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2. 172 Spatiotemporal architecting of skin dendritic cell directed immunity and tolerance

Author

Huang, Q., primary, Doane, A.S., additional, Liu, Y., additional, Valencia, J., additional, Nirschl, C., additional, Hsu, J., additional, Savitz, A., additional, Pradhan, K., additional, Jaiswal, A., additional, Song-Zhao, G., additional, Bale, M., additional, Ricardo-Gonzalez, R.R., additional, Locksley, R., additional, Lawrence, T., additional, Young, H., additional, Suarez-Farinas, M., additional, Elemento, O., additional, and Anandasabapathy, N., additional

Published
2023
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5. 037 A systems immunology approach to classify melanoma tumor infiltrating lymphocytes (TILs) informs and models overall survival

Author

Jaiswal, A., primary, Verma, A., additional, Dannenfelser, R., additional, Melssen, M., additional, Tirosh, I., additional, Izar, B., additional, Kim, T., additional, Nirschl, C., additional, Devi, S., additional, Olson, W., additional, Slingluff, C., additional, Engelhard, V., additional, Garraway, L., additional, Regev, A., additional, Yoon, C., additional, Troyanskaya, O., additional, Elemento, O., additional, Suarez-Farinas, M., additional, and Anandasabapathy, N., additional

Published
2022
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6. 646 A nuclear cAMP microdomain suppresses tumor growth by hippo pathway inactivation

Author

Drozdz, M., primary, Doane, A.S., additional, Alkallas, R., additional, Desman, G., additional, Bareja, R., additional, Reilly, M., additional, Bang, J., additional, Yusupova, M., additional, You, J., additional, Wang, J., additional, Verma, A., additional, Aguirre, K., additional, Kang, E., additional, Watson, I., additional, Elemento, O., additional, Piskounova, E., additional, Merghoub, T., additional, and Zippin, J., additional

Published
2022
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8. Conservation of copy number profiles during engraftment and passaging of patient-derived cancer xenografts

Author

Woo, X.Y., Giordano, J., Srivastava, A., Zhao, Z.-., Lloyd, M.W., de Bruijn, R., Suh, Y.-., Patidar, R., Chen, L., Scherer, S., Bailey, M.H., Yang, C.-., Cortes-Sanchez, E., Xi, Y., Wang, J., Wickramasinghe, J., Kossenkov, A.V., Rebecca, V.W., Sun, H., Mashl, R.J., Davies, S.R., Jeon, R., Frech, C., Randjelovic, J., Rosains, J., Galimi, F., Bertotti, A., Lafferty, A., O'Farrell, A.C., Modave, E., Lambrechts, D., ter Brugge, P., Marangoni, E., El Botty, R., Kim, H., Kim, J.-., Yang, H.-., Lee, C., Dean, D.A., Davis-Dusenbery, B., Evrard, Y.A., Doroshow, J.H., Welm, A.L., Welm, B.E., Lewis, M.T., Fang, B., Roth, J.A., Meric-Bernstam, F., Herlyn, M., Davies, M.A., Ding, L., Li, S., Govindan, R., Isella, C., Moscow, J.A., Trusolino, L., Byrne, A.T., Jonkers, J., Bult, C.J., Medico, E., Chuang, J.H., Robinson, P.N., Sanderson, B.J., Neuhauser, S.B., Dobrolecki, L.E., Zheng, X., Majidi, M., Zhang, R., Zhang, X., Akcakanat, A., Evans, K.W., Yap, T.A., Li, D., Yucan, E., Lanier, C.D., Saridogan, T., Kirby, B.P., M. J., H., Chen, H., Kopetz, S., Menter, D.G., Zhang, J., Westin, S.N., Kim, M.P., Dai, B., Gibbons, D.L., Tapia, C., Jensen, V.B., Boning, G., Minna, J.D., Park, H., Timmons, B.C., Girard, L., Fingerman, D., Liu, Q., Somasundaram, R., Xiao, M., Yennu-Nanda, V.G., Tetzlaff, M.T., Xu, X., Nathanson, K.L., Cao, S., Chen, F., Dipersio, J.F., Lim, K.H., C. X., M., Rodriguez, F.M., Van Tine, B.A., Wang-Gillam, A., Wendl, M.C., Wu, Y., Wyczalkowski, M.A., Yao, L., Jayasinghe, R., Aft, R.L., Fields, R.C., Luo, J., Fuh, K.C., Chin, V., Digiovanna, J., Grover, J., Koc, S., Seepo, S., Wallace, T., Pan, C.-., Chen, M.S., Carvajal-Carmona, L.G., Kirane, A.R., Cho, M., Gandara, D.R., Riess, J.W., Le, T., deVere White, R.W., Tepper, C.G., Zhang, H., Coggins, N.B., Lott, P., Estrada, A., Toal, T., Arana, A.M., Polanco-Echeverry, G., Rocha, S., A. -H., M., Mitsiades, N., Kaochar, S., O'Malley, B.W., Ellis, M.J., Hilsenbeck, S.G., Ittmann, M., Corso, S., Fiori, A., Giordano, S., van de Ven, M., Peeper, D.S., Miller, I., Bernado, C., Morancho, B., Ramirez, L., Arribas, J., Palmer, H.G., Piris-Gimenez, A., Soucek, L., Dahmani, A., Montaudon, E., Nemati, F., Dangles-Marie, V., Decaudin, D., Roman-Roman, S., Alferez, D.G., Spence, K., Clarke, R.B., Bentires-Alj, M., Chang, D.K., Biankin, A.V., Bruna, A., O'Reilly, M., Caldas, C., Casanovas, O., Gonzalez-Suarez, E., Munoz, P., Villanueva, A., Conte, N., Mason, J., Thorne, R., Meehan, T.F., Parkinson, H., Dudova, Z., Krenek, A., Stuchlik, D., Elemento, O., Inghirami, G., Golebiewska, A., Niclou, S.P., Wisman, G.B.A., de Jong, S., Kralova, P., Sedlacek, R., Claeys, E., Leucci, E., Borsani, M., Lanfrancone, L., Pelicci, P.G., Maelandsmo, G.M., Norum, J.H., Vinolo, E., Serra, V., and Leucci, Eleonora

Subjects
endocrine system diseases, Microarray, gene amplification, Whole Exome Sequencing, Mice, 0302 clinical medicine, Gene expression, Databases, Genetic, Gene duplication, Neoplasm Metastasis, Exome sequencing, Cancer, Regulation of gene expression, 0303 health sciences, Manchester Cancer Research Centre, adult, adult, animal experiment, animal model, animal tissue, breast cancer, microarray, DNA sequencing engraftment, gene amplification, tumor, xenograft, tumor-related gene, Polymorphism, Single Nucleotide/genetics, 3. Good health, Gene Expression Regulation, Neoplastic, 030220 oncology & carcinogenesis, microarray, hormones, hormone substitutes, and hormone antagonists, tumor, endocrine system, DNA sequencing engraftment, animal experiment, DNA Copy Number Variations/genetics, Biology, digestive system, DNA sequencing, Article, animal tissue, 03 medical and health sciences, breast cancer, Breast cancer, Genetics, medicine, Animals, Humans, xenograft, Gene, 030304 developmental biology, Settore MED/04 - Patologia Generale, Microarray analysis techniques, animal model, ResearchInstitutes_Networks_Beacons/mcrc, tumor-related gene, medicine.disease, Xenograft Model Antitumor Assays, Computational biology and bioinformatics, Cancer research, Human cancer
Abstract

Patient-derived xenografts (PDXs) are resected human tumors engrafted into mice for preclinical studies and therapeutic testing. It has been proposed that the mouse host affects tumor evolution during PDX engraftment and propagation, affecting the accuracy of PDX modeling of human cancer. Here, we exhaustively analyze copy number alterations (CNAs) in 1,451 PDX and matched patient tumor (PT) samples from 509 PDX models. CNA inferences based on DNA sequencing and microarray data displayed substantially higher resolution and dynamic range than gene expression-based inferences, and they also showed strong CNA conservation from PTs through late-passage PDXs. CNA recurrence analysis of 130 colorectal and breast PT/PDX-early/PDX-late trios confirmed high-resolution CNA retention. We observed no significant enrichment of cancer-related genes in PDX-specific CNAs across models. Moreover, CNA differences between patient and PDX tumors were comparable to variations in multiregion samples within patients. Our study demonstrates the lack of systematic copy number evolution driven by the PDX mouse host., Analysis of copy number alterations in 1,451 patient-derived xenografts (PDXs) and matched patient tumor samples shows strong conservation from patient tumors through late-passage PDXs and a lack of systematic copy number evolution driven by the mouse host.

Published
2021

9. Analytical demands to use whole-genome sequencing in precision oncology

Author

Meggendorfer, M, Jobanputra, V, Wrzeszczynski, KO, Roepman, P, de Bruijn, E, Cuppen, E, Buttner, R, Caldas, C, Grimmond, S, Mullighan, CG, Elemento, O, Rosenquist, R, Schuh, A, Haferlach, T, Meggendorfer, M, Jobanputra, V, Wrzeszczynski, KO, Roepman, P, de Bruijn, E, Cuppen, E, Buttner, R, Caldas, C, Grimmond, S, Mullighan, CG, Elemento, O, Rosenquist, R, Schuh, A, and Haferlach, T

Abstract

Interrogating the tumor genome in its entirety by whole-genome sequencing (WGS) offers an unprecedented insight into the biology and pathogenesis of cancer, with potential impact on diagnostics, prognostication and therapy selection. WGS is able to detect sequence as well as structural variants and thereby combines central domains of cytogenetics and molecular genetics. Given the potential of WGS in directing targeted therapeutics and clinical decision-making, we envision a gradual transition of the method from research to clinical routine. This review is one out of three within this issue aimed at facilitating this effort, by discussing in-depth analytical validation, clinical interpretation and clinical utility of WGS. The review highlights the requirements for implementing, validating and maintaining a clinical WGS pipeline to obtain high-quality patient-specific data in accordance with the local regulatory landscape. Every step of the WGS pipeline, which includes DNA extraction, library preparation, sequencing, bioinformatics analysis, and data storage, is considered with respect to its logistics, necessities, potential pitfalls, and the required quality management. WGS is likely to drive clinical diagnostics and patient care forward, if requirements and challenges of the technique are recognized and met.

Published
2022

10. Implementation of Whole-Genome and Transcriptome Sequencing Into Clinical Cancer Care

Author

Cuppen, E, Elemento, O, Rosenquist, R, Nikic, S, IJzerman, M, Zaleski, ID, Frederix, G, Levin, L-A, Mullighan, CG, Buettner, R, Pugh, TJ, Grimmond, S, Caldas, C, Andre, F, Custers, I, Campo, E, van Snellenberg, H, Schuh, A, Nakagawa, H, von Kalle, C, Haferlach, T, Froehling, S, Jobanputra, V, Cuppen, E, Elemento, O, Rosenquist, R, Nikic, S, IJzerman, M, Zaleski, ID, Frederix, G, Levin, L-A, Mullighan, CG, Buettner, R, Pugh, TJ, Grimmond, S, Caldas, C, Andre, F, Custers, I, Campo, E, van Snellenberg, H, Schuh, A, Nakagawa, H, von Kalle, C, Haferlach, T, Froehling, S, and Jobanputra, V

Abstract

PURPOSE: The combination of whole-genome and transcriptome sequencing (WGTS) is expected to transform diagnosis and treatment for patients with cancer. WGTS is a comprehensive precision diagnostic test that is starting to replace the standard of care for oncology molecular testing in health care systems around the world; however, the implementation and widescale adoption of this best-in-class testing is lacking. METHODS: Here, we address the barriers in integrating WGTS for cancer diagnostics and treatment selection and answer questions regarding utility in different cancer types, cost-effectiveness and affordability, and other practical considerations for WGTS implementation. RESULTS: We review the current studies implementing WGTS in health care systems and provide a synopsis of the clinical evidence and insights into practical considerations for WGTS implementation. We reflect on regulatory, costs, reimbursement, and incidental findings aspects of this test. CONCLUSION: WGTS is an appropriate comprehensive clinical test for many tumor types and can replace multiple, cascade testing approaches currently performed. Decreasing sequencing cost, increasing number of clinically relevant aberrations and discovery of more complex biomarkers of treatment response, should pave the way for health care systems and laboratories in implementing WGTS into clinical practice, to transform diagnosis and treatment for patients with cancer.

Published
2022

15. PRMT5 INHIBITION RESTARTS A PRO‐APOPTOTIC PROGRAM AND CREATES VULNERABILITY TO COMBINATION TREATMENT WITH BCL‐2 INHIBITOR VENETOCLAX IN MANTLE CELL LYMPHOMA

Author

Brown, F, primary, Hwang, I, additional, Sloan, S, additional, Hinterschied, C, additional, Helmig‐Mason, J, additional, Long, M, additional, Youssef, Y, additional, Chan, W, additional, Prouty, A, additional, Chung, J, additional, Zhang, Y, additional, Chen‐Kiang, S, additional, DiLiberto, M, additional, Elemento, O, additional, Sehgal, L, additional, Alinari, L, additional, Scherle, P, additional, Vaddi, K, additional, Lapalombella, R, additional, Paik, J, additional, and Baiocchi, R. A, additional

Published
2021
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18. Common deleterious germline variants shape the urothelial cancer genome

Author

Vosoughi, A, primary, Zhang, T, additional, Shohdy, KS, additional, Vlachostergios, PJ, additional, Wilkes, DC, additional, Tagawa, ST, additional, Nanus, SM, additional, Molina, AM, additional, Beltran, H, additional, Sternberg, CN, additional, Motanagh, S, additional, Robinson, BD, additional, Xiang, J, additional, Chung, WK, additional, Rubin, MA, additional, Elemento, O, additional, Sboner, A, additional, Mosquera, JM, additional, and Faltas, BM, additional

Published
2020
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19. Genomic Landscape of Reed-Sternberg Cells of Hodgkin Lymphoma from Children, Adolescents, and Young Adults

Author

Roshal, M, additional, Xiang, JZ, additional, Park, S, additional, Oberley, M, additional, Ruchdeschel, E, additional, Lim, M, additional, Wertheim, G, additional, Barth, M, additional, Horton, TM, additional, Bhinder, B, additional, Wha, Eng K, additional, He, F, additional, Zhang, W, additional, Tan, A, additional, Elemento, O, additional, and Giulino-Roth, L, additional

Published
2020
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21. Reconstruction of Patient-Specific Distal Airway Regeneration Patterns in COPD

Author

Mahjour, S.B., primary, Gomi, K., additional, Rustam, S., additional, Dolma, P., additional, Krishnan, J., additional, Bareja, R., additional, Hu, Y., additional, Elemento, O., additional, Zhang, T., additional, Xiang, J., additional, Urso, A., additional, D'Ovidio, F., additional, Randell, S.H., additional, Richmond, B.W., additional, Polosukhin, V.V., additional, Blackwell, T.S., additional, and Shaykhiev, R., additional

Published
2019
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22. Phenotype, penetrance, and treatment of 133 cytotoxic T-lymphocyte antigen 4-insufficient subjects

Author

Schwab, C., Gabrysch, A., Olbrich, P., Patino, V., Warnatz, K., Wolff, D., Hoshino, A., Kobayashi, M., Imai, K., Takagi, M., Dybedal, I., Haddock, J.A., Sansom, D.M., Lucena, J.M., Seidl, M., Schmitt-Graeff, A., Reiser, V., Emmerich, F., Frede, N., Bulashevska, A., Salzer, U., Schubert, Desiree, Hayakawa, S., Okada, S., Kanariou, M., Kucuk, Z.Y., Chapdelaine, H., Petruzelkova, L., Sumnik, Z., Sediva, A., Slatter, M., Arkwright, P.D., Cant, A., Lorenz, H.M., Giese, T., Lougaris, V., Plebani, A., Price, C., Sullivan, K.E., Moutschen, M., Litzman, J., Freiberger, T., Veerdonk, F.L. van de, Recher, M., Albert, M.H., Hauck, F., Seneviratne, S., Schmid, J., Kolios, A., Unglik, G., Klemann, C., Speckmann, C., Ehl, S., Leichtner, A., Blumberg, R., Franke, A., Snapper, S., Zeissig, S., Cunningham-Rundles, C., Giulino-Roth, L., Elemento, O., Duckers, G., Niehues, T., Fronkova, E., Kanderova, V., Platt, C.D., Chou, J., Chatila, T.A., Geha, R., McDermott, E., Bunn, S., Kurzai, M., Schulz, A., Alsina, L., Casals, F., Deya-Martinez, A., Hambleton, S., Kanegane, H., Tasken, K., Neth, O., Grimbacher, B., Schwab, C., Gabrysch, A., Olbrich, P., Patino, V., Warnatz, K., Wolff, D., Hoshino, A., Kobayashi, M., Imai, K., Takagi, M., Dybedal, I., Haddock, J.A., Sansom, D.M., Lucena, J.M., Seidl, M., Schmitt-Graeff, A., Reiser, V., Emmerich, F., Frede, N., Bulashevska, A., Salzer, U., Schubert, Desiree, Hayakawa, S., Okada, S., Kanariou, M., Kucuk, Z.Y., Chapdelaine, H., Petruzelkova, L., Sumnik, Z., Sediva, A., Slatter, M., Arkwright, P.D., Cant, A., Lorenz, H.M., Giese, T., Lougaris, V., Plebani, A., Price, C., Sullivan, K.E., Moutschen, M., Litzman, J., Freiberger, T., Veerdonk, F.L. van de, Recher, M., Albert, M.H., Hauck, F., Seneviratne, S., Schmid, J., Kolios, A., Unglik, G., Klemann, C., Speckmann, C., Ehl, S., Leichtner, A., Blumberg, R., Franke, A., Snapper, S., Zeissig, S., Cunningham-Rundles, C., Giulino-Roth, L., Elemento, O., Duckers, G., Niehues, T., Fronkova, E., Kanderova, V., Platt, C.D., Chou, J., Chatila, T.A., Geha, R., McDermott, E., Bunn, S., Kurzai, M., Schulz, A., Alsina, L., Casals, F., Deya-Martinez, A., Hambleton, S., Kanegane, H., Tasken, K., Neth, O., and Grimbacher, B.

Abstract

Item does not contain fulltext, BACKGROUND: Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is a negative immune regulator. Heterozygous CTLA4 germline mutations can cause a complex immune dysregulation syndrome in human subjects. OBJECTIVE: We sought to characterize the penetrance, clinical features, and best treatment options in 133 CTLA4 mutation carriers. METHODS: Genetics, clinical features, laboratory values, and outcomes of treatment options were assessed in a worldwide cohort of CTLA4 mutation carriers. RESULTS: We identified 133 subjects from 54 unrelated families carrying 45 different heterozygous CTLA4 mutations, including 28 previously undescribed mutations. Ninety mutation carriers were considered affected, suggesting a clinical penetrance of at least 67%; median age of onset was 11 years, and the mortality rate within affected mutation carriers was 16% (n = 15). Main clinical manifestations included hypogammaglobulinemia (84%), lymphoproliferation (73%), autoimmune cytopenia (62%), and respiratory (68%), gastrointestinal (59%), or neurological features (29%). Eight affected mutation carriers had lymphoma, and 3 had gastric cancer. An EBV association was found in 6 patients with malignancies. CTLA4 mutations were associated with lymphopenia and decreased T-, B-, and natural killer (NK) cell counts. Successful targeted therapies included application of CTLA-4 fusion proteins, mechanistic target of rapamycin inhibitors, and hematopoietic stem cell transplantation. EBV reactivation occurred in 2 affected mutation carriers after immunosuppression. CONCLUSIONS: Affected mutation carriers with CTLA-4 insufficiency can present in any medical specialty. Family members should be counseled because disease manifestation can occur as late as 50 years of age. EBV- and cytomegalovirus-associated complications must be closely monitored. Treatment interventions should be coordinated in clinical trials.

Published
2018

23. Global miRNA expression analysis identifies novel key regulators of plasma cell differentiation and malignant plasma cell

Author

Kassambara, A, Jourdan, M, Bruyer, A, Robert, N, Pantesco, V, Elemento, O, Klein, B, Moreaux, J, Institut de génétique humaine (IGH), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Département Hématologie biologique [CHRU Montpellier], Pôle Biologie-Pathologie [CHRU Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Weill Medical College of Cornell University [New York], Université de Montpellier (UM), Larose, Catherine, and Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)

Subjects
[SDV.GEN]Life Sciences [q-bio]/Genetics, [SDV]Life Sciences [q-bio], Plasma Cells, Computational Biology, Cell Differentiation, DNA-Binding Proteins, Gene Expression Regulation, Neoplastic, Repressor Proteins, MicroRNAs, Cell Transformation, Neoplastic, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Interferon Regulatory Factors, otorhinolaryngologic diseases, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Humans, Gene Regulatory Networks, Positive Regulatory Domain I-Binding Factor 1, RNA, Messenger, Transcriptional Elongation Factors, Multiple Myeloma, ComputingMilieux_MISCELLANEOUS, Transcription Factors
Abstract

International audience; MicroRNAs (miRNAs) are small noncoding RNAs that attenuate expression of their mRNA targets. Here, we developed a new method and an R package, to easily infer candidate miRNA–mRNA target interactions that could be functional during a given biological process. Using this method, we described, for the first time, a comprehensive integrated analysis of miRNAs and mRNAs during human normal plasma cell differentiation (PCD). Our results reveal 63 miRNAs with significant temporal changes in their expression during normal PCD. We derived a high-confidence network of 295 target relationships comprising 47 miRNAs and 141 targets. These relationships include new examples of miRNAs that appear to coordinately regulate multiple members of critical pathways associated with PCD. Consistent with this, we have experimentally validated a role for the miRNA-30b/c/d-mediated regulation of key PCD factors (IRF4, PRDM1, ELL2 and ARID3A). Furthermore, we found that 24 PCD stage-specific miRNAs are aberrantly overexpressed in multiple myeloma (MM) tumor plasma cells compared to their normal counterpart, suggesting that MM cells frequently acquired expression changes in miRNAs already undergoing dynamic expression modulation during normal PCD. Altogether, our analysis identifies candidate novel key miRNAs regulating networks of significance for normal PCD and malignant plasma cell biology

Published
2017

25. Abstract P6-07-10: The ERβ4 variant induce transformation of the normal breast mammary epithelial cell line MCF-10A; the ERβ variants ERβ2, ERβ4 and ERβ5 increase aggressiveness of TNBC by regulation of hypoxic signaling

Author

Faria, M, primary, Karami, S, additional, Granados-Principal, S, additional, Dey, P, additional, Verma, A, additional, Choi, DS, additional, Elemento, O, additional, Bawa-Khalfe1, T, additional, Chang, JC, additional, Gustafsson, J-A, additional, and Strom, AM, additional

Published
2018
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26. Abstract P2-09-01: T-cell receptor beta chain variable region (TRBV) expression patterns predict response to combined trastuzumab/lapatinib treatment in the NeoALTTO/BIG-1-06 trial

Author

Powles, R, primary, Redmond, D, additional, Sotiriou, C, additional, Loi, S, additional, Fumagalli, D, additional, Nuciforo, P, additional, Harbeck, N, additional, de Azambuja, E, additional, Sarp, S, additional, Di Cosimo, S, additional, Huober, J, additional, Baselga, J, additional, Piccart-Gebhart, M, additional, Elemento, O, additional, Hatzis, C, additional, and Pusztai, L, additional

Published
2018
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27. HARNESSING BTKI THERAPY BY CDK4/6I CONTROL OF T CELL SURVEILLANCE.

Author

Chen‐Kiang, S., Di Liberto, M., Huang, X., Inghirami, G., Martin, P., and Elemento, O.

Subjects
T cells, RNA sequencing, MANTLE cell lymphoma
Abstract

Primary resistance and progression on therapy were associated with a marked expansion of either long-live non-proliferating C3 cells or C2 cells that fuel the proliferating C4 cells. B Conclusion: b T cell surveillance plays a critical role in prolonging the ibrutinib response by CDK4/6 inhibition, implicating genome-guided combination therapy to overcome ibrutinib resistance in MCL. [Extracted from the article]

Published
2023
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38. Crystal Structure of the ER-alpha Ligand-binding Domain (Y537S) in Complex with the OBHS-ASC compound, 6-(4-((1R,4S,6R)-6-((4-bromophenoxy)sulfonyl)-3-(4-hydroxyphenyl)-7-oxabicyclo[2.2.1]hept-2-en-2-yl)phenoxy)hexanoic acid

Author

Nwachukwu, J.C., primary, Erumbi, R., additional, Srinivasan, S., additional, Bruno, N.E., additional, Nowak, J., additional, Izard, T., additional, Kojetin, D.J., additional, Elemento, O., additional, Katzenellenbogen, J.A., additional, and Nettles, K.W., additional

Published
2017
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40. Crystal Structure of the ER-alpha Ligand-binding Domain (Y537S) in Complex with the estradiol derivative, (8S,9S,13S,14S,17S)-16-(3-methoxybenzyl)-13-methyl-7,8,9,11,12,13,14,15,16,17-decahydro-6H-cyclopenta[a]phenanthrene-3,17-diol

Author

Nwachukwu, J.C., primary, Erumbi, R., additional, Srinivasan, S., additional, Bruno, N.E., additional, Nowak, J., additional, Izard, T., additional, Kojetin, D.J., additional, Elemento, O., additional, Katzenellenbogen, J.A., additional, and Nettles, K.W., additional

Published
2017
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41. Crystal Structure of the ER-alpha Ligand-binding Domain (Y537S) in Complex with the Arene Core OBHS derivative, 4-bromophenyl 4,4''-dihydroxy-[1,1':2',1''-terphenyl]-4'-sulfonate

Author

Nwachukwu, J.C., primary, Erumbi, R., additional, Srinivasan, S., additional, Bruno, N.E., additional, Nowak, J., additional, Izard, T., additional, Kojetin, D.J., additional, Elemento, O., additional, Katzenellenbogen, J.A., additional, and Nettles, K.W., additional

Published
2017
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45. Crystal Structure of the ER-alpha Ligand-binding Domain (Y537S) in Complex with the OBHS-ASC compound, 7-(4-((1R,4S,6R)-6-((3-chlorophenoxy)sulfonyl)-3-(4-hydroxyphenyl)-7-oxabicyclo[2.2.1]hept-2-en-2-yl)phenoxy)heptanoic acid

Author

Nwachukwu, J.C., primary, Erumbi, R., additional, Srinivasan, S., additional, Bruno, N.E., additional, Nowak, J., additional, Izard, T., additional, Kojetin, D.J., additional, Elemento, O., additional, Katzenellenbogen, J.A., additional, and Nettles, K.W., additional

Published
2017
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46. Crystal Structure of the ER-alpha Ligand-binding Domain (Y537S) in Complex with the Methyl(phenyl)amino-substituted Estrogen, (8R,9S,13S,14S,17S)-13-methyl-17-(methyl(phenyl)amino)-7,8,9,11,12,13,14,15,16,17-decahydro-6H-cyclopenta[a]phenanthren-3-ol

Author

Nwachukwu, J.C., primary, Srinivasan, S., additional, Bruno, N.E., additional, Nowak, J., additional, Kojetin, D.J., additional, Elemento, O., additional, Katzenellenbogen, J.A., additional, and Nettles, K.W., additional

Published
2017
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47. Crystal Structure of the ER-alpha Ligand-binding Domain (Y537S) in Complex with the OBHS-ASC analog, (E)-6-(4-((1R,4S,6R)-6-((4-bromophenoxy)sulfonyl)-3-(4-hydroxyphenyl)-7-oxabicyclo[2.2.1]hept-2-en-2-yl)phenyl)hex-5-enoic acid

Author

Nwachukwu, J.C., primary, Srinivasan, S., additional, Bruno, N.E., additional, Nowak, J., additional, Kojetin, D.J., additional, Elemento, O., additional, Katzenellenbogen, J.A., additional, and Nettles, K.W., additional

Published
2017
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50. Crystal Structure of the ER-alpha Ligand-binding Domain (Y537S) in Complex with the Cyclofenil-ASC derivative, ethyl (E)-3-(4-(bicyclo[3.3.1]nonan-9-ylidene(4-hydroxyphenyl)methyl)phenyl)acrylate

Author

Nwachukwu, J.C., primary, Erumbi, R., additional, Srinivasan, S., additional, Bruno, N.E., additional, Nowak, J., additional, Izard, T., additional, Kojetin, D.J., additional, Elemento, O., additional, Katzenellenbogen, J.A., additional, and Nettles, K.W., additional

Published
2017
Full Text
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