , Fowler Nathan H. , Flowers Christopher R. , Strati Paolo , Westin Jason R. , Neelapu Sattva S. , Nastoupil Loretta J. , Vega Francisco , Wang Linghua , Green Michael R.
Published: April 2023

Supplementary Data from Follicular Lymphoma Microenvironment Characteristics Associated with Tumor Cell Mutations and MHC Class II Expression
Data from PRPS-ST: A Protocol-Agnostic Self-training Method for Gene Expression–Based Classification of Blood Cancers
Authors: Jiang Aixiang , Hilton Laura K. , Tang Jeffrey , Rushton Christopher K. , Grande Bruno M. , Scott David W. , Morin Ryan D.
Published: April 2023

Abstract
Gene expression classifiers are gaining increasing popularity for stratifying tumors into subgroups with distinct biological features. A fundamental limitation shared by current classifiers is the requirement for comparable training and testing datasets. Here, we describe a self-training implementation of our probability ratio-based classification prediction score method (PRPS-ST), which facilitates the porting of existing classification models to other gene expression datasets. In comparison with gold standards, we demonstrate favorable performance of PRPS-ST in gene expression–based classification of diffuse large B-cell lymphoma (DLBCL) and B-lineage acute lymphoblastic leukemia (B-ALL) using a diverse variety of gene expression data types and preprocessing methods, including in classifications with a high degree of class imbalance. Tumors classified by our method were significantly enriched for prototypical genetic features of their respective subgroups. Interestingly, this included cases that were unclassifiable by established methods, implying the potential enhanced sensitivity of PRPS-ST.
Significance:
The adoption of binary classifiers such as cell of origin (COO) has been thwarted, in part, by the challenges imposed by batch effects and continual evolution of gene expression technologies. PRPS-ST resolves this by enabling classifiers to be ported across platforms while retaining high accuracy.

This article is highlighted in the In This Issue feature, p. 215
Data from Bortezomib Induces Anti–Multiple Myeloma Immune Response Mediated by cGAS/STING Pathway Activation
Authors: Gulla Annamaria , Morelli Eugenio , Samur Mehmet K. , Botta Cirino , Hideshima Teru , Bianchi Giada , Fulciniti Mariateresa , Malvestiti Stefano , Prabhala Rao H. , Talluri Srikanth , Wen Kenneth , Tai Yu-Tzu , Richardson Paul G. , Chauhan Dharminder , Sewastianik Tomasz , Carrasco Ruben D. , Munshi Nikhil C. , Anderson Kenneth C.
Published: April 2023

Abstract
The proteasome inhibitor bortezomib induces apoptosis in multiple myeloma cells and has transformed patient outcome. Using in vitro as well as in vivo immunodeficient and immunocompetent murine multiple myeloma models, we here show that bortezomib also triggers immunogenic cell death (ICD), characterized by exposure of calreticulin on dying multiple myeloma cells, phagocytosis of tumor cells by dendritic cells, and induction of multiple myeloma–specific immunity. We identify a bortezomib-triggered specific ICD gene signature associated with better outcome in two independent cohorts of patients with multiple myeloma. Importantly, bortezomib stimulates multiple myeloma cell immunogenicity via activation of the cGAS/STING pathway and production of type I IFNs, and STING agonists significantly potentiate bortezomib-induced ICD. Our study therefore delineates mechanisms whereby bortezomib exerts immunotherapeutic activity and provides the framework for clinical trials of STING agonists with bortezomib to induce potent tumor-specific immunity and improve patient outcome in multiple myeloma.
Significance:
Our study demonstrates that cGAS/STING-dependent immunostimulatory activity mediates bortezomib anti-myeloma activity in experimental models and associates with clinical response to bortezomib in patients with multiple myeloma. These findings provide the rationale for clinical evaluation of STING agonists to further potentiate anti–multiple myeloma immune response.

See related commentary by Zitvogel and Kroemer, p. 405.

This article is highlighted in the In This Issue feature, p. 403
Data from Translational Activation of ATF4 through Mitochondrial Anaplerotic Metabolic Pathways Is Required for DLBCL Growth and Survival
Authors: Li Meng , Teater Matthew R. , Hong Jun Young , Park Noel R. , Duy Cihangir , Shen Hao , Wang Ling , Chen Zhengming , Cerchietti Leandro , Davidson Shawn M. , Lin Hening , Melnick Ari M.
Published: April 2023

Abstract
Diffuse large B-cell lymphomas (DLBCL) are broadly dependent on anaplerotic metabolism regulated by mitochondrial SIRT3. Herein we find that translational upregulation of ATF4 is coupled with anaplerotic metabolism in DLBCLs due to nutrient deprivation caused by SIRT3 driving rapid flux of glutamine into the tricarboxylic acid (TCA) cycle. SIRT3 depletion led to ATF4 downregulation and cell death, which was rescued by ectopic ATF4 expression. Mechanistically, ATF4 translation is inhibited in SIRT3-deficient cells due to the increased pools of amino acids derived from compensatory autophagy and decreased glutamine consumption by the TCA cycle. Absence of ATF4 further aggravates this state through downregulation of its target genes, including genes for amino acid biosynthesis and import. Collectively, we identify a SIRT3–ATF4 axis required to maintain survival of DLBCL cells by enabling them to optimize amino acid uptake and utilization. Targeting ATF4 translation can potentiate the cytotoxic effect of SIRT3 inhibitor to DLBCL cells.
Significance:
We discovered the link between SIRT3 and ATF4 in DLBCL cells, which connected lymphoma amino acid metabolism with ATF4 translation via metabolic stress signals. SIRT3–ATF4 axis is required in DLBCL cells regardless of subtype, which indicates a common metabolic vulnerability in DLBCLs and can serve as a therapeutic target.

This article is highlighted in the In This Issue feature, p. 1
Data from Patients Recently Treated for B-lymphoid Malignancies Show Increased Risk of Severe COVID-19
Authors: Rubinstein Samuel M. , Bhutani Divaya , Lynch Ryan C. , Hsu Chih-Yuan , Shyr Yu , Advani Shailesh , Mesa Ruben A. , Mishra Sanjay , Mundt Daniel P. , Shah Dimpy P. , Sica R. Alejandro , Stockerl-Goldstein Keith E. , Stratton Catherine , Weiss Matthias , Beeghly-Fadiel Alicia , Accordino Melissa , Assouline Sarit E. , Awosika Joy , Bakouny Ziad , Bashir Babar , Berg Stephanie , Bilen Mehmet Asim , Castellano Cecilia A. , Cogan Jacob C. , KC Devendra , Friese Christopher R. , Gupta Shilpa , Hausrath Daniel , Hwang Clara , Johnson Nathalie A. , Joshi Monika , Kasi Anup , Klein Elizabeth J. , Koshkin Vadim S. , Kuderer Nicole M. , Kwon Daniel H. , Labaki Chris , Latif Tahir , Lau Eric , Li Xuanyi , Lyman Gary H. , McKay Rana R. , Nagaraj Gayathri , Nizam Amanda , Nonato Taylor K. , Olszewski Adam J. , Polimera Hyma V. , Portuguese Andrew J. , Puc Matthew M. , Razavi Pedram , Rosovski Rachel , Schmidt Andrew , Shah Sumit A. , Shastri Aditi , Su Christopher , Torka Pallawi , Wise-Draper Trisha M. , Zubiri Leyre , Warner Jeremy L. , Thompson Michael A.
Published: April 2023

Abstract
Patients with B-lymphoid malignancies have been consistently identified as a population at high risk of severe COVID-19. Whether this is exclusively due to cancer-related deficits in humoral and cellular immunity, or whether risk of severe COVID-19 is increased by anticancer therapy, is uncertain. Using data derived from the COVID-19 and Cancer Consortium (CCC19), we show that patients treated for B-lymphoid malignancies have an increased risk of severe COVID-19 compared with control populations of patients with non–B-lymphoid malignancies. Among patients with B-lymphoid malignancies, those who received anticancer therapy within 12 months of COVID-19 diagnosis experienced increased COVID-19 severity compared with patients with non–recently treated B-lymphoid malignancies, after adjustment for cancer status and several other prognostic factors. Our findings suggest that patients recently treated for a B-lymphoid malignancy are at uniquely high risk for severe COVID-19.
Significance:
Our study suggests that recent therapy for a B-lymphoid malignancy is an independent risk factor for COVID-19 severity. These findings provide rationale to develop mitigation strategies targeted at the uniquely high-risk population of patients with recently treated B-lymphoid malignancies.

This article is highlighted in the In This Issue feature, p. 171
Data from Type I but Not Type II Calreticulin Mutations Activate the IRE1α/XBP1 Pathway of the Unfolded Protein Response to Drive Myeloproliferative Neoplasms
Authors: Ibarra Juan , Elbanna Yassmin A. , Kurylowicz Katarzyna , Ciboddo Michele , Greenbaum Harrison S. , Arellano Nicole S. , Rodriguez Deborah , Evers Maria , Bock-Hughes Althea , Liu Chenyu , Smith Quinn , Lutze Julian , Baumeister Julian , Kalmer Milena , Olschok Kathrin , Nicholson Benjamin , Silva Diane , Maxwell Luke , Dowgielewicz Jonathan , Rumi Elisa , Pietra Daniela , Casetti Ilaria Carola , Catricala Silvia , Koschmieder Steffen , Gurbuxani Sandeep , Schneider Rebekka K. , Oakes Scott A. , Elf Shannon E.
Published: April 2023

Abstract
Approximately 20% of patients with myeloproliferative neoplasms (MPN) harbor mutations in the gene calreticulin (CALR), with 80% of those mutations classified as either type I or type II. While type II CALR-mutant proteins retain many of the Ca2+ binding sites present in the wild-type protein, type I CALR-mutant proteins lose these residues. The functional consequences of this differential loss of Ca2+ binding sites remain unexplored. Here, we show that the loss of Ca2+ binding residues in the type I mutant CALR protein directly impairs its Ca2+ binding ability, which in turn leads to depleted endoplasmic reticulum (ER) Ca2+ and subsequent activation of the IRE1α/XBP1 pathway of the unfolded protein response. Genetic or pharmacologic inhibition of IRE1α/XBP1 signaling induces cell death in type I mutant but not type II mutant or wild-type CALR-expressing cells, and abrogates type I mutant CALR-driven MPN disease progression in vivo.
Significance:
Current targeted therapies for CALR-mutated MPNs are not curative and fail to differentiate between type I- versus type II-driven disease. To improve treatment strategies, it is critical to identify CALR mutation type–specific vulnerabilities. Here we show that IRE1α/XBP1 represents a unique, targetable dependency specific to type I CALR-mutated MPNs.

This article is highlighted in the In This Issue feature, p. 265
Supplementary Figure 1 from Phase I Trial of Autologous RNA-electroporated cMET-directed CAR T cells Administered Intravenously in Patients with Melanoma & Breast Carcinoma
Authors: Shah Payal D , Huang Alexander C. , Xu Xiaowei , Orlowski Robert , Amaravadi Ravi K , Schuchter Lynn M. , Zhang Paul , Tchou Julia , Matlawski Tina , Cervini Amanda , Shea Joanne , Gilmore Joan , Lledo Lester , Dengel Karen , Marshall Amy , Wherry E. John , Linette Gerald P , Brennan Andrea Lynne , Gonzalez Vanessa E , Kulikovskaya Irina , Lacey Simon F , Plesa Gabriela , June Carl H , Vonderheide Robert H , Mitchell Tara C
Published: April 2023

Supplementary Figure 1. : Representative immunohistochemical staining for Subject 74 with metastatic melanoma; lymph node biopsy. Panel A: pS6 staining prior to infusion; Panel B: pS6 staining at post-infusion biopsy; Panel C: Ki-67 staining prior to infusion; Panel D: Ki-67 staining at post-infusion biopsy.
Supplementary Data from Chimeric Antigen Receptors Directed at Mutant KRAS Exhibit an Inverse Relationship Between Functional Potency and Neoantigen Selectivity
Authors: Tokatlian Talar , Asuelime Grace E. , Naradikian Martin S. , Mock Jee-Young , Daris Mark E. , Martin Aaron D. , Toledo Warshaviak Dora , Kamb Alexander , Hamburger Agnes E.
Published: April 2023

S.Figures 1-5 and S.Table 1
Supplementary Table 1 from Resolving the Heterogeneous Tumor-Centric Cellular Neighborhood through Multiplexed, Spatial Paracrine Interactions in the Setting of Immune Checkpoint Blockade
Authors: Maus Rachel L.G. , Leontovich Alexey A. , Moore Raymond M. , Becher Laura , Nevala Wendy K. , Flotte Thomas J. , Guo Ruifeng , Schimke Jill M. , Dicke Betty A. , Yan Yiyi , Markovic Svetomir N.
Published: April 2023

Antibody reagents and validation for MxIF panel design
Supplement 5 from The Vaginal Microbiome is Associated with Endometrial Cancer Grade and Histology
Authors: Hakimjavadi Hesamedin , George Sophia H. , Taub Michael , Dodds Leah V. , Sanchez-Covarrubias Alex P. , Huang Marilyn , Pearson J. Matt , Slomovitz Brian M. , Kobetz Erin N. , Gharaibeh Raad , Sowamber Ramlogan , Pinto Andre , Chamala Srikar , Schlumbrecht Matthew P.
Published: April 2023

Microbial abundance by histotype
Supplementary Figures S1-S8 from The Tankyrase Inhibitor OM-153 Demonstrates Antitumor Efficacy and a Therapeutic Window in Mouse Models
Authors: Brinch Shoshy A. , Amundsen-Isaksen Enya , Espada Sandra , Hammarström Clara , Aizenshtadt Aleksandra , Olsen Petter A. , Holmen Lone , Høyem Merete , Scholz Hanne , Grødeland Gunnveig , Sowa Sven T. , Galera-Prat Albert , Lehtiö Lari , Meerts Ilonka A.T.M. , Leenders Ruben G.G. , Wegert Anita , Krauss Stefan , Waaler Jo
Published: April 2023

Supplementary Figure S1. Chemical structures of selected tankyrase inhibitors. Supplementary Figure S2. OM-153 specifically inhibits TNKS1/2 and WNT/β-catenin signaling. Supplementary Figure S3. OM-153 specifically inhibits cell growth of an APC-mutated colon carcinoma cell line. Supplementary Figure S4. OM-153 shows an anti-proliferative effect in human cancer cell lines. Supplementary Figure S5. OM-153 inhibits WNT/β-catenin, YAP and MYC signaling in human cancer cell lines. Supplementary Figure S6. OM-153 inhibits the WNT/β-catenin signaling pathway and shows anti-tumor effect in a human colon carcinoma xenograft model. Supplementary Figure S7. Combined OM-153 and anti-PD-1 treatment confers anti-tumor effect in mouse melanoma. Supplementary Figure S8. PO-BID treatment with 10 mg/kg OM-153 does not reduce body weight and food consumption or induce toxicity in mice.
Supplemental Table 1 from Race-associated Molecular Changes in Gynecologic Malignancies
Authors: Asare Amma , Yao Hui , Lara Olivia D. , Wang Ying , Zhang Lin , Sood Anil K.
Published: April 2023

Differentially expressed transcripts in Pan-Gyn cohort EA vs AA
Supplemental Figure S2 from Race-associated Molecular Changes in Gynecologic Malignancies
Authors: Asare Amma , Yao Hui , Lara Olivia D. , Wang Ying , Zhang Lin , Sood Anil K.
Published: April 2023

Analysis of mRNA expression by tumor type
Figure S3 from Targeting the Ezrin Adaptor Protein Sensitizes Metastatic Breast Cancer Cells to Chemotherapy and Reduces Neoadjuvant Therapy–induced Metastasis
Authors: Hoskin Victoria , Ghaffari Abdi , Laight Brian J. , SenGupta Sandip , Madarnas Yolanda , Nicol Christopher J.B. , Elliott Bruce E. , Varma Sonal , Greer Peter A.
Published: April 2023

Automated analysis of pTERM staining in metastatic lesions and adjacent normal lung tissue
Figure S1 from Targeting the Ezrin Adaptor Protein Sensitizes Metastatic Breast Cancer Cells to Chemotherapy and Reduces Neoadjuvant Therapy–induced Metastasis
Authors: Hoskin Victoria , Ghaffari Abdi , Laight Brian J. , SenGupta Sandip , Madarnas Yolanda , Nicol Christopher J.B. , Elliott Bruce E. , Varma Sonal , Greer Peter A.
Published: April 2023

Correlation analysis of ezrin levels with DOX or DTX sensitivity
Supplementary Fig S2 from Development of an Automated Liquid Biopsy Assay for Methylated Markers in Advanced Breast Cancer
Authors: Fackler Mary Jo , Tulac Suzana , Venkatesan Neesha , Aslam Adam J. , de Guzman Timothy N. , Mercado-Rodriguez Claudia , Cope Leslie M. , Downs Bradley M. , Vali Abdul Hussain , Ding Wanjun , Lehman Jennifer , Denbow Rita , Reynolds Jeffrey , Buckley Morgan E. , Visvanathan Kala , Umbricht Christopher B. , Wolff Antonio C. , Stearns Vered , Bates Michael , Lai Edwin W. , Sukumar Saraswati
Published: April 2023

Figure shows the analytical sensitivity of LBx-BCM based detection of fully methylated DNA (0-300 copies) spiked into normal serum separately for each gene in the panel in 10-11 replicate assays
Table S6 from A Phenogenetic Axis that Modulates Clinical Manifestation and Predicts Treatment Outcome in Primary Myeloid Neoplasms
Authors: Shen Qiujin , Feng Yahui , Gong Xiaowen , Jia Yujiao , Gao Qingyan , Jiao Xiaokang , Qi Saibing , Liu Xueou , Wei Hui , Huang Bingqing , Zhao Ningning , Song Xiaoqiang , Ma Yueshen , Liang Shihao , Zhang Donglei , Qin Li , Wang Ying , Qu Shiqiang , Zou Yao , Chen Yumei , Guo Ye , Yi Shuhua , An Gang , Jiao Zengtao , Zhang Song , Li Linfeng , Yan Jun , Wang Huijun , Song Zhen , Mi Yingchang , Qiu Lugui , Zhu Xiaofan , Wang Jianxiang , Xiao Zhijian , Chen Junren
Published: April 2023

Table S6. Gene mutation rates in THAMP and comparisons with AACR GENIE 10.0-public.
Supplementary Figures S1-S7 from Neoantigen Presentation and IFNγ Signaling on the Same Tumor-associated Macrophage are Necessary for CD4 T Cell–mediated Antitumor Activity in Mice
Authors: Perez-Diez Ainhoa , Liu Xiangdong , Matzinger Polly
Published: April 2023

Fig S1 shows that sorted CD4 T cells used in Figure 2 lack APC

Fig S2 shows that CD4 T cells in all chimeric mice shown in Figure 3 were primed by the immunizations

Fig S3 shows that CD4 T cells first arrive at the tumor site around day 6

Fig S4 shows the proteins secreted by TAMs that are not changed by in vivo interaction with tumor specific CD4 T cells

Fig S5 shows the cytokines produced by sorted CD4 TILs after anti-CD3 and anti-CD28 in vitro stimulation

Fig S6 shows that in vivo blockade of TNF-alpha does not inhibit the CD4 mediated anti-tumor effect

Fig S7 shows the factors characteristic of the TAMs re-education by CD4 T cells that are independent of IFN-gamma

Fig S8 shows that the CD4 mediated in vivo phenotypic switch of TAMs is not dependent on CD40L
Supplementary Experimental Procedures from Neoantigen Presentation and IFNγ Signaling on the Same Tumor-associated Macrophage are Necessary for CD4 T Cell–mediated Antitumor Activity in Mice
Authors: Perez-Diez Ainhoa , Liu Xiangdong , Matzinger Polly
Published: April 2023

Supplementary Materials and Methods
Supplemental Table S2 from BRCA1-Associated RING Domain-1 (BARD1) Loss and GBP1 Expression Enhance Sensitivity to DNA Damage in Ewing Sarcoma
Authors: Maurer Lisa M. , Daley Jessica D. , Mukherjee Elina , Venier Rosemarie E. , Julian Claire M. , Bailey Nathanael G. , Jacobs Michelle F. , Kumar-Sinha Chandan , Raphael Haley , Periyapatna Nivitha , Weiss Kurt , Janeway Katherine A. , Mody Rajen , Lucas Peter C. , McAllister-Lucas Linda M. , Bailey Kelly M.
Published: April 2023

Prevalence of somatic DNA damage repair gene variants in Ewing cell lines included in original studies of PARP inhibition.
Supplemental Figure S3 from BRCA1-Associated RING Domain-1 (BARD1) Loss and GBP1 Expression Enhance Sensitivity to DNA Damage in Ewing Sarcoma
Authors: Maurer Lisa M. , Daley Jessica D. , Mukherjee Elina , Venier Rosemarie E. , Julian Claire M. , Bailey Nathanael G. , Jacobs Michelle F. , Kumar-Sinha Chandan , Raphael Haley , Periyapatna Nivitha , Weiss Kurt , Janeway Katherine A. , Mody Rajen , Lucas Peter C. , McAllister-Lucas Linda M. , Bailey Kelly M.
Published: April 2023

Interferon-gamma-induced GBP1 expression in A673 Ewing sarcoma cells.
Fig S4 from World Trade Center Dust Exposure Promotes Cancer in PTEN-deficient Mouse Prostates
Authors: Wang Lin , Xu Yitian , Zhang Licheng , Kang Kyeongah , Kobryn Andriy , Portman Kensey , Gordon Ronald E , Pan Ping-Ying , Taioli Emanuela , Aaronson Stuart A , Chen Shu-Hsia , Mulholland David J
Published: April 2023

Fig. S4. Effect of direct introduction of WTC dust to the mouse prostate. A, Approach injecting solubilized WTC dust (2x 1 μl injections per prostate) and evaluation 6-8 weeks later. B, Histological low magnification image showing prostate enlargement after dust injection. C, Gross images showing a PBS control injected prostate (panel 1) and prostates with WTC dust injection (panels 2, 3, 4). D, Histological high magnification view showing immune cell infiltration in WTC dust injected prostate. E, Gene expression profiles for two independent prostates injected with WTC dust normalized to PBS control prostates (bars: B, C1, C3 = 2000 μM, C2, C4 = 5000 μM, D = 250 μM).
Table S2 from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome
Authors: Silwal-Pandit Laxmi , Stålberg Stina M. , Johansson Henrik J. , Mermelekas Georgios , Lothe Inger Marie B. , Skrede Martina L. , Dalsgaard Astrid Marie , Nebdal Daniel J. H. , Helland Åslaug , Lingjærde Ole Christian , Labori Knut Jørgen , Skålhegg Bjørn S. , Lehtiö Janne , Kure Elin H.
Published: April 2023

Histological composition of the samples along with assigned transcriptomics and proteomics classifications for PDAC
Fig S2 from World Trade Center Dust Exposure Promotes Cancer in PTEN-deficient Mouse Prostates
Authors: Wang Lin , Xu Yitian , Zhang Licheng , Kang Kyeongah , Kobryn Andriy , Portman Kensey , Gordon Ronald E , Pan Ping-Ying , Taioli Emanuela , Aaronson Stuart A , Chen Shu-Hsia , Mulholland David J
Published: April 2023

Fig. S2. Volcano plots showing gene expression profiles for C57BL/6 mouse organs at 7d and 21d after WTC dust exposure normalized to PBS control mice (n=3).
Fig S1 from World Trade Center Dust Exposure Promotes Cancer in PTEN-deficient Mouse Prostates
Authors: Wang Lin , Xu Yitian , Zhang Licheng , Kang Kyeongah , Kobryn Andriy , Portman Kensey , Gordon Ronald E , Pan Ping-Ying , Taioli Emanuela , Aaronson Stuart A , Chen Shu-Hsia , Mulholland David J
Published: April 2023

Fig. S1. Percentage increases of metals detected by mass spectrometry in lung (A), spleen (B) and prostate (C)
found in mice receiving WTC dust normalized to control, PBS nasal instillation (n=8 per organ).
Table S11 from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome
Authors: Silwal-Pandit Laxmi , Stålberg Stina M. , Johansson Henrik J. , Mermelekas Georgios , Lothe Inger Marie B. , Skrede Martina L. , Dalsgaard Astrid Marie , Nebdal Daniel J. H. , Helland Åslaug , Lingjærde Ole Christian , Labori Knut Jørgen , Skålhegg Bjørn S. , Lehtiö Janne , Kure Elin H.
Published: April 2023

Proteins (and the assigned module) identified in our dataset overlapping with the proteins with significantly higher abundance in PDAC tumor tissue compared to adjacent tissue/normal ducts in the study of Cao et al.2021
Table S10A and S10B from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome
Authors: Silwal-Pandit Laxmi , Stålberg Stina M. , Johansson Henrik J. , Mermelekas Georgios , Lothe Inger Marie B. , Skrede Martina L. , Dalsgaard Astrid Marie , Nebdal Daniel J. H. , Helland Åslaug , Lingjærde Ole Christian , Labori Knut Jørgen , Skålhegg Bjørn S. , Lehtiö Janne , Kure Elin H.
Published: April 2023

Differential expression analysis of M2 and M4 proteins between PDAC and tumor adjacent tissue samples (Wilcoxon-rank sum test)
Table S1 from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome
Authors: Silwal-Pandit Laxmi , Stålberg Stina M. , Johansson Henrik J. , Mermelekas Georgios , Lothe Inger Marie B. , Skrede Martina L. , Dalsgaard Astrid Marie , Nebdal Daniel J. H. , Helland Åslaug , Lingjærde Ole Christian , Labori Knut Jørgen , Skålhegg Bjørn S. , Lehtiö Janne , Kure Elin H.
Published: April 2023

Patients and samples overview
Materials Spreadsheet MS1 from WEE1 Inhibition Augments CDC7 (DDK) Inhibitor–induced Cell Death in Ewing Sarcoma by Forcing Premature Mitotic Entry and Mitotic Catastrophe
Authors: Martin Jeffrey C. , Sims Jennie R. , Gupta Ajay , Bakin Andrei V. , Ohm Joyce Ellen
Published: April 2023

This table provides additional information about the materials used in this study.
Supplementary Figures S1-S9 from NetrinG1+ Cancer-Associated Fibroblasts Generate Unique Extracellular Vesicles that Support the Survival of Pancreatic Cancer Cells Under Nutritional Stress
Authors: Raghavan Kristopher S. , Francescone Ralph , Franco-Barraza Janusz , Gardiner Jaye C. , Vendramini-Costa Débora B. , Luong Tiffany , Pourmandi Narges , Andren Anthony , Kurimchak Alison , Ogier Charline , Campbell Paul M. , Duncan James S. , Lyssiotis Costas A. , Languino Lucia R. , Cukierman Edna
Published: April 2023

Supplementary Figure 1. Confirmation that CAFs produce ECMs distinct from NLFs. Supplementary Figure 2. Direct co-culture of CAFs support PDAC cells during nutrient-deprivation. Supplementary Figure 3. Additional CAF cell lines generate sEVs that rescue PDAC cells from nutrient deprivation-induced apoptosis. Supplementary Figure 4. NetG1+ CAF-sEVs support PDAC cell survival in a NGL-1 dependent manner. Supplementary Figure 5. NetG1 expression in CAFs is necessary for sEV-mediated survival of nutrient-deprived PDAC cells. Supplementary Figure 6. NetG1 ablation does not affect the uptake of sEV cargo in PDAC cells. Supplementary Figure 7. sEV supernatant contains DNPs enriched with sub-exosome sized EVs. Supplementary Figure 8. Enriched gene ontology clusters from proteomic and metabolomic analysis comparing sEV and DNP fractions. Supplementary Figure 9. EV cargo requires transfer in intact vesicles to provide tumor-supportive effect.
Figure S1 from A Phase I Study of Pelabresib (CPI-0610), a Small-Molecule Inhibitor of BET Proteins, in Patients with Relapsed or Refractory Lymphoma
Authors: Blum Kristie A. , Supko Jeffrey G. , Maris Michael B. , Flinn Ian W. , Goy Andre , Younes Anas , Bobba Suresh , Senderowicz Adrian M. , Efuni Sergey , Rippley Ronda , Colak Gozde , Trojer Patrick , Abramson Jeremy S.
Published: April 2023

CONSORT diagram of patient disposition throughout study
Supplementary Figure 1 from Remodeling of the Tumor Microenvironment Through PAK4 Inhibition Sensitizes Tumors to Immune Checkpoint Blockade
Authors: Abril-Rodriguez Gabriel , Torrejon Davis Y. , Karin Daniel , Campbell Katie M. , Medina Egmidio , Saco Justin D. , Galvez Mildred , Champhekar Ameya S. , Perez-Garcilazo Ivan , Baselga-Carretero Ignacio , Singh Jas , Comin-Anduix Begoña , Puig-Saus Cristina , Ribas Antoni
Published: April 2023

Supplementary Figure 1: Impact of PAK4 deletion on the expression of chemokines.
Supplementary Table 2 from Protein Kinase C Alpha is a Central Node for Tumorigenic Transcriptional Networks in Human Prostate Cancer
Authors: Cooke Mariana , Zhang Xuyao , Zhang Suli , Eruslanov Evgeniy , Lal Priti , Daniel Reba E. , Feldman Michael D. , Abba Martin C. , Kazanietz Marcelo G.
Published: April 2023

Pathway and GO enrichment analysis.
Supplementary Figure 1 from Protein Kinase C Alpha is a Central Node for Tumorigenic Transcriptional Networks in Human Prostate Cancer
Authors: Cooke Mariana , Zhang Xuyao , Zhang Suli , Eruslanov Evgeniy , Lal Priti , Daniel Reba E. , Feldman Michael D. , Abba Martin C. , Kazanietz Marcelo G.
Published: April 2023

Time-dependent expression of PKCalpha in prostate cancer cells after RNAi silencing with three different siRNA duplexes.
Supplementary Data S1 from The RPL/RPS Gene Signature of Melanoma CTCs Associates with Brain Metastasis
Authors: Bowley Tetiana Y. , Lagutina Irina V. , Francis Carol , Sivakumar Sinduja , Selwyn Reed G. , Taylor Erik , Guo Yan , Fahy Bridget N. , Tawfik Bernard , Marchetti Dario
Published: April 2023

Supplemental figures and tables
Supplementary Figures S1-S7 from The Combination of Radiotherapy and Complement C3a Inhibition Potentiates Natural Killer cell Functions Against Pancreatic Cancer
Authors: Sodji Quaovi H. , Nambiar Dhanya K. , Viswanathan Vignesh , von Eyben Rie , Colburg Deana , Binkley Michael S. , Li Caiyun G. , Olcina Monica M. , Chang Daniel T. , Le Quynh-Thu , Giaccia Amato J.
Published: April 2023

Supplementary Figure S1: Proportion of total NK cell in the tumor microenvironment of 138 pancreatic cancer patients based on the CIBERSORTx analysis of TCGA. Supplementary Figure S2: Immunohistochemical staining of NK cells (Red circle) using NKp46. Supplementary Figure S3: Pan02 tumor in C57BL/6 mice as a syngeneic mouse model. Supplementary Figure S4: Representative flow cytometry gating strategy for NK cells (a) and percent of NK cells relative to immune cells in the C3aR antagonist-treated and vehicle-treated tumors (b). Supplementary Figure S5: Flow cytometry gating strategy for B cells (B220+), CD4+ T cells, CD8+ T cells, macrophages (Gr1-CD11b+F4/80+) and myeloid derived suppressor cells (MDSC) (Gr1+CD11b+) in the spleen, vehicle-treated (control) tumor and C3aR antagonist-treated tumor. Supplementary Figure S6: C3aR antagonism does not impact immune cell infiltration in the spleen of vehicle-treated and C3aR antagonist-treated mice. Supplementary Figure S7: Depletion of NK cells and CD8+ T cells and confirmatory analysis of depletion and survival of Pan02 tumor-bearing mice.
Supplementary Figure S7 from Mitochondrial Matrix Protease ClpP Agonists Inhibit Cancer Stem Cell Function in Breast Cancer Cells by Disrupting Mitochondrial Homeostasis
Authors: Greer Yoshimi Endo , Hernandez Lidia , Fennell Emily M.J. , Kundu Manjari , Voeller Donna , Chari Raj , Gilbert Samuel F. , Gilbert Thomas S.K. , Ratnayake Shashikala , Tang Binwu , Hafner Markus , Chen Qingrong , Meerzaman Daoud , Iwanowicz Edwin , Annunziata Christina M. , Graves Lee M. , Lipkowitz Stanley
Published: April 2023

The effects of ClpP agonists and other mitochondria-targeting drugs on Myc and HIF pathway