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Journal articles on the topic "Caleb T"
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Whitlark, Jason. "Listen, Understand, Obey: Essays on Hebrews in Honor of Gareth Lee Cockerill ed. by Caleb T. Friedman." Catholic Biblical Quarterly 82, no. 1 (2020): 164–65. http://dx.doi.org/10.1353/cbq.2020.0040.
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Borker, Parth, Yi Bao, Yuanyuan Qiao, Arul Chinnaiyan, Jae Eun Choi, Yuping Zhang, Rahul Mannan, et al. "Abstract 7479: Targeting the lipid kinase PIKfyve upregulates surface expression of MHC class I to augment cancer immunotherapy." Cancer Research 84, no. 6_Supplement (March 22, 2024): 7479. http://dx.doi.org/10.1158/1538-7445.am2024-7479.
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Abstract The widespread success of cancer immunotherapies suggests a promising future - but has been subverted by unresponsiveness and resistance. Current research has furthered the understanding of immunotherapy resistance through the findings of “hot” (responsive) and “cold” (unresponsive) tumors. Here, we focus on the genetic and pharmacological inhibition of PIKfyve, a lipid kinase regulator of autophagic flux and lysosomal biogenesis. We find that inhibition of PIKfyve results in the upregulation of major histocompatibility complex class I (MHC-I) surface expression in cancer cells (through inhibition of autophagic flux), resulting in increased CD8+ T cell-mediated cancer cell death. These findings were corroborated in multiple syngeneic mouse models, which also displayed increased intratumoral functional CD8+ T cells. In addition, the Pikfyve-depletion antitumor responses are CD8+ T cell and MHC-I dependent - as CD8+ T cell and B2m knockout rescued tumor growth - resulting in improved response to immune checkpoint blockable (ICB), adoptive cell therapy, and a therapeutic vaccine. Further, high PIKfyve expression predicts poor ICB response and is prognostic of poor survival in ICB-treated cohorts. Ultimately, these findings collectively suggest PIKfyve as an effective target to enhance immunotherapies through elevation of MHC-I surface expression in cancer cells, and accordingly, PIKfyve inhibitors have novel potential to increase immunotherapy response in cancer patients. Citation Format: Parth Borker, Yi Bao, Yuanyuan Qiao, Arul Chinnaiyan, Jae Eun Choi, Yuping Zhang, Rahul Mannan, Caleb Cheng, Tongchen He, Yang Zheng, Jiali Yu, Mahnoor Gondal, Gabriel Cruz, Sara Sara Grove, Xuhong Cao, Fengyun Su, Rui Wang, Yu Chang, Ilona Kryczek, Marcin Cieslik, Michael D. Green, Weiping Zou. Targeting the lipid kinase PIKfyve upregulates surface expression of MHC class I to augment cancer immunotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7479.
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Liu, Vincent, Katalin Sandor, Bence Daniel, Lionel Berthoin, Shan Sabri, Sofia Panagiotopoulou, Yajie Yin, et al. "Abstract 1701: Single-cell multi-omic profiling and clonal tracing of the human gynecological tumor microenvironment." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1701. http://dx.doi.org/10.1158/1538-7445.am2022-1701.
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Abstract Tumor initiation and progression are the result of a close interplay between malignant cells and immune cells. While single-cell genomics has enabled the molecular dissection of the cellular heterogeneity underlying complex cancers, many facets of tumor microenvironments remain unresolved. In particular, the ontogeny of myeloid cells have not been fully understood in human tumors, although the source and expansion of macrophages have been suggested to underlie tumor development and metastasis in mice. In an effort to comprehensively characterize these tumor microenvironments, we profiled endometrial, ovarian, and metastatic tumors from 16 patients using CITE-seq (an atlas of 258,810 cells) and mitochondrial single-cell ATAC-seq (mtscATAC-seq; consisting of 173,820 cells). Our multi-omic analyses reveal the heterogeneity of tumor-infiltrating immune cells at clonal, epigenetic, transcriptomic, and proteomic levels. Notably, all tumor types harbored diverse exhausted T cell subsets, including terminal and precursor exhausted T cells, and gamma/delta T cells. Clonal somatic variant analysis between tumor tissues and peripheral blood mononuclear cells identified blood-derived monocytes, rather than embryonically derived cells, as the origin of macrophages within gynecological tumors. Further, our analyses show that macrophages expand minimally within the tumor microenvironment, suggesting that they may be continuously replenished by blood, an observation that may facilitate new approaches for cancer immunotherapy. In total, our dataset represents the first multi-modal single cell atlas of gynecologic tumors and reveals distinct features of T cell heterogeneity and myeloid expansions in complex tumor microenvironments. Citation Format: Vincent Liu, Katalin Sandor, Bence Daniel, Lionel Berthoin, Shan Sabri, Sofia Panagiotopoulou, Yajie Yin, Kamir Hiam-Galvez, Rene Sit, Zi Fan, Brendan Galvin, Omar Khan, Natalie Bezman, Jane Grogan, Brooke Howitt, Grace Zheng, Caleb Lareau, Ansuman Satpathy. Single-cell multi-omic profiling and clonal tracing of the human gynecological tumor microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1701.
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Hurvitz, Sara, Sung-Bae Kim, Wei-Pang Chung, Seock-Ah Im, Yeon Hee Park, Roberto Hegg, Min-Hwan Kim, et al. "Abstract GS3-01: Trastuzumab deruxtecan (T-DXd; DS-8201a) vs. trastuzumab emtansine (T-DM1) in patients (pts) with HER2+ metastatic breast cancer (mBC): subgroup analyses from the randomized phase 3 study DESTINY-Breast03." Cancer Research 82, no. 4_Supplement (February 15, 2022): GS3–01—GS3–01. http://dx.doi.org/10.1158/1538-7445.sabcs21-gs3-01.
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Abstract Background: T-DXd is a HER2-targeting antibody-drug conjugate approved for the treatment of pts with advanced HER2+ mBC based on the DESTINY-Breast01 study (NCT03248492). DESTINY-Breast03 (NCT03529110) isa randomized, multicenter, open-label, phase 3 study assessing the efficacy and safety of T-DXd vs. T-DM1 in pts with HER2+ mBC previously treated with trastuzumab and taxane. In the primary analysis, T-DXd demonstrated a clinically meaningful and statistically significant improvement in PFS vs. T-DM1 (Corteset al, ESMO 2021). In this exploratory analysis, we provide additional efficacy and safety data in subgroups, including in pts with brain metastases (BMs). Methods: Pts were randomly assigned 1:1 to receive 5.4 mg/kg T-DXd or 3.6 mg/kg T-DM1 Q3W. Pts with clinically stable BMs were eligible. Lesions were measured per modified Response Evaluation Criteria in Solid Tumors version 1.1. The primary endpoint was progression-free survival (PFS) determined by blinded independent central review (BICR). PFS and overall response rate (ORR) were analyzed for subgroups.Sites of progression and post-end-of-study therapies were also investigated. Results: At data cutoff (May 21, 2021), 524 pts were randomly assigned to T-DXd (n=261) orT-DM1 (n=263). T-DXd demonstrated superior PFS by BICR vs. T-DM1 (HR, 0.28 [95%CI, 0.22-0.37]; P=7.8 x 10-22); median (m) PFS by BICR was not reached (95% CI, 18.5-NE) for T-DXd compared with 6.8 mo (95% CI, 5.6-8.2) forT-DM1. For pts with stable BMs at baseline (n=82), mPFS was 15.0 mo (95% CI,12.5-22.2) for T-DXd vs. 3.0 mo (95% CI, 2.8-5.8) for T-DM1 (HR, 0.25 [95% CI,0.31-0.45)]. Overall, confirmed ORR for T-DXd was 79.7% vs. 34.2% for T-DM1.For patients with stable BMs at baseline, ORR was 67.4% for T-DXd vs. 20.5% forT-DM1. Consistent PFS and ORR benefit was also observed across other subgroups(Table 1). At data cutoff, 84 (32.2%) pts treated with T-DXd had progressive disease (PD) versus 155 (58.9%) with T-DM1. In pts with stable BMs in the T-DXd arm, 48.8% of pts (21/43) had PD. In pts with stable BMs in the T-DM1 arm, 69.2%of pts (27/39) had PD. Data on sites of progression will be presented. Further analyses are underway and will be presented. Overall, the safety profile of T-DXd was manageable and comparable with its known safety profile. Adjudicated drug-related interstitial lung disease/pneumonitis was reported in 27 (10.5%) pts treated with T-DXd and 5 (1.9%) pts treated with T-DM1 overall, with no grade 4 or 5 events. Additional new safety data will be presented. Conclusion: DESTINY-Breast03,the first-reported randomized phase 3 trial comparing T-DXd to standard of care, met the primary endpoint with T-DXd demonstrating superior PFS vs. T-DM1and T-DXd had a manageable safety profile. In this exploratory analysis, consistent PFS and ORR benefit with T-DXd vs. T-DM1 was observed across subgroups in pts with HER2+ mBC previously treated with trastuzumab and taxane, including in pts with BMs. Table 1.Subgroup Analyses forPFS and ORR of T-DXd versus T-DM1PFS by BICR HR (95% CI)Absolute ORR Difference (T-DXd-T-DM1) (95% CI)All patients (N=524)0.28 (0.22-0.37)45.5 (37.6-53.4)Hormone receptorPositive (n=272)0.32 (0.22-0.46)47.3 (36.1-58.4)Negative (n=248)0.30 (0.20-0.44)43.2 (31.5-55.0)Prior pertuzumabYes (n=320)0.31 (0.22-0.43)46.7 (36.5-56.9)No (n=204)0.30 (0.19-0.47)43.6 (30.5-56.7)Prior lines of therapya0-1 (n=258)0.33 (0.23-0.48)39.3 (27.3-51.2)≥2 (n=266)0.28 (0.19-0.41)51.6 (40.9-62.4)Visceral disease Yes (n=384)0.28 (0.21-0.38)48.3 (39.1-57.6)No (n=140)0.32 (0.17-0.58)39.1 (23.6-54.6)Brain metastases at baseline Yes (n=82)0.25 (0.13-0.45)46.9 (25.6-68.3)No (n=442)0.30 (0.22-0.40)45.5 (36.9-54.1) Citation Format: Sara Hurvitz, Sung-Bae Kim, Wei-Pang Chung, Seock-Ah Im, Yeon Hee Park, Roberto Hegg, Min-Hwan Kim, Ling-Ming Tseng, Vanessa Petry, Chi-Feng Chung, Hiroji Iwata, Erika Hamilton, Giuseppe Curigliano, Binghe Xu, Caleb Lee, Yali Liu, Jillian Cathcart, Emarjola Bako, Sunil Verma, Javier Cortés. Trastuzumab deruxtecan (T-DXd; DS-8201a) vs. trastuzumab emtansine (T-DM1) in patients (pts) with HER2+ metastatic breast cancer (mBC): subgroup analyses from the randomized phase 3 study DESTINY-Breast03 [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr GS3-01.
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Fan, Zenghua, David Y. Oh, Anthony Wong, Katsuto Shinohara, Hao Nguyen, Caleb Hwang, Hewitt Chang, et al. "Abstract 4988: Responders to combination radiation and PD-1 blockade demonstrate reduced myeloid immunosuppression and enhanced interferon signaling in oligometastatic prostate cancer patients." Cancer Research 84, no. 6_Supplement (March 22, 2024): 4988. http://dx.doi.org/10.1158/1538-7445.am2024-4988.
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Abstract Background: Prostate cancer is unresponsive to current immunotherapies such as checkpoint inhibitors. Overcoming this “cold” environment requires rational combination of therapeutic modalities that can prime anti-tumor immunity. Radiation is a potential candidate; however it remains unclear how it should be most productively combined with immunotherapies. Methods: We completed an investigator-initiated clinical trial of newly diagnosed men with oligometastatic, hormone-sensitive prostate cancer (mHSPC, NCT03007732). Patients were randomized to receive anti-PD-1 x 13 cycles (pembrolizumab, Arm 1, n=12), or anti-PD-1 with intraprostatic injections of TLR9 agonist SD-101 (Arm 2, n=11). All patients received SBRT to the prostate tumor during cycle 1, and concomitant hormonal therapy with a GnRH agonist and abiraterone. Response was assessed as PSA < nadir + 2 ng/mL at 15 months after ceasing all cancer therapies. For unbiased correlative immune interrogation of these patients, fresh paired biopsies of primary prostate tumor and PBMCs both before and after radiation and immunotherapy were analyzed by multi-omic single-cell genomics to assess changes with treatment, including T cell repertoire changes. Results: Fourteen of 21 evaluable patients responded by PSA criteria with 3 patients not yet reaching 15 months of post-treatment follow-up. Adverse events included expected IRAEs from anti-PD-1, and flu-like symptoms from SD-101, with no unexpected AEs. Single-cell analysis of tumor biopsies reveals treatment-induced decreases in cytotoxic T cell populations and increases in both immunostimulatory LAMP3+ dendritic cells and immunosuppressive SPP1+ myeloid populations. Treatment increased interferon (IFN) signaling in most myeloid subsets while strongest in LAMP3+ DCs. Compared to non-responders, responders showed less immunosuppression at baseline with depletion of myeloid cells and enhanced IFN activity on LAMP3+ DCs, and treatment-induced IFN activity on cytotoxic T cells. TLR9 agonism also specifically enhanced IFN responses, persistence of cytotoxic T cell clonotypes, and enhanced antigen presentation in tumor cells. Circulating T cells in blood detected shared clones with tissue showing enrichment in cytotoxic phenotype and association with responders. Conclusions: Responders to combination radiation and anti-PD-1 blockade have decreased myeloid immunosuppression and enhanced IFN activity prior to treatment in oligometastatic prostate cancer. This may identify patients likely to respond, and baseline immune setpoints that can be enhanced with improved immunotherapy strategies. Acknowledgements: This work was supported by the Prostate Cancer Foundation and Merck. Merck Sharp & Dohme LLC, Rahway, NJ, USA provided drug and financial support for the study. Citation Format: Zenghua Fan, David Y. Oh, Anthony Wong, Katsuto Shinohara, Hao Nguyen, Caleb Hwang, Hewitt Chang, Alec Starzinski, Tony Li, Christopher De Leon, Marissa Gin, Eliezer Van Allen, Li Zhang, Rahaul R. Aggarwal, Terence W. Friedlander, Eric J. Small, Felix Y. Feng, Lawrence Fong. Responders to combination radiation and PD-1 blockade demonstrate reduced myeloid immunosuppression and enhanced interferon signaling in oligometastatic prostate cancer patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4988.
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Lafargue, Audrey M., Hailun Wang, Sivarajan T. Chettiar, Rajendra P. Gajula, Amol C. Shetty, Yang Song, Brian W. Simons, et al. "Abstract 2968: TWIST1-induced suppression of oncogene-induced senescence in non-small cell lung cancer requires the transactivation domain of TWIST1." Cancer Research 84, no. 6_Supplement (March 22, 2024): 2968. http://dx.doi.org/10.1158/1538-7445.am2024-2968.
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Abstract Non-small cell lung carcinoma (NSCLC) is a major cause of cancer mortality. High expression of the epithelial-to-mesenchymal transition transcription factor TWIST1 is strongly associated with metastatic cancers and treatment resistance. Additionally, TWIST1 can upregulate O-GlcNAcylation which (1) is required to suppress fail-safe programs such as oncogene (KRasG12D)-induced senescence (OIS) to accelerate tumorigenesis in primary NSCLC tumors, and (2) is a potential modulator of DNA repair/radiation response. To decipher the domains and transcriptional targets required for tumorigenicity and radioresistance, we created a novel genetically engineered mouse model (GEMM) allowing tetracycline-inducible expression in the lung epithelium (via lung specific CCSP-reverse tetracycline transactivator (C)) of KRasG12D (R) with Twist1wt (T) or with Twist1F191G transactivation-null mutant (F). CRT mice had shorter tumor-free survival and more aggressive tumors compared to CR/CRF mice indicating that the Twist1 transactivation domain is required for Twist1-dependent tumorigenesis acceleration. Also, Twist1wt expression promoted radioresistance in cell lines and GEMMs. Contrary to CRT, CRF showed a progressive loss of Twist1F191G expression over time suggesting no functionality/no selective advantage. CRT lung tumors had higher proliferation (Ki67) and lower cell-cycle arrest (p16) compared to CR/CRF suggesting that the transactivation domain of Twist1 is important for the suppression of OIS. Supporting these data, we observed in non-cancer Human Bronchial Epithelial Cell (HBEC) that the co-expression of human TWIST1wt (HBEC-TWIST1wt) could suppress HRasG12V-induced senescence while the transactivation-null TWIST1F187G mutant (HBEC-TWIST1F187G) could not. Additionally, HBEC expressing HRasG12V-TWIST1wt had enhanced tumorigenic/invasive programs. Interestingly, we observed that the inhibition of O-GlcNAcylation rescued OIS in HBEC-HRasG12V-TWIST1wt while the stimulation of O-GlcNAcylation in HBEC-HRasG12V-TWIST1F187G suppressed OIS. Furthermore, TWIST1wt expression with HRasG12V modulated MYC downstream targets and the inhibition of MYC activity using the novel MYC inhibitor MYCi975 in HBEC-HRasG12V-TWIST1wt also rescued OIS induction. Altogether, these results suggest that TWIST1 may suppress OIS via MYC signaling and nominate MYCi975 as a means to activate latent OIS programs. In this context, MYC inhibiting strategies could serve as a therapeutic sensitizer for TWIST1-positive NSCLC. This work and our future studies on TWIST1 toward the control of OIS, O-GlcNAcylation and of mechanisms of radioresistance may help to identify new potential NSCLC therapeutic strategies. Citation Format: Audrey M. Lafargue, Hailun Wang, Sivarajan T. Chettiar, Rajendra P. Gajula, Amol C. Shetty, Yang Song, Brian W. Simons, Triet Nguyen, Christine Lam, Francesca A. Carrieri, Caleb Smack, Nick Connis, Dipanwita Dutta Chowdhury, Jinhee Chang, Danielle Council, Katriana Nugent, Ismaeel Siddiqui, Kekoa Taparra, Mohammad Rezaee, Natasha Zachara, Zachary S. Morris, Christopher McFarland, Sarki Abba Abdulkadir, Christine L. Hann, Phuoc T. Tran. TWIST1-induced suppression of oncogene-induced senescence in non-small cell lung cancer requires the transactivation domain of TWIST1 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 2968.
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Tien, Jean C., Yu Chang, Yuping Zhang, Jonathan Chou, Yunhui Cheng, Xiaoju Wang, Jianzhang Yang, et al. "Abstract PR010: CDK12 loss promotes prostate cancer development while exposing vulnerabilities to paralog-based synthetic lethality." Molecular Cancer Therapeutics 23, no. 6_Supplement (June 10, 2024): PR010. http://dx.doi.org/10.1158/1538-8514.synthleth24-pr010.
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Abstract Biallelic loss of cyclin-dependent kinase 12 (CDK12) defines a unique molecular subtype of metastatic castration-resistant prostate cancer (mCRPC). It remains unclear, however, whether CDK12 loss per se is sufficient to drive prostate cancer development—either alone, or in the context of other genetic alterations—and whether CDK12-mutant tumors exhibit sensitivity to specific pharmacotherapies. Here, we demonstrate that tissue-specific Cdk12 ablation is sufficient to induce preneoplastic lesions and robust T cell infiltration in the mouse prostate. Allograft-based CRISPR screening demonstrated that Cdk12 loss is positively associated with Trp53 inactivation but negatively associated with Pten inactivation—akin to what is observed in human mCRPC. Consistent with this, ablation of Cdk12 in prostate organoids with concurrent Trp53 loss promotes their proliferation and ability to form tumors in mice, while Cdk12knockout in the Pten-null prostate cancer mouse model abrogates tumor growth. Bigenic Cdk12 and Trp53 loss allografts represent a new syngeneic model for the study of androgen receptor (AR)-positive, luminal prostate cancer. Notably, Cdk12/Trp53 loss prostate tumors are sensitive to immune checkpoint blockade. Cdk12-null organoids (either with or without Trp53 co-ablation) and patient-derived xenografts from tumors with CDK12 inactivation are highly sensitive to inhibition or degradation of its paralog kinase, CDK13. Together, these data identify CDK12 as a bona fidetumor suppressor gene with impact on tumor progression and lends support to paralog-based synthetic lethality as a promising strategy for treating CDK12-mutant mCRPC. Citation Format: Jean C. Tien, Yu Chang, Yuping Zhang, Jonathan Chou, Yunhui Cheng, Xiaoju Wang, Jianzhang Yang, Rahul Mannan, Palak Shah, Xiao-Ming Wang, Abbey Todd, Sanjana Eyunni, Caleb Cheng, Xuhong Cao, Yi Bao, James Neiswender, Rachel Brough, Stephen Pettitt, Estefania Labanca, Yuzhuo Wang, Marcin Cieslik, Christopher J. Lord, Ke Ding, Arul M. Chinnaiyan. CDK12 loss promotes prostate cancer development while exposing vulnerabilities to paralog-based synthetic lethality [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Expanding and Translating Cancer Synthetic Vulnerabilities; 2024 Jun 10-13; Montreal, Quebec, Canada. Philadelphia (PA): AACR; Mol Cancer Ther 2024;23(6 Suppl):Abstract nr PR010.
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Dai, Chaobin, Bin Zhang, Yunyang Liao, Qicai Liu, Feiguang Wu, Xiaoting Lv, Kai Zeng, and Xiaofeng Zhu. "CALCB rs3829222 T/T Genotype and Low Expression of CALCB Are High-Risk Factors for Adenoid Cystic Carcinoma of Salivary Gland." Disease Markers 2021 (June 12, 2021): 1–5. http://dx.doi.org/10.1155/2021/5546858.
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Objectives. To investigate the relationship between polymorphisms of calcitonin-related peptide gene II (beta-calcitonin gene-related peptide (βCGRP), CALCB) and serum CGRP levels in salivary adenoid cystic carcinoma. Materials and Methods. Using the polymerase chain reaction (PCR) technique, the full-length amplification and genotype analysis of CALCB genes were performed in 39 patients with adenoid cystic carcinoma of salivary gland and 158 normal controls. The gene frequencies of major genotype of CALCB in adenoid cystic carcinoma of salivary gland and normal control group were analyzed. Enzyme-linked immunosorbent assay (ELISA) was used to evaluate serum calcitonin gene-related peptide (CGRP) and its concentration of alpha and beta subtypes. Results. Univariate logistic regression analysis showed that the CALCB rs2839222 T/T genotype was closely related to the occurrence of salivary adenoid cystic carcinoma, with a correlation coefficient of 3.89. Conclusions. The serum CGRP concentration in the salivary adenoid cystic carcinoma group was 1.56 times that of the normal control group. The αCGRP subtype was significant, which was 3.02 times that of the normal control. The polymorphism of βCGRP gene is associated with genetic susceptibility to salivary adenoid cystic carcinoma, and serum CGRP and βCGRP can be used as novel markers of salivary adenoid cystic carcinoma.
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BUENO, VINICIUS R., MORGAN R. GOSTEL, and GUSTAVO HEIDEN. "The spiraling story of Tyleropappus and a new name for Calea (Asteraceae: Neurolaeneae) from Venezuela." Phytotaxa 622, no. 1 (October 24, 2023): 75–84. http://dx.doi.org/10.11646/phytotaxa.622.1.5.
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Tyleropappus was described in 1931 by Greenman and is characterized by its spiral, alternate leaves and epaleaceous receptacle. Throughout its taxonomic history, the genus was placed into the tribes Helenieae and Neurolaeneae, often treated as the sister genus of Geissopappus, which is currently a synonym of Calea. Later, Tyleropappus was synonymized with Calea; however, when its synonymization was proposed, the sole species in the genus, T. dichotomus, had not been synonymized under a previously described species nor properly transferred to Calea. Ongoing taxonomic studies in Neurolaeneae have provided opportunities to clarify the challenging taxonomic history of this monotypic genus. We confirm the synonymy of Tyleropappus in Calea; however, we recognize T. dichotomus as a distinct species that should be accepted in Calea. Nonetheless, the name C. dichotoma already exists, and is a synonym of C. ternifolia. Therefore, we propose the new name C. spiralis to accommodate this species, which is morphologically similar to C. linearifolia. The former can be distinguished from the latter by the spiral, alternate (vs. decussate) arrangement of leaves, receptacle epaleaceous (vs. oligopaleaceous) and cypselae hirsute (vs. glabrous). We also provide a detailed description of the species, the first map of its geographic occurrence, an illustration with diagnostic characters, and the first taxonomic key for the Nana clade of Calea.
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Alkashgari, Hossam, Cornelia Stoian, Caleb Ruiz-Jimenez, Jacqueline Coats, Carlos A. Casiano, Sinisa Dovat, and Kimberly J. Payne. "Abstract 1528: Molecular mechanisms of TSLP as a therapy for CRLF2 B-Cell acute lymphoblastic leukemia." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1528. http://dx.doi.org/10.1158/1538-7445.am2022-1528.
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Abstract B-cell acute lymphoblastic leukemia (B-ALL) is the most common type of leukemia in children. B-ALL characterized by cytokine receptor-like factor 2 (CRLF2) overexpression (CRLF2 B-ALL) has a survival rate of <30% and is the highest risk sub-group of B-ALL in both adults and children. CRLF2 is a receptor component for the cytokine thymic stromal lymphopoietin (TSLP). TSLP plays a role in the survival and proliferation of B-cell precursors, thus explaining the oncogenic role of increased CRLF2 signaling in CRLF2 B-ALL. To our surprise, we found that high-levels of TSLP eliminated leukemia cells in patient-derived xenograft (PDX) models of CRLF2 B-ALL. CRLF2 and IL-7 receptor-alpha (IL-7Ra) form the heterodimer type-I cytokine receptor for TSLP cytokine. Binding of TSLP to its CRLF2 receptor complex induces JAK-STAT5 and PI3K-AKT pathway signals. TSLP shares the IL-7Ra with Interleukin 7 (IL-7) which has a heterodimer receptor consisting of IL-7Ra and the common gamma chain. High-levels of IL-7 (50 ng/ml) have been shown to induce IL-7Ra internalization and degradation in T-cells. We hypothesize that high-level TSLP induces internalization and degradation of IL-7Ra leading to CRLF2 signal inhibition, death of CRLF2 B-ALL cells and the anti-leukemia effects that we have observed in PDX mice. To test this hypothesis, we treated CRLF2 B-ALL cell lines with different TSLP concentrations to observe the effect of TSLP on its receptor and CRLF2 signaling. Flow cytometry data showed that continuous or a pulse of high-dose TSLP induced a loss of surface IL-7Ra expression for up to 24 hours. Phosphorylation assays showed that cells cultured with high-dose TSLP were unresponsive to subsequent TSLP-induced phosphorylation events (pSTAT5 and pRPS6), indicating CRLF2 signal inhibition. In conclusion, high-dose TSLP induces loss of (IL-7Ra) and inhibition of CRLF2 signaling. These results suggest that TSLP exerts its anti-leukemia effects by shutting down CRLF2-mediated signals possibly via the loss of the IL-7Ra receptor component. Citation Format: Hossam Alkashgari, Cornelia Stoian, Caleb Ruiz-Jimenez, Jacqueline Coats, Carlos A. Casiano, Sinisa Dovat, Kimberly J. Payne. Molecular mechanisms of TSLP as a therapy for CRLF2 B-Cell acute lymphoblastic leukemia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1528.
Dissertations / Theses on the topic "Caleb T"
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Cazoir, David-Alexandre. "Traitement d'eaux huileuses par photocatalyse h��t��rog��ne : application �� la d��pollution des eaux de cales." Phd thesis, Universit�� Claude Bernard - Lyon I, 2011. http://tel.archives-ouvertes.fr/tel-00745779.
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Afin de r��duire la quantit�� d'hydrocarbures d��vers��s dans le milieu marin, les navires de la flotte marchande et, depuis peu, les navires militaires sont tenus de contr��ler leurs rejets huileux. Par exemple, seules les eaux de cales dont la concentration en huile (indice hydrocarbure) est inf��rieure �� 15 ppmv peuvent ��tre d��vers��es en mer (Marpol 73/78). Au-del�� de cette teneur, et si le stockage �� bord n'est pas envisageable, un traitement avant rejet devient alors in��vitable. Cependant, les traitements actuels des eaux de cales se sont av��r��s jusqu'ici insuffisants. La photocatalyse h��t��rog��ne, m��thode largement utilis��e dans le cas du traitement d'effluents gazeux et liquides, a ainsi ��t�� propos��e dans ce travail. L'abattement de l'indice hydrocarbure a ��t�� suivi par analyse GC-MS. D��s lors, apr��s avoir mis en ��vidence la faisabilit�� et les limites du proc��d�� batch, un r��acteur photocatalytique �� a��ration diffus��e (DAPR) a ��t�� d��velopp�� afin de rem��dier au manque d'oxyg��ne dissous de l'effluent r��el. Comparativement au traitement dans le r��acteur batch, une meilleure efficacit�� de la d��gradation a ��t�� observ��e dans le DAPR. Cependant, l'analyse parall��le (ATD-GC-MS) de l'��volution de la composition de la phase gazeuse a montr�� qu'une quantit�� non n��gligeable de compos��s organiques volatils (COV) y ��taient alors ��mis. Enfin, les nalcanes ont ��t�� identifi��s comme ��tant les compos��s les plus r��fractaires au traitement photocatalytique et le pentad��cane a alors ��t�� choisi comme polluant mod��le des eaux de cales pour une analyse cin��tique.
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Gesse, Pascal [Verfasser], T. J. J. [Gutachter] Müller, and Jörg [Gutachter] Pietruszka. "Konsekutive 5-, 6- und 7-Komponentensynthesen auf Basis von Ugi-Vierkomponenten-CALB-Aminolyse-Ein-Topf-Sequenzen / Pascal Gesse ; Gutachter: T. J. J. Müller, Jörg Pietruszka." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1203872429/34.
Full textBook chapters on the topic "Caleb T"
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Sefryn, Penrose. "Creative Destruction and Neoliberal Landscapes: Post-industrial Archaeologies Beyond Ruins." In Contemporary Archaeology and the City. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198803607.003.0018.
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‘[T]he problem that is usually being visualized is how capitalism administers existing structures, whereas the relevant problem is how it creates and destroys them’, wrote the Austrian economist, Josef Schumpeter in Capitalism, Socialism and Democracy, in 1942 (84). He was describing his discipline’s response to creative destruction; the process of continuous reinvention within capitalist markets. Like Schumpeter’s visualizing economists, are archaeologists in danger of bolstering a static view? Of pushing a preservation-of-decay agenda, appealing to a mass diagnosis of the rot of modernity? Ruin studies within contemporary and historical archaeology frequently present an overtly anti-capitalist critique, within an aesthetic conception of things and place, sometimes accompanied by an anti-heritage stance (cf. González-Ruibal, Chapter 7). In recent years archaeologists have recognized and at times moved away from, the problem of aestheticization, but continue to parade an underdog status for the stationary object that reverts to an uneasy stasis—an object from the ground—without an acknowledgement of the movement and change that both contemporary and historical archaeology have worked so hard to develop (e.g. Aldred 2014; Beaudry and Parno 2013; Holtorf and Piccini 2009). This can lead to a tendency to critique without fully situating ruin—site, place—in process, despite benchmark studies (e.g. Gosden 2004). Pictures capture a moment. A ruin illustrates an end. Memory mourns the past. What remains, decays. In this chapter I address some of the landscapes considered epitomic of neoliberalism: the ‘winners’ in the landscape of capitalism, and consider whether current archaeological approaches to the contemporary have inadvertently, or indeed overtly, disqualified them from analysis. I present case studies that illustrate the ‘creative’ side of ‘creative destruction’—the larges-cale landscape transformation of deindustrialized areas. These sites were transformed through governmental interventions in policy—privatization, public–private investment frameworks, changes to the planning system— with the intention of transforming declined industrial areas into economic success stories in line with the push towards a service economy, away from industry. There is of course another side to this story: as Arthur Marwick observed the reinvigoration of declined industrial areas is often characterized by ‘a growing mismatch between the characteristics of those seeking work and the kind of jobs which [a]re available’ (Marwick 2003: 153).
Conference papers on the topic "Caleb T"
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Harris, L., J. Parker, G. Broadwater, V. Schulz, K. Halligan, K. Geyda, A. Seidman, et al. "Genome-Wide Profiling of Archived Material from CALGB 9840 and 9342 for Paclitaxel (P) and Trastuzumab (T) Response Biomarkers Using Gene Expression and Copy Number Analysis." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4032.
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Zhang, Jun, Yiyao Liu, Mingxing Wen, Yufeng Yue, Haoyuan Zhang, and Danwei Wang. "L2V2T2Calib: Automatic and Unified Extrinsic Calibration Toolbox for Different 3D LiDAR, Visual Camera and Thermal Camera." In 2023 IEEE Intelligent Vehicles Symposium (IV). IEEE, 2023. http://dx.doi.org/10.1109/iv55152.2023.10186657.
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Hoadley, Katherine A., William T. Barry, Brandelyn N. Pitcher, Joel S. Parker, Matthew D. Wilkerson, William Irvin, Norah Lynn Henry, et al. "Abstract S3-06: Mutational analysis of CALGB 40601 (Alliance), a neoadjuvant phase III trial of weekly paclitaxel (T) and trastuzumab (H) with or without lapatinib (L) for HER2-positive breast cancer." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-s3-06.
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Tanioka, M., C. Fan, LA Carey, T. Hyslop, BN Pitcher, JA Parker, KA Hoadley, et al. "Abstract S3-05: Integrated analysis of multidimensional genomic data on CALGB 40601 (Alliance), a randomized neoadjuvant phase III trial of weekly paclitaxel (T) and trastuzumab (H) with or without lapatinib (L) for HER2-positive breast cancer." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-s3-05.
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Shulman, LN, C. Cirrincione, DA Berry, HP Becker, E. Perez, R. O'Regan, S. Martino, JN Atkins, C. Hudis, and E. Winer. "Abstract S6-3: Four vs 6 Cycles of Doxorubicin and Cyclophosphamide (AC) or Paclitaxel (T) as Adjuvant Therapy for Breast Cancer in Women with 0-3 Positive Axillary Nodes: CALGB 40101 — A 2x2 Factorial Phase III Trial: First Results Comparing 4 vs 6 Cycles of Therapy." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-s6-3.
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Xiaozhi Wang and Neil Pegg, ISSC 2022 Editors. "Proceedings of the 21st International Ship and Offshore Structures Congress VOLUME 3 Discussions." In 21st International Ship and Offshore Structures Congress Volume 3 Discussions. SNAME, 2022. http://dx.doi.org/10.5957/issc-2022-discussion-vol-3.
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Committee I.1: Environment Alexander Babanin (Chair); Mariana Bernardino; Franz von Bock und Polach; Ricardo Campos,; Jun Ding; Sanne van Essen; Tomaso Gaggero; Maryam Haroutunian; Vanessa Katsardi; Alexander Nilva; Arttu Polojarvi; Erik Vanem; Jungyong Wang; Huidong Zhang; Tingyao Zhu Floor Discussers: Florian Sprenger; Carlos Guedes Soares; Henk den Besten Committee I.2: Loads Ole Andreas Hermundstad (Chair); Shuhong Chai; Guillaume de Hauteclocque; Sheng Dong; Chih-Chung Fang; Thomas B. Johannessen; Celso Morooka; Masayoshi Oka; Jasna Prpić-Oršić; Alessandro Sacchet; Mahmud Sazidy; Bahadir Ugurlu; Roberto Vettor; Peter Wellens Official Discusser: Hayden Marcollo Committee II-1: Quasi-Static Response James Underwood (Chair); Erick Alley; Jerolim Andrić Dario Boote; Zhen Gao; Ad Van Hoeve; Jasmin Jelovica; Yasumi Kawamura; Yooil Kim; Jian Hu Liu; Sime Malenica; Heikki Remes; Asokendu Samanta; Krzysztof Woloszyk; Deqing Yang Official Discusser: Prof. T. Yoshikwa Committee II.2: Dynamic Response Gaute Storhaug (Chair); Daniele Dessi; Sharad Dhavalikar; Ingo Drummen; Michael Holtmann; Young-Cheol Huh; Lorenzo Moro; Andre Paiva; Svein Sævik; Rong-Juin Shyu; Shan Wang; Sue Wang; WenWei Wu; Yasuhira Yamada; Guiyong Zhang Floor Discussers: Ling Zhu; Tomoki Takami; Anriette (Annie) Bekker; Bruce Quinton; Robert Sielski Committee III.1: Ultimate Strength Paul E. Hess (Chair); Chen An; Lars Brubak; Xiao Chen; Jinn Tong Chiu; Jurek Czujko; Ionel Darie; Guoqing Feng; Marco Gaiotti; Beom Seon Jang; Adnan Kefal; Sukron Makmun; Jonas Ringsberg; Jani Romanoff; Saad Saad-Eldeen; Ingrid Schipperen; Kristjan Tabri; Yikun Wang; Daisuke Yanagihara Official Discusser: Jørgen Amdahl Committee III.2: Fatigue and Fracture Yordan Garbatov (Chair); Sigmund K Ås; Henk Den Besten; Philipp Haselbach; Adrian Kahl; Dale Karr; Myung Hyun Kim; Junjie Liu; Marcelo Igor Lourenço de Souza; Wengang Mao; Eeva Mikkola; Naoki Osawa; Fredhi Agung Prasetyo; Mauro Sicchiero; Suhas Vhanmane; Marta Vicente del Amo; Jingxia Yue Official Discusser Weicheng Cui Floor Discussers: Robert Sielski; Sören Ehlers; Stephane Paboeuf; Teresa Magoga Committee IV.1: Design Principles and Criteria Matthew Collette (Chair); Piero Caridis; Petar Georgiev; Torfinn Hørte; Han Koo Jeong; Rafet emek Kurt; Igor Ilnytskiy; Tetsuo Okada; Charles Randall; Zbigniew Sekulski; Matteo Sidari; Zhihu Zhan; Ling Zhu Official Discusser: Enrico Rizzuto Committee IV.2: Design Methods Andrea Ivaldi (Chair); Abbas Bayatfar; Jean-David Caprace; Gennadiy Egorov; Svein Erling Heggelund; Shinichi Hirakawa; Jung Min Kwon; Dan Mcgreer; Pero Prebeg; Robert Sielski; Mark Slagmolen; Adam Sobey; Wenyong Tang; Jiameng Wu Official Discusser: Mario Dogliani Committee V.1: Accidental Limit States Bruce Quinton; Gaetano De Luca; Topan Firmandha; Mihkel Körgesaar; Hervé Le Sourne; Ken Nahshon; Gabriele Notaro; Kourosh Parsa; Smiljko Rudan; Katsuyuki Suzuki; Osiris Valdez Banda; CareyWalters; Deyu Wang; Zhaolong Yu Official Discusser: Manolis Samuelides Committee V.2: Experimental Methods Sören Ehlers (Chair); Nagi Abdussamie; Kim Branner; ShiXiao Fu; Martijn Hoogeland; Kari Kolari; Paul Lara; Constantine Michailides; Hideaki Murayama; Cesare Rizzo; Jung Kwan Seo; Patrick Kaeding Official Discusser: Giles Thomas Committee V.3: Materials and Fabrication Technology Lennart Josefson (Chair); Konstantinos Anyfantis; Bianca de Carvalho Pinheiro; Bai-Qiao Chen; Pingsha Dong; Nicole Ferrari; Koji Gotoh; James Huang; Matthias Krause; Kun Liu; Stephane Paboeuf; Stephen van Duin; Fang Wang; Albert Zamarin Official Discusser: Frank Roland Floor Discussers Alessandro Caleo; Agnes Marie Horn; Krzysztof Woloszyk; Robert Sielski Committee V.4: Offshore Renewable Energy Atanasios Kolios (Chair); Kyong-Hwan Kim; Chen Hsing Cheng; Elif Oguz; Pablo Morato; Freeman Ralph; Chuang Fang; Chunyan Ji; Marc Le Boulluec; Thomas Choisnet; Luca Greco; Tomoaki Utsunomiya; Kourosh Rezanejad; Charles Rawson; Jose Miguel Rodrigues Official Discusser: Amy Robertson Committee V.5: Special Vessels Darren Truelock (Chair); Jason Lavroff; Dustin Pearson; Zbigniew (Jan) Czaban; Hanbing Luo; Fuhua Wang; Ivan Catipovic; Ermina Begovic; Yukichi Takaoka; Claudia Loureiro; Chang Yong Song; Esther Garcia; Alexander Egorov; Jean-Baptiste Souppez; Pradeep Sensharma; Rachel Nicholls-Lee Official Discusser: Jaye Falls Floor Discussers: Jasmin Jelovica; Stephane Paboeuf; Sören Ehlers Committee V.6: Ocean Space Utilization Sebastian Schreier (Chair); Felice Arena; Harry Bingham; Nuno Fonseca; Zhiqiang Hu; Debabrata Karmakar; Ekaterina Kim; Hui Li; Pengfei Liu; Motohiko Murai; Spiro J Pahos; Chao Tian; George Wang Official Discusser: Hideyuki Suzuki Floor Discussers: Robert Sielski; Sue Wang; Sarat Mohapatra; Gaute Storhaug; Henk den Besten Committee V.7: Structural Longevity Iraklis Lazakis (Chair); Bernt Leira; Nianzhong Chen; Geovana Drumond; Chi-Fang Lee; Paul Jurisic; Bin Liu; Alysson Mondoro; Pooria Pahlavan; Xinghua Shi; Ha Cheol Song; Tadashi Sugimura; Christian Jochum; Tommaso Coppola Official Discusser: Timo de Beer Floor Discusser: Krzysztof Woloszyk Committee V.8: Subsea Technology Agnes Marie Horn (Chair); Tauhid Rahman; Ilson Pasqualino; Menglan Duan; Zhuang Kang; Michael Rye Andersen; Yoshihiro Konno; Chunsik Shim; Angelo Teixeira; Selda Oterkus; Blair Thornton; Brajendra Mishra Official Discusser: Segen F. Estefen