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12. Induction of Autologous Graft-versus-Host Disease: Results of a Randomized Prospective Clinical Trial in Patients with Poor Risk Lymphoma

Author

Bolaños-Meade, Javier, Garrett-Mayer, Elizabeth, Luznik, Leo, Anders, Viki, Webb, Jennifer, Fuchs, Ephraim J., Huff, Carol Ann, Matsui, William, Borrello, Ivan M., Brodsky, Robert, Kasamon, Yvette L., Swinnen, Lode J., Flinn, Ian W., Ambinder, Richard F., Jones, Richard J., Hess, Allan D., and Vogelsang, Georgia B.

Published
2007
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24. Thalidomide for the treatment of chronic graft-versus-host disease

Author

Vogelsang, Georgia B., Farmer, Evan R., Hess, Allan D., Altamonte, Viki, Beschorner, William E., Jabs, Douglas A., Corio, Russell L., Levin, L. Stefon, Colvin, Michael O., Wingard, John R., and Santos, George W.

Subjects
Graft versus host reaction -- Drug therapy, Thalidomide -- Health aspects
Abstract

Thalidomide may be an effective and safe treatment for patients with chronic graft-versus-host disease (GVHD). Chronic GVHD occurs in patients who receive bone marrow transplants, and high-risk chronic GVHD can cause death. Among 44 patients with chronic GVHD who were treated with oral thalidomide, 23 had refractory GVHD, or GVHD that did not respond to conventional treatment, and 21 had high-risk GVHD. Twenty-eight patients (64%) survived; 18 (78%) with refractory GVHD and 10 (48%) with high-risk GVHD. Fourteen patients (32%) had complete recovery after treatment, 12 patients (27%) had partial recovery after treatment, and 18 patients (41%) had no response to treatment. The major side effects were sleepiness, which occurred in 91% of the patients, and constipation, which occurred in half the patients.

Published
1992

25. Identification and characterization of a spontaneous ovarian carcinoma in Lewis rats

Author

Sharrow Allison C, Ronnett Brigitte M, Thoburn Christopher J, Barber James P, Giuntoli Robert L, Armstrong Deborah K, Jones Richard J, and Hess Allan D

Subjects
Gynecology and obstetrics, RG1-991
Abstract

Abstract Background Ovarian carcinoma is the fourth most common cause of death from cancer in women. Limited progress has been made toward improving the survival rate of patients with this disease in part because of the lack of a good animal model. We present here a model of spontaneous ovarian carcinoma arising in a normal Lewis rat. Methods A spontaneously occurring tumor of the left ovary was found in a normal Lewis rat during necropsy, which was sectioned for histological examination and placed into single cell suspension. Tumor cells were passaged in vivo by intraperitoneal injection into immunocompetent Lewis rats, and in vitro culture resulted in generation of a cell line. Tumor cells were examined by flow cytometry for expression of estrogen receptor α, progesterone receptor, androgen receptor, her-2/neu, epithelial cell adhesion molecule, and CA125. β-catenin expression and cellular localization was assessed by immunocytochemistry. RNA was harvested for gene expression profiling and studying the expression of cytokines. Results The tumor, designated FNAR, could be serially transplanted into Lewis rats and propagated as a cell line in vitro, maintaining the properties of the original tumor. The FNAR cells displayed striking morphologic similarities to human ovarian carcinoma, resembling the endometrioid carcinoma subtype of surface epithelial neoplasms. The cells expressed estrogen receptor α, progesterone receptor, androgen receptor, her-2/neu, epithelial cell adhesion molecule, CA125, and nuclear β-catenin. A gene expression profile showed upregulation of a number of genes that are also upregulated in human ovarian carcinoma. Conclusion This reliable model of ovarian carcinoma should be helpful in better understanding the biology of the disease as well as the development of novel treatment strategies.

Published
2010
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35. Osteoblasts Protect AML Cells from SDF-1-Induced Apoptosis

Author

Kremer, Kimberly N., Dudakovic, Amel, McGee-Lawrence, Meghan E., Philips, Rachael L., Hess, Allan D., Smith, B. Douglas, van Wijnen, Andre J., Karp, Judith E., Kaufmann, Scott H., Westendorf, Jennifer J., and Hedin, Karen E.

Subjects
Receptors, CXCR4, Osteoblasts, Reverse Transcriptase Polymerase Chain Reaction, Osteocalcin, Gene Expression, Apoptosis, Cell Differentiation, Mesenchymal Stem Cells, U937 Cells, Alkaline Phosphatase, Flow Cytometry, Article, Chemokine CXCL12, Coculture Techniques, Cell Line, Mice, Inbred C57BL, Luminescent Proteins, Leukemia, Myeloid, hemic and lymphatic diseases, Cell Line, Tumor, Acute Disease, Animals, Humans, Cells, Cultured
Abstract

The bone marrow provides a protective environment for acute myeloid leukemia (AML) cells that often allows leukemic stem cells to survive standard chemotherapeutic regimens. Targeting these leukemic stem cells within the bone marrow is critical for preventing relapse. We recently demonstrated that SDF-1, a chemokine abundant in the bone marrow, induces apoptosis in AML cell lines and in patient samples expressing high levels of its receptor, CXCR4. Here we show that a subset of osteoblast lineage cells within the bone marrow can protect AML cells from undergoing apoptosis in response to the SDF-1 naturally present in that location. In co-culture systems, osteoblasts at various stages of differentiation protected AML cell lines and patient isolates from SDF-1-induced apoptosis. The differentiation of the osteoblast cell lines, MC3T3 and W-20-17, mediated this protection via a cell contact-independent mechanism. In contrast, bone marrow-derived mesenchymal cells, the precursors of osteoblasts, induced apoptosis in AML cells via a CXCR4-dependent mechanism and failed to protect AML cells from exogenously added SDF-1. These results indicate that osteoblasts in the process of differentiation potently inhibit the SDF-1-driven apoptotic pathway of CXCR4-expressing AML cells residing in the bone marrow. Drugs targeting this protective mechanism could potentially provide a new approach to treating AML by enhancing the SDF-1-induced apoptosis of AML cells residing within the bone marrow microenvironment.

Published
2014

38. mTOR Dual Inhibitor Induced Cytotoxicity Depends on 4EBP1/c-Myc/Puma and NFkB/Egr-1/Bim Pathways in Human Lymphoid Malignancies

Author

Yun, Seongseok, primary, Vincelette, Nicole D., additional, Knorr, Katherine L. B., additional, Almada, Luciana L., additional, Schneider, Paula A., additional, Peterson, Kevin L., additional, Flatten, Karen S., additional, Hess, Allan D., additional, Smith, B. Douglas, additional, Karp, Judith E., additional, Fernandez-Zapico, Martin E., additional, and Kaufmann, Scott H., additional

Published
2015
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44. Protein Kinase Cβ Modulates Ligand-induced Cell Surface Death Receptor Accumulation: A MECHANISTIC BASIS FOR ENZASTAURIN-DEATH LIGAND SYNERGY*

Author

Meng, Xue Wei, Heldebrant, Michael P., Flatten, Karen S., Loegering, David A., Dai, Haiming, Schneider, Paula A., Gomez, Timothy S., Peterson, Kevin L., Trushin, Sergey A., Hess, Allan D., Smith, B. Douglas, Karp, Judith E., Billadeau, Daniel D., and Kaufmann, Scott H.

Subjects
Fas Ligand Protein, Indoles, Tumor Necrosis Factor-alpha, Mechanisms of Signal Transduction, Enzyme Activators, Apoptosis, HL-60 Cells, Isoenzymes, Jurkat Cells, Protein Transport, Receptors, TNF-Related Apoptosis-Inducing Ligand, Protein Kinase C beta, Carcinogens, Humans, Tetradecanoylphorbol Acetate, fas Receptor, Phosphorylation, Protein Kinase C, Cell Proliferation, Signal Transduction
Abstract

Although treatment with the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) is known to protect a subset of cells from induction of apoptosis by death ligands such as Fas ligand and tumor necrosis factor-alpha-related apoptosis-inducing ligand, the mechanism of this protection is unknown. This study demonstrated that protection in short term apoptosis assays and long term proliferation assays was maximal when Jurkat or HL-60 human leukemia cells were treated with 2-5 nm PMA. Immunoblotting demonstrated that multiple PKC isoforms, including PKCalpha, PKCbeta, PKCepsilon, and PKC, translocated from the cytosol to a membrane-bound fraction at these PMA concentrations. When the ability of short hairpin RNA (shRNA) constructs that specifically down-regulated each of these isoforms was examined, PKCbeta shRNA uniquely reversed PMA-induced protection against cell death. The PKCbeta-selective small molecule inhibitor enzastaurin had a similar effect. Although mass spectrometry suggested that Fas is phosphorylated on a number of serines and threonines, mutation of these sites individually or collectively had no effect on Fas-mediated death signaling or PMA protection. Further experiments demonstrated that PMA diminished ligand-induced cell surface accumulation of Fas and DR5, and PKCbeta shRNA or enzastaurin reversed this effect. Moreover, enzastaurin sensitized a variety of human tumor cell lines and clinical acute myelogenous leukemia isolates, which express abundant PKCbeta, to tumor necrosis factor-alpha related apoptosis-inducing ligand-induced death in the absence of PMA. Collectively, these results identify a specific PKC isoform that modulates death receptor-mediated cytotoxicity as well as a small molecule inhibitor that mitigates the inhibitory effects of PKC activation on ligand-induced death receptor trafficking and cell death.

Published
2009

50. Osteoblasts Protect AML Cells From SDF-1-Induced Apoptosis

Author

Kremer, Kimberly N., primary, Dudakovic, Amel, additional, McGee-Lawrence, Meghan E., additional, Philips, Rachael L., additional, Hess, Allan D., additional, Smith, B. Douglas, additional, van Wijnen, Andre J., additional, Karp, Judith E., additional, Kaufmann, Scott H., additional, Westendorf, Jennifer J., additional, and Hedin, Karen E., additional

Published
2014
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