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159 results on '"Kornblau S. M."'

6. P576: A PHASE I/II STUDY OF MILADEMETAN (DS3032B) IN COMBINATION WITH LOW DOSE CYTARABINE WITH OR WITHOUT VENETOCLAX IN ACUTE MYELOID LEUKEMIA

Author

Senapati, J., primary, Ishizawa, J., additional, Abbas, H. A., additional, Loghavi, S., additional, Borthakur, G., additional, Issa, G. C., additional, Dara, S. I., additional, Pourebrahim, R., additional, Daver, N., additional, Jabbour, E. J., additional, Kornblau, S. M., additional, Pemmaraju, N., additional, Garcia-Manero, G., additional, Ravandi, F., additional, Muftuoglu, M., additional, Khoury, J., additional, DiNardo, C., additional, and Andreeff, M., additional

Published
2022
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7. Ordering of mutations in acute myeloid leukemia with partial tandem duplication of MLL (MLL-PTD)

Author

Sun, Q-Y, Ding, L-W, Tan, K-T, Chien, W, Mayakonda, A, Lin, D-C, Loh, X-Y, Xiao, J-F, Meggendorfer, M, Alpermann, T, Garg, M, Lim, S-L, Madan, V, Hattori, N, Nagata, Y, Miyano, S, Yeoh, A EJ, Hou, H-A, Jiang, Y-Y, Takao, S, Liu, L-Z, Tan, S-Z, Lill, M, Hayashi, M, Kinoshita, A, Kantarjian, H M, Kornblau, S M, Ogawa, S, Haferlach, T, Yang, H, and Koeffler, H P

Published
2017
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17. Erratum: Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

Author

Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K T, Alpermann, T, Kuo, M C, Rostami, S, Matthews, J, Sanada, M, Liu, L-Z, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H A, Malnassy, G, Ma, T, Garg, M, Ding, L W, Sun, Q Y, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, R A, Powell, B L, Lübbert, M, Chng, W J, Tien, H F, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, S M, Kantarjian, H M, Nowak, D, Hofmann, W K, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L Y, Mathews, V, and Koeffler, H P

Published
2016
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18. Molecular patterns of response and treatment failure after frontline venetoclax combinations in older patients with AML

Author

DiNardo, C. D., primary, Tiong, I. S., additional, Quaglieri, A., additional, MacRaild, S., additional, Loghavi, S., additional, Brown, F. C., additional, Thijssen, R., additional, Pomilio, G., additional, Ivey, A., additional, Salmon, J. M., additional, Glytsou, C., additional, Fleming, S. A., additional, Zhang, Q., additional, Ma, H., additional, Patel, K. P., additional, Kornblau, S. M., additional, Xu, Z., additional, Chua, C. C., additional, Chen, Xufeng, additional, Blombery, P., additional, Flensburg, C., additional, Cummings, N., additional, Aifantis, I., additional, Kantarjian, H., additional, Huang, D. C. S., additional, Roberts, A. W., additional, Majewski, I. J., additional, Konopleva, M., additional, and Wei, A. H., additional

Published
2020
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21. Author Correction: Metabolic gatekeeper function of B-lymphoid transcription factors (Nature (2017) DOI: 10.1038/nature21076)

Author

Chan L. N., Chan, L, Chen, Z, Braas, D, Lee, J, Xiao, G, Geng, H, Cosgun, K, Hurtz, C, Shojaee, S, Cazzaniga, V, Schjerven, H, Ernst, T, Hochhaus, A, Kornblau, S, Konopleva, M, Pufall, M, Cazzaniga, G, Liu, G, Milne, T, Koeffler, H, Ross, T, Sanchez-Garcia, I, Borkhardt, A, Yamamoto, K, Dickins, R, Graeber, T, Muschen, M, Chan L. N., Chen Z., Braas D., Lee J. -W., Xiao G., Geng H., Cosgun K. N., Hurtz C., Shojaee S., Cazzaniga V., Schjerven H., Ernst T., Hochhaus A., Kornblau S. M., Konopleva M., Pufall M. A., Cazzaniga G., Liu G. J., Milne T. A., Koeffler H. P., Ross T. S., Sanchez-Garcia I., Borkhardt A., Yamamoto K. R., Dickins R. A., Graeber T. G., Muschen M., Chan L. N., Chan, L, Chen, Z, Braas, D, Lee, J, Xiao, G, Geng, H, Cosgun, K, Hurtz, C, Shojaee, S, Cazzaniga, V, Schjerven, H, Ernst, T, Hochhaus, A, Kornblau, S, Konopleva, M, Pufall, M, Cazzaniga, G, Liu, G, Milne, T, Koeffler, H, Ross, T, Sanchez-Garcia, I, Borkhardt, A, Yamamoto, K, Dickins, R, Graeber, T, Muschen, M, Chan L. N., Chen Z., Braas D., Lee J. -W., Xiao G., Geng H., Cosgun K. N., Hurtz C., Shojaee S., Cazzaniga V., Schjerven H., Ernst T., Hochhaus A., Kornblau S. M., Konopleva M., Pufall M. A., Cazzaniga G., Liu G. J., Milne T. A., Koeffler H. P., Ross T. S., Sanchez-Garcia I., Borkhardt A., Yamamoto K. R., Dickins R. A., Graeber T. G., and Muschen M.

Abstract

In Fig. 3c of this Letter, the the effects of CRISPR-Cas9-mediated deletion of NR3C1, TXNIP and CNR2 in patient-derived B-lineage leukaemia cells were shown. For curves depicting NR3C1 (left graph), data s for TXNIP (middle graph) were inadvertently plotted. This figure has been corrected online, and the original Fig. 3c is shown as Supplementary Information to this Amendment for transparency. The error does not affect the conclusions of the Letter. In addition, Source Data files have been added for the Figs. 1-4 and Extended Data Figs. 1-10 of the original Letter.

Published
2018

22. Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

Author

Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K, Alpermann, T, Kuo, M, Rostami, S, Matthews, J, Sanada, M, Liu, L, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H, Malnassy, G, Ma, T, Garg, M, Ding, L, Sun, Q, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, R, Powell, B, Lubbert, M, Chng, W, Tien, H, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, S, Kantarjian, H, Nowak, D, Hofmann, W, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L, Mathews, V, Koeffler, H, Madan V., Shyamsunder P., Han L., Mayakonda A., Nagata Y., Sundaresan J., Kanojia D., Yoshida K., Ganesan S., Hattori N., Fulton N., Tan K. -T., Alpermann T., Kuo M. -C., Rostami S., Matthews J., Sanada M., Liu L. -Z., Shiraishi Y., Miyano S., Chendamarai E., Hou H. -A., Malnassy G., Ma T., Garg M., Ding L. -W., Sun Q. -Y., Chien W., Ikezoe T., Lill M., Biondi A., Larson R. A., Powell B. L., Lubbert M., Chng W. J., Tien H. -F., Heuser M., Ganser A., Koren-Michowitz M., Kornblau S. M., Kantarjian H. M., Nowak D., Hofmann W. -K., Yang H., Stock W., Ghavamzadeh A., Alimoghaddam K., Haferlach T., Ogawa S., Shih L. -Y., Mathews V., Koeffler H. P., Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K, Alpermann, T, Kuo, M, Rostami, S, Matthews, J, Sanada, M, Liu, L, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H, Malnassy, G, Ma, T, Garg, M, Ding, L, Sun, Q, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, R, Powell, B, Lubbert, M, Chng, W, Tien, H, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, S, Kantarjian, H, Nowak, D, Hofmann, W, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L, Mathews, V, Koeffler, H, Madan V., Shyamsunder P., Han L., Mayakonda A., Nagata Y., Sundaresan J., Kanojia D., Yoshida K., Ganesan S., Hattori N., Fulton N., Tan K. -T., Alpermann T., Kuo M. -C., Rostami S., Matthews J., Sanada M., Liu L. -Z., Shiraishi Y., Miyano S., Chendamarai E., Hou H. -A., Malnassy G., Ma T., Garg M., Ding L. -W., Sun Q. -Y., Chien W., Ikezoe T., Lill M., Biondi A., Larson R. A., Powell B. L., Lubbert M., Chng W. J., Tien H. -F., Heuser M., Ganser A., Koren-Michowitz M., Kornblau S. M., Kantarjian H. M., Nowak D., Hofmann W. -K., Yang H., Stock W., Ghavamzadeh A., Alimoghaddam K., Haferlach T., Ogawa S., Shih L. -Y., Mathews V., and Koeffler H. P.

Abstract

Acute promyelocytic leukemia (APL) is a subtype of myeloid leukemia characterized by differentiation block at the promyelocyte stage. Besides the presence of chromosomal rearrangement t(15;17), leading to the formation of PML-RARA (promyelocytic leukemia-retinoic acid receptor alpha) fusion, other genetic alterations have also been implicated in APL. Here, we performed comprehensive mutational analysis of primary and relapse APL to identify somatic alterations, which cooperate with PML-RARA in the pathogenesis of APL. We explored the mutational landscape using whole-exome (n=12) and subsequent targeted sequencing of 398 genes in 153 primary and 69 relapse APL. Both primary and relapse APL harbored an average of eight non-silent somatic mutations per exome. We observed recurrent alterations of FLT3, WT1, NRAS and KRAS in the newly diagnosed APL, whereas mutations in other genes commonly mutated in myeloid leukemia were rarely detected. The molecular signature of APL relapse was characterized by emergence of frequent mutations in PML and RARA genes. Our sequencing data also demonstrates incidence of loss-of-function mutations in previously unidentified genes, ARID1B and ARID1A, both of which encode for key components of the SWI/SNF complex. We show that knockdown of ARID1B in APL cell line, NB4, results in large-scale activation of gene expression and reduced in vitro differentiation potential.

Published
2016

24. Cathepsin G is broadly expressed in acute myeloid leukemia and is an effective immunotherapeutic target

Author

Alatrash, G, primary, Garber, H R, additional, Zhang, M, additional, Sukhumalchandra, P, additional, Qiu, Y, additional, Jakher, H, additional, Perakis, A A, additional, Becker, L, additional, Yoo, S Y, additional, Dwyer, K C, additional, Coombes, K, additional, Talukder, A H, additional, John, L S St, additional, Senyukov, V, additional, Lee, D A, additional, Sergeeva, A, additional, He, H, additional, Ma, Q, additional, Armistead, P M, additional, Roszik, J, additional, Mittendorf, E A, additional, Molldrem, J J, additional, Hawke, D, additional, Lizee, G, additional, and Kornblau, S M, additional

Published
2016
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25. Ordering of mutations in acute myeloid leukemia with partial tandem duplication of MLL (MLL-PTD)

Author

Sun, Q-Y, primary, Ding, L-W, additional, Tan, K-T, additional, Chien, W, additional, Mayakonda, A, additional, Lin, D-C, additional, Loh, X-Y, additional, Xiao, J-F, additional, Meggendorfer, M, additional, Alpermann, T, additional, Garg, M, additional, Lim, S-L, additional, Madan, V, additional, Hattori, N, additional, Nagata, Y, additional, Miyano, S, additional, Yeoh, A E J, additional, Hou, H-A, additional, Jiang, Y-Y, additional, Takao, S, additional, Liu, L-Z, additional, Tan, S-Z, additional, Lill, M, additional, Hayashi, M, additional, Kinoshita, A, additional, Kantarjian, H M, additional, Kornblau, S M, additional, Ogawa, S, additional, Haferlach, T, additional, Yang, H, additional, and Koeffler, H P, additional

Published
2016
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26. Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

Author

Madan, V, primary, Shyamsunder, P, additional, Han, L, additional, Mayakonda, A, additional, Nagata, Y, additional, Sundaresan, J, additional, Kanojia, D, additional, Yoshida, K, additional, Ganesan, S, additional, Hattori, N, additional, Fulton, N, additional, Tan, K-T, additional, Alpermann, T, additional, Kuo, M-C, additional, Rostami, S, additional, Matthews, J, additional, Sanada, M, additional, Liu, L-Z, additional, Shiraishi, Y, additional, Miyano, S, additional, Chendamarai, E, additional, Hou, H-A, additional, Malnassy, G, additional, Ma, T, additional, Garg, M, additional, Ding, L-W, additional, Sun, Q-Y, additional, Chien, W, additional, Ikezoe, T, additional, Lill, M, additional, Biondi, A, additional, Larson, R A, additional, Powell, B L, additional, Lübbert, M, additional, Chng, W J, additional, Tien, H-F, additional, Heuser, M, additional, Ganser, A, additional, Koren-Michowitz, M, additional, Kornblau, S M, additional, Kantarjian, H M, additional, Nowak, D, additional, Hofmann, W-K, additional, Yang, H, additional, Stock, W, additional, Ghavamzadeh, A, additional, Alimoghaddam, K, additional, Haferlach, T, additional, Ogawa, S, additional, Shih, L-Y, additional, Mathews, V, additional, and Koeffler, H P, additional

Published
2016
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29. Targeted therapy of AML new concepts

Author

Andreeff, M., Milella, M., Carter, B. Z., Tabe, Y., Maria Rosaria RICCIARDI, Sneed, T., Ruvolo, P., Contractor, R., Tsao, T., Schober, W., Evans, R., Mcqueen, T., Zeng, Z., Kornblau, S. M., Mccubrey, J., Estey, E., Mills, G. B., Reed, J. C., and Konopleva, M.

Subjects
Antineoplastic Agents, Apoptosis, Humans, Leukemia, Myelocytic, Acute, Receptors, Cytoplasmic and Nuclear, Signal Transduction, Transcription Factors, Leukemia, Myeloid, Acute, Leukemia, Cytoplasmic and Nuclear, Receptors, Humans, Receptors, Cytoplasmic and Nuclear, Antineoplastic Agents, Apoptosis, Acute, Signal Transduction, Transcription Factors
Published
2004

31. Apoptosis repressor with caspase recruitment domain is regulated by MAPK/PI3K and confers drug resistance and survival advantage to AML

Author

Mak, P. Y., primary, Mak, D. H., additional, Mu, H., additional, Shi, Y., additional, Ruvolo, P., additional, Ruvolo, V., additional, Jacamo, R., additional, Burks, J. K., additional, Wei, W., additional, Huang, X., additional, Kornblau, S. M., additional, Andreeff, M., additional, and Carter, B. Z., additional

Published
2013
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32. p53 pathway dysfunction is highly prevalent in acute myeloid leukemia independent of TP53mutational status

Author

Quintás-Cardama, A, Hu, C, Qutub, A, Qiu, Y H, Zhang, X, Post, S M, Zhang, N, Coombes, K, and Kornblau, S M

Abstract

TP53mutations are associated with the lowest survival rates in acute myeloid leukemia (AML). In addition to mutations, loss of p53 function can arise via aberrant expression of proteins that regulate p53 stability and function. We examined a large AML cohort using proteomics, mutational profiling and network analyses, and showed that (1) p53 stabilization is universal in mutant TP53samples, it is frequent in samples with wild-type TP53, and in both cases portends an equally dismal prognosis; (2) the p53 negative regulator Mdm2 is frequently overexpressed in samples retaining wild-type TP53alleles, coupled with absence of p21 expression and dismal prognosis similar to that of cases with p53 stabilization; (3) AML samples display unique patterns of p53 pathway protein expression, which segregate prognostic groups with distinct cure rates; (4) such patterns of protein activation unveil potential AML vulnerabilities that can be therapeutically exploited.

Published
2017
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35. Evidence of a role for the novel zinc-finger transcription factor ZKSCAN3 in modulating Cyclin D2 expression in multiple myeloma

Author

Yang, L, primary, Wang, H, additional, Kornblau, S M, additional, Graber, D A, additional, Zhang, N, additional, Matthews, J A, additional, Wang, M, additional, Weber, D M, additional, Thomas, S K, additional, Shah, J J, additional, Zhang, L, additional, Lu, G, additional, Zhao, M, additional, Muddasani, R, additional, Yoo, S-Y, additional, Baggerly, K A, additional, and Orlowski, R Z, additional

Published
2010
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41. Mylotarg (gemtuzumab ozogamicin) therapy is associated with hepatic venoocclusive disease in patients who have not received stem cell transplantation.

Author

Giles, Francis J., Kantarjian, Hagop M., Kornblau, Steve M., Thomas, Deborah A., Garcia-Manero, Guillermo, Waddelow, Tracey A., David, Cynthia L., Phan, Alexandria T., Colburn, Dawn E., Rashid, Asif, Estey, Elihu H., Giles, F J, Kantarjian, H M, Kornblau, S M, Thomas, D A, Garcia-Manero, G, Waddelow, T A, David, C L, Phan, A T, and Colburn, D E

Published
2001
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43. Production and culture of HSVtk transduced suicidal lymphocytes induces variable changes in the lymphocyte subset composition.

Author

Marini, F C and Kornblau, S M

Subjects
*BONE marrow transplantation, *GRAFT versus host disease, *T cells
Abstract

Allogeneic bone marrow transplant followed by donor lymphocyte infusion (DLI) is limited by T cell-mediated graft-versus-host disease (GVHD). A potential solution to alleviate uncontrolled GVHD is to create a controllable suicidal lymphocyte using retroviral transduction of the herpes simplex virus thymidine kinase gene (HSVtk) into the T cell graft. Should GVHD arise, the administration of ganciclovir (GCV) should eliminate the causal T cells. The culture conditions and expansion protocols required to produce suicidal lymphocytes may affect the composition of the T cell product. In this report we describe how T cells from individual donor samples respond to the same culture condition in highly varied ways. Among five donors, two demonstrated predominant expansion of CD4+ cells (with a decrease of CD8+), two donors resulted in predominately CD8+ cells, and one donor developed mainly dual positive CD8+/CD56+ cells. We observed a 20-fold expansion of T cells during the 14 day protocol. The function of the T cells was not affected by the transduction procedures (as tested by 51Cr release assays). In contrast to suicidal lymphocytes prepared using entire T cell populations, T cells pre-selected into CD3+/CD4+ or CD3+/CD8+ subpopulations prior to culture maintained their initial phenotype during the 14 day culture period, with little or no drift. Results from clinical trials using suicidal lymphocytes may be confounded by variance in lymphocyte subset compositions (LSC) and optimal use of suicidal lymphocytes may require separate culture and transduction to control the LSC delivered to the patient. [ABSTRACT FROM AUTHOR]

Published
1999
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44. Expression of Bcl-2-related genes in normal and AML progenitors: changes induced by chemotherapy and retinoic acid.

Author

Andreeff, M, Jiang, S, Zhang, X, Konopleva, M, Estrov, Z, Snell, V E, Xie, Z, Okcu, M F, Sanchez-Williams, G, Dong, J, Estey, E H, Champlin, R C, Kornblau, S M, Reed, J C, and Zhao, S

Subjects
LEUKEMIA, CELLS
Abstract

The expression of Bcl-2 family members was examined in normal and leukemic hematopoietic cells. Immature hematopoietic progenitor cells (CD34+/33-/13-) did not express Bcl-2 but Bcl-XL, the majority of CD34 cells expressed Bcl-2, Bcl-XL and BAD, and normal promyelocytes (CD34-/33+) lacked expression of both Bcl-2 and Bcl-XL, while leukemic CD34+progenitors and promyelocytes expressed these anti-apoptotic proteins. In AML, Bcl-2 expression was higher on CD34+ than on all AML cells, however, expression of Bcl-2 or Bcl-XL did not predict achievement of complete remission. Surprisingly, low Bcl-2 content was associated with poor survival in a group of patients with poor prognosis cytogenetics. The anti-apoptotic BAD protein was found to be expressed in AML, but was phosphorylated in 41/42 samples. Phosphorylation was found at both sites, Ser 112 and Ser 136. During induction chemotherapy, Bcl-2 levels of CD34 cells increased significantly. In the context of evidence for small numbers of leukemic CD34+ cells expressing very high levels of Bcl-2 prior to therapy, this finding is interpreted as a survival advantage of Bcl-2 overexpressing progenitors and rapid elimination of cells with low Bcl-2. Bcl-2 and Bcl-XL were both expressed in minimal residual disease cells. Downregulation of Bcl-2 mRNA and protein was observed by ATRA and the combination of Ara-C, followed by ATRA, resulted in markedly increased cytotoxicity in HL-60 cells, as compared to Ara-C alone or ATRA followed by Ara-C. Implications of these findings for the development of new therapeutic strategies for AML are discussed. [ABSTRACT FROM AUTHOR]

Published
1999
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45. Regulation of AML2/CBFA3 in hematopoietic cells through the retinoic acid receptor alpha-dependent signaling pathway.

Author

Le, X F, Groner, Y, Kornblau, S M, Gu, Y, Hittelman, W N, Levanon, D, Mehta, K, Arlinghaus, R B, and Chang, K S

Abstract

AML2 is a member of the acute myelogenous leukemia, AML family of transcription factors. The biologic functions of AML1 and AML3 have been well characterized; however, the functional role of AML2 remains unknown. In this study, we found that AML2 protein expressed predominantly in cells of hematopoietic origin is a nuclear serine phosphoprotein associated with the nuclear matrix, and its expression is not cell cycle-related. In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. A synthetic retinoic acid derivative, 4HPR, which neither activates RA receptor (RAR) alpha nor retinoic X receptor alpha was unable to induce the expression of AML2. A RAR-selective activator, TTNPB, induced AML2 expression similar to RA. Our study further showed that AGN193109, a potent RARalpha antagonist, suppressed AML2 expression induced by RA and that a retinoic X receptor pan agonist AGN194204 had no effect on its expression. Taken together, these studies conclusively demonstrated that the expression of AML2 in HL-60 cells is regulated through the RARalpha-specific signaling pathway. Our study further showed that after all-trans-retinoic acid priming, AML2 expression could be augmented by vitamin D(3). Based on these studies we hypothesize that AML2 expression is normally regulated by retinoid/vitamin D nuclear receptors mainly through the RARalpha-dependent signaling pathway and that it may play a role in hematopoietic cell differentiation.

Published
1999

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