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2. Germline Aberrations in Pancreatic Cancer: Implications for Clinical Care

Author

Casolino, Raffaella, Corbo, Vincenzo, Beer, Philip, Hwang, Chang-il, Paiella, Salvatore, Silvestri, Valentina, Ottini, Laura, and Biankin, Andrew V

Subjects
Cancer, Orphan Drug, Digestive Diseases, Rare Diseases, Pancreatic Cancer, Genetics, Clinical Trials and Supportive Activities, Clinical Research, Prevention, Biotechnology, 2.1 Biological and endogenous factors, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Aetiology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Good Health and Well Being, germline, pancreatic cancer, BRCA, PARP inhibitors, precision prevention, familial pancreatic cancer, Oncology and Carcinogenesis
Abstract

Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis and represents a major public health issue, as both its incidence and mortality are expecting to increase steeply over the next years. Effective screening strategies are lacking, and most patients are diagnosed with unresectable disease precluding the only chance of cure. Therapeutic options for advanced disease are limited, and the treatment paradigm is still based on chemotherapy, with a few rare exceptions to targeted therapies. Germline variants in cancer susceptibility genes-particularly those involved in mechanisms of DNA repair-are emerging as promising targets for PDAC treatment and prevention. Hereditary PDAC is part of the spectrum of several syndromic disorders, and germline testing of PDAC patients has relevant implications for broad cancer prevention. Germline aberrations in BRCA1 and BRCA2 genes are predictive biomarkers of response to poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor olaparib and platinum-based chemotherapy in PDAC, while mutations in mismatch repair genes identify patients suitable for immune checkpoint inhibitors. This review provides a timely and comprehensive overview of germline aberrations in PDAC and their implications for clinical care. It also discusses the need for optimal approaches to better select patients for PARP inhibitor therapy, novel therapeutic opportunities under clinical investigation, and preclinical models for cancer susceptibility and drug discovery.

Published
2022

4. Prediction of acute myeloid leukaemia risk in healthy individuals.

Author

Abelson, Sagi, Collord, Grace, Ng, Stanley WK, Weissbrod, Omer, Mendelson Cohen, Netta, Niemeyer, Elisabeth, Barda, Noam, Zuzarte, Philip C, Heisler, Lawrence, Sundaravadanam, Yogi, Luben, Robert, Hayat, Shabina, Wang, Ting Ting, Zhao, Zhen, Cirlan, Iulia, Pugh, Trevor J, Soave, David, Ng, Karen, Latimer, Calli, Hardy, Claire, Raine, Keiran, Jones, David, Hoult, Diana, Britten, Abigail, McPherson, John D, Johansson, Mattias, Mbabaali, Faridah, Eagles, Jenna, Miller, Jessica K, Pasternack, Danielle, Timms, Lee, Krzyzanowski, Paul, Awadalla, Philip, Costa, Rui, Segal, Eran, Bratman, Scott V, Beer, Philip, Behjati, Sam, Martincorena, Inigo, Wang, Jean CY, Bowles, Kristian M, Quirós, J Ramón, Karakatsani, Anna, La Vecchia, Carlo, Trichopoulou, Antonia, Salamanca-Fernández, Elena, Huerta, José M, Barricarte, Aurelio, Travis, Ruth C, Tumino, Rosario, Masala, Giovanna, Boeing, Heiner, Panico, Salvatore, Kaaks, Rudolf, Krämer, Alwin, Sieri, Sabina, Riboli, Elio, Vineis, Paolo, Foll, Matthieu, McKay, James, Polidoro, Silvia, Sala, Núria, Khaw, Kay-Tee, Vermeulen, Roel, Campbell, Peter J, Papaemmanuil, Elli, Minden, Mark D, Tanay, Amos, Balicer, Ran D, Wareham, Nicholas J, Gerstung, Moritz, Dick, John E, Brennan, Paul, Vassiliou, George S, and Shlush, Liran I

Subjects
Humans, Disease Progression, Genetic Predisposition to Disease, Prevalence, Risk Assessment, Age Factors, Mutagenesis, Mutation, Models, Genetic, Adult, Aged, Middle Aged, Health, Female, Male, Leukemia, Myeloid, Acute, Electronic Health Records, Models, Genetic, Leukemia, Myeloid, Acute, General Science & Technology
Abstract

The incidence of acute myeloid leukaemia (AML) increases with age and mortality exceeds 90% when diagnosed after age 65. Most cases arise without any detectable early symptoms and patients usually present with the acute complications of bone marrow failure1. The onset of such de novo AML cases is typically preceded by the accumulation of somatic mutations in preleukaemic haematopoietic stem and progenitor cells (HSPCs) that undergo clonal expansion2,3. However, recurrent AML mutations also accumulate in HSPCs during ageing of healthy individuals who do not develop AML, a phenomenon referred to as age-related clonal haematopoiesis (ARCH)4-8. Here we use deep sequencing to analyse genes that are recurrently mutated in AML to distinguish between individuals who have a high risk of developing AML and those with benign ARCH. We analysed peripheral blood cells from 95 individuals that were obtained on average 6.3 years before AML diagnosis (pre-AML group), together with 414 unselected age- and gender-matched individuals (control group). Pre-AML cases were distinct from controls and had more mutations per sample, higher variant allele frequencies, indicating greater clonal expansion, and showed enrichment of mutations in specific genes. Genetic parameters were used to derive a model that accurately predicted AML-free survival; this model was validated in an independent cohort of 29 pre-AML cases and 262 controls. Because AML is rare, we also developed an AML predictive model using a large electronic health record database that identified individuals at greater risk. Collectively our findings provide proof-of-concept that it is possible to discriminate ARCH from pre-AML many years before malignant transformation. This could in future enable earlier detection and monitoring, and may help to inform intervention.

Published
2018

5. Interpreting and integrating genomic tests results in clinical cancer care: Overview and practical guidance

Author

Casolino, Raffaella, primary, Beer, Philip A., additional, Chakravarty, Debyani, additional, Davis, Melissa B., additional, Malapelle, Umberto, additional, Mazzarella, Luca, additional, Normanno, Nicola, additional, Pauli, Chantal, additional, Subbiah, Vivek, additional, Turnbull, Clare, additional, Westphalen, C. Benedikt, additional, and Biankin, Andrew V., additional

Published
2024
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9. The human myeloproliferative disorders : molecular pathogenesis and clonal heterogeneity

Author

Beer, Philip and Green, Anthony

Subjects
616.15, Myeloproliferative disorder, Myeloid, Leukaemia
Abstract

The classical myeloproliferative disorders (MPD), comprising essential thrombocythaemia (ET), polycythaemia vera (PV) and idiopathic myelofibrosis (IMF), are clonal premalignant haematopoietic neoplasms associated with activating mutations in signalling pathway molecules and a variable tendency to develop acute myeloid leukaemia (AML). This thesis examined genotype-phenotype associations of JAK2 and MPL mutations, the presence of clonal diversity in the MPD and the genetic events associated with progressive disease. Mutations in MPL were identified in 4% of ET and 7% of IMF but not in PV. Three different acquired MPL mutations were identified, one of which had been reported as an inherited allele. Although MPL mutations did not delineate a distinct clinical or histopathological subtype of ET, molecular testing provides an important new tool in the diagnostic armamentarium. Clones homozygous for the JAK2 V617F mutation were identified in female but not male patients with ET, suggesting that gender differences may be important in the determination of disease phenotype. In patients with two acquired genetic alterations, a signalling pathway mutation and a cytogenetic abnormality were usually present within the same clone. By contrast, coexistence of two signalling pathway mutations indicated the presence of biclonal disease that in two patients had arisen independently and not from a shared founder clone. RAS mutations were identified as potential cooperating events in patients with JAK2 or MPL mutant IMF. In patients developing AML following a JAK2 V617F-positive MPD, those with V617F-positive leukaemia had progressed via an accelerated phase of disease and harboured acquired alterations of RUNX1 or EVI1. V617F-negative leukaemias tended to follow directly from ET or PV, and loss of the JAK2 mutation by reversion to wild-type due to mitotic recombination, gene deletion or gene conversion was excluded. The thesis concludes with a discussion of how clonal heterogeneity can be integrated into current models of MPD disease pathogenesis.

Published
2009
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10. Societal challenges of precision medicine: Bringing order to chaos

Author

Becker, Robert, Beer, Philip, Bergh, Jonas, Bogaerts, Jan, Dovedi, Simon, Fojo, Antonio T., Gerstung, Moritz, Golfinopoulos, Vassilis, Hewitt, Stephen, Hochhauser, Daniel, Juhl, Hartmut, Kinders, Robert, Lillie, Thomas, Herbert, Kim Lyerly, Maheswaran, Shyamala, Mesri, Mehdi, Nagai, Sumimasa, Norstedt, Irene, O'Connor, Daniel, Oliver, Kathy, Oyen, Wim J.G., Pignatti, Francesco, Polley, Eric, Rosenfeld, Nitzan, Schellens, Jan, Schilsky, Richard, Schneider, Erasmus, Senderowicz, Adrian, Tenhunen, Olli, van Dongen, Augustinus, Vietz, Christine, Wilking, Nils, Salgado, Roberto, Moore, Helen, Martens, John W.M., Lively, Tracy, Malik, Shakun, McDermott, Ultan, Michiels, Stefan, Moscow, Jeffrey A., Tejpar, Sabine, McKee, Tawnya, and Lacombe, Denis

Published
2017
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13. Genetic modification of primary human B cells to model high-grade lymphoma

Author

Caeser, Rebecca, Di Re, Miriam, Krupka, Joanna A., Gao, Jie, Lara-Chica, Maribel, Dias, João M. L., Cooke, Susanna L., Fenner, Rachel, Usheva, Zelvera, Runge, Hendrik F. P., Beer, Philip A., Eldaly, Hesham, Pak, Hyo-Kyung, Park, Chan-Sik, Vassiliou, George S., Huntly, Brian J. P., Mupo, Annalisa, Bashford-Rogers, Rachael J. M., and Hodson, Daniel J.

Published
2019
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16. Figures S1 - S6 from Preclinical Development and First-in-Human Study of KA2507, a Selective and Potent Inhibitor of Histone Deacetylase 6, for Patients with Refractory Solid Tumors

Author

Tsimberidou, Apostolia M., primary, Beer, Philip A., primary, Cartwright, Carrie A., primary, Haymaker, Cara, primary, Vo, Henry H., primary, Kiany, Simin, primary, Cecil, Alexander R.L., primary, Dow, James, primary, Haque, Kemal, primary, Silva, Franck A., primary, Coe, Lucy, primary, Berryman, Helen, primary, Bone, Elisabeth A., primary, Nogueras-Gonzalez, Graciela M., primary, Vining, David, primary, McElwaine-Johnn, Hilary, primary, and Wistuba, Ignacio I., primary

Published
2023
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17. Table S7 from The Driver Mutational Landscape of Ovarian Squamous Cell Carcinomas Arising in Mature Cystic Teratoma

Author

Cooke, Susanna L., primary, Ennis, Darren, primary, Evers, Lisa, primary, Dowson, Suzanne, primary, Chan, Mei Yen, primary, Paul, James, primary, Hirschowitz, Lynn, primary, Glasspool, Rosalind M., primary, Singh, Naveena, primary, Bell, Sarah, primary, Day, Elizabeth, primary, Kochman, Agata, primary, Wilkinson, Nafisa, primary, Beer, Philip, primary, Martin, Sancha, primary, Millan, David, primary, Biankin, Andrew V., primary, and McNeish, Iain A., primary

Published
2023
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18. Figure S3 from The Driver Mutational Landscape of Ovarian Squamous Cell Carcinomas Arising in Mature Cystic Teratoma

Author

Cooke, Susanna L., primary, Ennis, Darren, primary, Evers, Lisa, primary, Dowson, Suzanne, primary, Chan, Mei Yen, primary, Paul, James, primary, Hirschowitz, Lynn, primary, Glasspool, Rosalind M., primary, Singh, Naveena, primary, Bell, Sarah, primary, Day, Elizabeth, primary, Kochman, Agata, primary, Wilkinson, Nafisa, primary, Beer, Philip, primary, Martin, Sancha, primary, Millan, David, primary, Biankin, Andrew V., primary, and McNeish, Iain A., primary

Published
2023
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19. Supplementary methods and legends from The Driver Mutational Landscape of Ovarian Squamous Cell Carcinomas Arising in Mature Cystic Teratoma

Author

Cooke, Susanna L., primary, Ennis, Darren, primary, Evers, Lisa, primary, Dowson, Suzanne, primary, Chan, Mei Yen, primary, Paul, James, primary, Hirschowitz, Lynn, primary, Glasspool, Rosalind M., primary, Singh, Naveena, primary, Bell, Sarah, primary, Day, Elizabeth, primary, Kochman, Agata, primary, Wilkinson, Nafisa, primary, Beer, Philip, primary, Martin, Sancha, primary, Millan, David, primary, Biankin, Andrew V., primary, and McNeish, Iain A., primary

Published
2023
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20. Supplementary Tables S1-S8 from Preclinical Development and First-in-Human Study of KA2507, a Selective and Potent Inhibitor of Histone Deacetylase 6, for Patients with Refractory Solid Tumors

Author

Tsimberidou, Apostolia M., primary, Beer, Philip A., primary, Cartwright, Carrie A., primary, Haymaker, Cara, primary, Vo, Henry H., primary, Kiany, Simin, primary, Cecil, Alexander R.L., primary, Dow, James, primary, Haque, Kemal, primary, Silva, Franck A., primary, Coe, Lucy, primary, Berryman, Helen, primary, Bone, Elisabeth A., primary, Nogueras-Gonzalez, Graciela M., primary, Vining, David, primary, McElwaine-Johnn, Hilary, primary, and Wistuba, Ignacio I., primary

Published
2023
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21. CTP Synthase 1 Is a Novel Therapeutic Target in Lymphoma

Author

Asnagli, Hélène, primary, Minet, Norbert, additional, Pfeiffer, Christina, additional, Hoeben, Eef, additional, Lane, Rebecca, additional, Laughton, David, additional, Birch, Louise, additional, Jones, Geraint, additional, Novak, Andrew, additional, Parker, Andrew E., additional, Ludwig, Heinz, additional, Fischer, Alain, additional, Latour, Sylvain, additional, and Beer, Philip A., additional

Published
2023
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26. STP938, a Selective CTPS1 Inhibitor, Shows Single Agent Activity and Synergy with BCL2 Inhibition in Preclinical Models of Mantle Cell Lymphoma

Author

Chiron, David, primary, Menoret, Emmanuelle, additional, Kervoelen, Charlotte, additional, Maïga, Sophie, additional, Bellanger, Celine, additional, Tessoulin, Benoit, additional, Touzeau, Cyrille, additional, Asnagli, Hélène, additional, Parker, Andy, additional, Beer, Philip, additional, and Pellat-Deceunynck, Catherine, additional

Published
2022
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30. Barcoding reveals complex clonal dynamics of de novo transformed human mammary cells

Author

Nguyen, Long V., Pellacani, Davide, Lefort, Sylvain, Kannan, Nagarajan, Osako, Tomo, Makarem, Maisam, Cox, Claire L., Kennedy, William, Beer, Philip, Carles, Annaick, Moksa, Michelle, Bilenky, Misha, Balani, Sneha, Babovic, Sonja, Sun, Ivan, Rosin, Miriam, Aparicio, Samuel, Hirst, Martin, and Eaves, Connie J.

Subjects
Mammary glands -- Physiological aspects, Breast cancer -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation, Physiological aspects
Abstract

Most human breast cancers have diversified genomically and biologically by the time they become clinically evident (1-3). Early events involved in their genesis and the cellular context in which these events occur have thus been difficult to characterize. Here we present the first formal evidence of the shared and independent ability of basal cells and luminal progenitors, isolated from normal human mammary tissue and transduced with a single oncogene ([KRAS.sup.GI2D]), to produce serially transplantable, polyclonal, invasive ductal carcinomas within 8 weeks of being introduced either subrenally or subcutaneously into immunodeficient mice (4). DNA barcoding (5,6) of the initial cells revealed a dramatic change in the numbers and sizes of clones generated from them within 2 weeks, and the first appearance of many 'new' clones in tumours passaged into secondary recipients. Both primary and secondary tumours were phenotypically heterogeneous and primary tumours were categorized transcriptionally as 'normal-like'. This system challenges previous concepts that carcinogenesis in normal human epithelia is necessarily a slow process requiring the acquisition of multiple driver mutations. It also presents the first description of initial events that accompany the genesis and evolution of malignant human mammary cell populations, thereby contributing new understanding of the rapidity with which heterogeneity in their properties can develop., To investigate the susceptibility of different normal human mammary cell types to transformation under the influence of known oncogenes, we isolated [CD49f.sup.+][EpCAM.sup.low] basal cells (BCs), [CD49f.sup.+][EpCAM.sup.+] luminal progenitors (LPs), [CD49f.sup.-][EpCAM.sup.+] [...]

Published
2015

36. Genomic characterization of hepatoid tumors: context matters

Author

Lawlor, Rita T., primary, Mafficini, Andrea, additional, Sciammarella, Concetta, additional, Cantù, Cinzia, additional, Rusev, Borislav C., additional, Piredda, Maria L., additional, Antonello, Davide, additional, Grimaldi, Sonia, additional, Bonizzato, Giada, additional, Sperandio, Nicola, additional, Marchegiani, Giovanni, additional, Malleo, Giuseppe, additional, Pea, Antonio, additional, Salvia, Roberto, additional, Mombello, Aldo, additional, Mazzoleni, Guido, additional, Nottegar, Alessia, additional, Hanspeter, Esther, additional, Riva, Giulio, additional, Tomezzoli, Anna, additional, Bencivenga, Maria, additional, de Manzoni, Giovanni, additional, Pedron, Serena, additional, Paolino, Gaetano, additional, Mattiolo, Paola, additional, Brosens, Lodewijk A., additional, Silvestris, Nicola, additional, Fassan, Matteo, additional, Cooke, Susanna L., additional, Beer, Philip A., additional, Milella, Michele, additional, Adsay, Volkan N., additional, Cheng, Liang, additional, Scarpa, Aldo, additional, and Luchini, Claudio, additional

Published
2021
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37. Sequential inverse dysregulation of the RNA helicases DDX3X and DDX3Y facilitates MYC-driven lymphomagenesis

Author

Gong, Chun, primary, Krupka, Joanna A., additional, Gao, Jie, additional, Grigoropoulos, Nicholas F., additional, Giotopoulos, George, additional, Asby, Ryan, additional, Screen, Michael, additional, Usheva, Zelvera, additional, Cucco, Francesco, additional, Barrans, Sharon, additional, Painter, Daniel, additional, Zaini, Nurmahirah Binte Mohammed, additional, Haupl, Björn, additional, Bornelöv, Susanne, additional, Ruiz De Los Mozos, Igor, additional, Meng, Wei, additional, Zhou, Peixun, additional, Blain, Alex E., additional, Forde, Sorcha, additional, Matthews, Jamie, additional, Khim Tan, Michelle Guet, additional, Burke, G.A. Amos, additional, Sze, Siu Kwan, additional, Beer, Philip, additional, Burton, Cathy, additional, Campbell, Peter, additional, Rand, Vikki, additional, Turner, Suzanne D., additional, Ule, Jernej, additional, Roman, Eve, additional, Tooze, Reuben, additional, Oellerich, Thomas, additional, Huntly, Brian J., additional, Turner, Martin, additional, Du, Ming-Qing, additional, Samarajiwa, Shamith A., additional, and Hodson, Daniel J., additional

Published
2021
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39. The JAK2 46/1 haplotype predisposes to MPL-mutated myeloproliferative neoplasms

Author

Jones, Amy V., Campbell, Peter J., Beer, Philip A., Schnittger, Susanne, Vannucchi, Alessandro M., Zoi, Katerina, Percy, Melanie J., McMullin, Mary Frances, Scott, Linda M., Tapper, William, Silver, Richard T., Oscier, David, Harrison, Claire N., Grallert, Harald, Kisialiou, Aliaksei, Strike, Paul, Chase, Andrew J., Green, Anthony R., and Cross, Nicholas C.P.

Published
2010
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42. Homologous Recombination Deficiency in Pancreatic Cancer: A Systematic Review and Prevalence Meta-Analysis

Author

Casolino, Raffaella, primary, Paiella, Salvatore, additional, Azzolina, Danila, additional, Beer, Philip A., additional, Corbo, Vincenzo, additional, Lorenzoni, Giulia, additional, Gregori, Dario, additional, Golan, Talia, additional, Braconi, Chiara, additional, Froeling, Fieke E. M., additional, Milella, Michele, additional, Scarpa, Aldo, additional, Pea, Antonio, additional, Malleo, Giuseppe, additional, Salvia, Roberto, additional, Bassi, Claudio, additional, Chang, David K., additional, and Biankin, Andrew V., additional

Published
2021
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43. Preclinical and phase I studies of KA2237, a selective and potent inhibitor of PI3K β/δ in relapsed refractory B cell lymphoma

Author

Nastoupil, Loretta J., primary, Neelapu, Sattva S., additional, Davis, Richard Eric, additional, Samaniego, Felipe, additional, Fowler, Nathan H., additional, Westin, Jason, additional, Lee, Hun Ju, additional, Wang, Michael, additional, Hagemeister, Fredrick, additional, Cecil, Alexander R. L., additional, Dow, James, additional, Haque, Kemal, additional, Silva, Franck A., additional, Whale, Andrew, additional, Lensun, Letitia, additional, Bone, Elisabeth A., additional, McElwaine-Johnn, Hilary, additional, and Beer, Philip A., additional

Published
2021
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44. CTPS1 is a novel therapeutic target in multiple myeloma which synergizes with inhibition of CHEK1, ATR or WEE1

Author

Pfeiffer, Christina, Grandits, Alexander M., Asnagli, Hélène, Schneller, Anja, Huber, Julia, Zojer, Niklas, Schreder, Martin, Parker, Andrew E., Bolomsky, Arnold, Beer, Philip A., and Ludwig, Heinz

Abstract

Targeting nucleotide biosynthesis is a proven strategy for the treatment of cancer but is limited by toxicity, reflecting the fundamental nucleotide requirement of dividing cells. The rate limiting step in de novo pyrimidine synthesis is of interest, being catalyzed by two homologous enzymes, CTP synthase 1 (CTPS1) and CTPS2, that could be differentially targeted. Herein, analyses of publicly available datasets identified an essential role for CTPS1 in multiple myeloma (MM), linking high expression of CTPS1 (but not CTPS2) with advanced disease and poor outcomes. In cellular experiments, CTPS1knockout induced apoptosis of MM cell lines. Exposure of MM cells to STP-B, a novel and highly selective pharmacological inhibitor of CTPS1, inhibited proliferation, induced S phase arrest and led to cell death by apoptosis. Mechanistically, CTPS1 inhibition by STP-B activated DNA damage response (DDR) pathways and induced double-strand DNA breaks which accumulated in early S phase. Combination of STP-B with pharmacological inhibitors of key components of the DDR pathway (ATR, CHEK1 or WEE1) resulted in synergistic growth inhibition and early apoptosis. Taken together, these findings identify CTPS1 as a promising new target in MM, either alone or in combination with DDR pathway inhibition.

Published
2023
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45. Cooperativity of imprinted genes inactivated by acquired chromosome 20q deletions

Author

Aziz, Athar, Baxter, E. Joanna, Edwards, Carol, Cheong, Clara Yujing, Ito, Mitsuteru, Bench, Anthony, Kelley, Rebecca, Silber, Yvonne, Beer, Philip A., Chng, Keefe, Renfree, Marilyn B., McEwen, Kirsten, Gray, Dionne, Nangalia, Jyoti, Mufti, Ghulam J., Hellstrom-Lindberg, Eva, Kiladjian, Jean-Jacques, McMullin, Mary Frances, Campbell, Peter J., Ferguson-Smith, Anne C., and Green, Anthony R.

Subjects
Gene expression -- Analysis, Genetic research -- Methods, Chromosome deletion -- Research, Cancer -- Research -- Genetic aspects, Health care industry
Abstract

Large regions of recurrent genomic loss are common in cancers; however, with a few well-characterized exceptions, how they contribute to tumor pathogenesis remains largely obscure. Here we identified primate-restricted imprinting [...]

Published
2013
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46. Use of JAK inhibitors in the management of myelofibrosis: a revision of the British Committee for Standards in Haematology Guidelines for Investigation and Management of Myelofibrosis 2012

Author

Reilly, John T., McMullin, Mary Frances, Beer, Philip A., Butt, Nauman, Conneally, Eibhlin, Duncombe, Andrew S., Green, Anthony R., Mikhaeel, George, Gilleece, Marie H., Knapper, Steven, Mead, Adam J., Mesa, Ruben A., Sekhar, Mallika, and Harrison, Claire N.

Published
2014
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49. Preclinical Development and First-in-Human Study of KA2507, a Selective and Potent Inhibitor of Histone Deacetylase 6, for Patients with Refractory Solid Tumors

Author

Tsimberidou, Apostolia M., primary, Beer, Philip A., additional, Cartwright, Carrie A., additional, Haymaker, Cara, additional, Vo, Henry H., additional, Kiany, Simin, additional, Cecil, Alexander R.L., additional, Dow, James, additional, Haque, Kemal, additional, Silva, Franck A., additional, Coe, Lucy, additional, Berryman, Helen, additional, Bone, Elisabeth A., additional, Nogueras-Gonzalez, Graciela M., additional, Vining, David, additional, McElwaine-Johnn, Hilary, additional, and Wistuba, Ignacio I., additional

Published
2021
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