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2. Oxygen carrying nanoemulsions and respiratory hyperoxia eliminate tumor hypoxia-induced suppression and improve cancer immunotherapy

Author

Halpin-Veszeleiova, Katarina, primary, Mallouh, Michael, additional, Apro, Ashley, additional, Romero, Nuria, additional, Bahr, Camille, additional, Shin, Maureen, additional, Ward, Kelly, additional, Rosenberg, Laura, additional, Sitkovsky, Michail V., additional, Spiess, Bruce, additional, and Hatfield, Stephen M., additional

Published
2024
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3. Antihypoxic oxygenation agents with respiratory hyperoxia to improve cancer immunotherapy

Author

Hatfield, Stephen M. and Sitkovsky, Michail V.

Subjects
Cancer treatment -- Methods, Respiratory symptoms -- Drug therapy, Respiratory system agents -- Usage, Cyclic adenosine monophosphate -- Health aspects, Chemical inhibitors -- Usage, Immunotherapy -- Methods, Health care industry
Abstract

Hypoxia/HIF-1[alpha]- and extracellular adenosine/A2 adenosine receptor-mediated immunosuppression protects tissues from collateral damage by antipathogen immune cells. However, this mechanism also protects cancerous tissues by inhibiting antitumor immune cells in hypoxic and extracellular adenosine-rich tumors that are the most resistant to current therapies. Here, we explain a potentially novel, antiimmunosuppressive reasoning to justify strategies using respiratory hyperoxia and oxygenation agents in cancer treatment. Earlier attempts to use oxygenation of tumors as a monotherapy or to improve radiotherapy have failed because oxygenation protocols were not combined with immunotherapies of cancer. In contrast, the proposal for therapeutic use of antihypoxic oxygenation described here was motivated by the need to prevent the hypoxia/ HIF-1[alpha]-driven accumulation of extracellular adenosine to (a) unleash antitumor immune cells from inhibition by intracellular cAMP and (b) prevent immunosuppressive transcription of cAMP response element- and hypoxia response elementcontaining immunosuppressive gene products (e.g., TGF-[beta]). Use of oxygenation agents together with inhibitors of the A2A adenosine receptor may be required to enable the most effective cancer immunotherapy. The emerging outcomes of clinical trials of cancer patients refractory to all other treatments provide support for the molecular and immunological mechanismbased approach to cancer immunotherapy described here., Introduction It has long been recognized that tumors are immunosuppressive, which explains the peaceful coexistence of tumors and tumor-reactive immune cells in the same cancer patient (the Hellstrom paradox) and [...]

Published
2020
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5. Table S3. Gene Set Enrichment Analysis (GSEA) C2 gene sets. from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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6. Data from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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7. Table S2. Gene Set Enrichment Analysis (GSEA) C5 GO gene sets. from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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8. Figure S1. Quantitative RT-PCR validation of ixazomib genes. from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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9. Supplementary Legends from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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10. Table S4. Key genes involved with anti-proteasomal response in L428 cells. from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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11. Figure S3. Inhibition of histone acetyl transferase (HAT). from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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12. Table S1. Common upstream regulators. from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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13. Table S5. DAVID functional classification of ixazomib genes. from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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14. Figure S2. Network representation of Gene Set Enrichment Analysis (GSEA) for Biological pathways. from Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, primary, Abermil, Nasséra, primary, Passero, Frank, primary, Sharma, Jaya, primary, Coyle, Michael, primary, Kritharis, Athena, primary, Kandela, Irawati, primary, Hlatky, Lynn, primary, Sitkovsky, Michail V., primary, Mazar, Andrew, primary, Gartenhaus, Ronald B., primary, and Evens, Andrew M., primary

Published
2023
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28. Immunomodulatory and neuroprotective effects of inosine

Author

Hasko, Gyorgy, Sitkovsky, Michail V., and Szabo, Csaba

Subjects
Cytology -- Research, Biological sciences, Chemistry, Pharmaceuticals and cosmetics industries
Abstract

Adenosine has been considered as a potential immunomodulatory and neuroprotective agent for 30 years. Inosine, a major degradation product of adenosine, was thought originally to have no biological effects. However, recent studies demonstrate that inosine has potent immunomodulatory and neuroprotective effects. Inosine enhances mast-cell degranulation, attenuates the production of pro-inflammatory mediators by macrophages, lymphocytes and neutrophils, and is protective in animal models of sepsis, ischemia--reperfusion and autoimmunity. Inosine preserves the viability of glial cells and neuronal cells during hypoxia, and stimulates axonal regrowth after injury. The biological actions of inosine might involve effects on adenosine receptors, poly(ADP-ribose) polymerase and cellular energy levels. In this article, we review recent observations indicating that it might be possible to exploit inosine therapeutically for the treatment of tissue damage caused by inflammation and ischemia.

Published
2004

33. Ecto-protein kinases: ecto-domain phosphorylation as a novel target for pharmacological manipulation?

Author

Redegeld, Frank A., Caldwell, Charles C., and Sitkovsky, Michail V.

Subjects
Protein kinases, Phosphorylation -- Research, Biological sciences, Chemistry, Pharmaceuticals and cosmetics industries
Abstract

An increasing number of studies document the presence of protein kinases facing outwards at the cell surface of a diverse array of cells. These ecto-protein kinases phosphorylate cell-surface proteins and soluble extracellular substrates, and thus could affect many physiological processes involving cell-cell contacts, cellular differentiation and proliferation, ion fluxes and cellular activation. To date, only limited attention has been paid to exploring ecto-protein kinases as possible pharmacological targets. Here, the identification and physiological role of ecto-protein kinases in different biological systems is described; it is suggested that ecto-protein kinases are attractive and novel candidates for pharmacological manipulation under various (patho)physiological conditions.

Published
1999

43. Hostile, Hypoxia-A2-Adenosinergic Tumor Biology as the Next Barrier to the Tumor Immunologists

Author

Sitkovsky, Michail V., Hatfield, Stephen, Abbott, Robert, Belikoff, Bryan, Lukashev, Dmitry, and Ohta, Akio

Subjects
Receptor, Adenosine A2A, Neoplasms, T-Lymphocytes, Immune Tolerance, Humans, Immunotherapy, Hypoxia-Inducible Factor 1, alpha Subunit, Article, Cell Hypoxia, Signal Transduction
Abstract

The hypoxia-driven and A2A or A2B adenosine receptors (A2AR/A2BR)-mediated (“Hypoxia-A2-Adenosinergic”) and T cell autonomous immunosuppression was first recognized as critical and non-redundant in protection of normal tissues from inflammatory damage and autoimmunity. However, this immunosuppressive mechanism is high-jacked by bacteria and tumors to misguidedly protect pathogens and cancerous tissues. The inhibitors of Hypoxia-A2-Adenosinergic pathway represent the conceptually novel type of immunological co-adjuvants to be combined with cancer vaccines, adoptive cell transfer and/or blockade of immunological negative regulators in order to further prolong survival and minimize side effects. In support of this approach are preclinical studies and findings that some human cancers are resistant to chemotherapies and immunotherapies due to the tumor-generated extracellular adenosine and intracellular cAMP-elevating A2AR and A2BR on anti-tumor T and NK cells. Among co-adjuvants are i) antagonists of A2AR/A2BR; ii) extracellular adenosine-degrading drugs; iii) inhibitors of adenosine generation by CD39/CD73 ecto-enzymes and iv) inhibitors of the hypoxia-HIF-1 alpha signaling. It is emphasized that even after the multi-combinatorial blockade of immunological negative regulators the anti-tumor T and NK cells would be still vulnerable to inhibition by hypoxia and A2AR and A2BR. The advantage of combining these co-adjuvants with the blockade of the CTLA4-A and/or PD-1 is in expectations of additive or even synergistic effects of targeting both immunological and physiological tumor-protecting mechanisms. Yet to be tested is the potential capacity of co-adjuvants to minimize the side effects of blockade of CTLA-4 and/or PD1 by decreasing the dose of blocking antibodies or by eliminating the need in dual blockade.

Published
2014

44. Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma

Author

Ravi, Dashnamoorthy, primary, Beheshti, Afshin, additional, Abermil, Nasséra, additional, Passero, Frank, additional, Sharma, Jaya, additional, Coyle, Michael, additional, Kritharis, Athena, additional, Kandela, Irawati, additional, Hlatky, Lynn, additional, Sitkovsky, Michail V., additional, Mazar, Andrew, additional, Gartenhaus, Ronald B., additional, and Evens, Andrew M., additional

Published
2016
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45. Immunological mechanisms of the antitumor effects of supplemental oxygenation

Author

Hatfield, Stephen M., primary, Kjaergaard, Jorgen, additional, Lukashev, Dmitriy, additional, Schreiber, Taylor H., additional, Belikoff, Bryan, additional, Abbott, Robert, additional, Sethumadhavan, Shalini, additional, Philbrook, Phaethon, additional, Ko, Kami, additional, Cannici, Ryan, additional, Thayer, Molly, additional, Rodig, Scott, additional, Kutok, Jeffrey L., additional, Jackson, Edwin K., additional, Karger, Barry, additional, Podack, Eckhard R., additional, Ohta, Akio, additional, and Sitkovsky, Michail V., additional

Published
2015
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46. Differentiation stage-specific requirement in HIF-1α-regulated glycolytic pathway during murine B cell development in bone marrow1

Author

Kojima, Hidefumi, Kobayashi, Ayano, Sakurai, Daisuke, Kanno, Yumiko, Hase, Hidenori, Takahashi, Riichi, Totsuka, Yoshikazu, Semenza, Gregg L., Sitkovsky, Michail V., and Kobata, Tetsuji

Subjects
B-Lymphocytes, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression, Bone Marrow Cells, Cell Differentiation, Flow Cytometry, Hematopoietic Stem Cells, Hypoxia-Inducible Factor 1, alpha Subunit, Article, Mice, Inbred C57BL, Mice, Gene Expression Regulation, Animals, Glycolysis
Abstract

Hypoxia-inducible factor (HIF)-1alpha plays a central role in oxygen homeostasis and energy supply by glycolysis in many cell types. We previously reported that an HIF-1alpha gene deficiency caused abnormal B cell development and autoimmunity. In this study we show that HIF-1alpha-enabled glycolysis during B cell development is required in a developmental stage-specific manner. Supporting this conclusion are observations that the glycolytic pathway in HIF-1alpha-deficient B220(+) bone marrow cells is much less functionally effective than in wild-type control cells. The expression of genes encoding the glucose transporters and the key glycolytic enzyme, 6-phosphofructo-2-kinase/fructose-2,6-bishosphatase 3, was greatly reduced in HIF-1alpha-deficient cells. The compensatory adaptation to the defect of glycolysis was reflected in higher levels of expression of respiratory chain-related genes and TCA cycle-related genes in HIF-1alpha-deficient cells than in wild-type cells. In agreement with these findings, HIF-1alpha-deficient cells used pyruvate more efficiently than wild-type cells. The key role of HIF-1alpha-enabled glycolysis in bone marrow B cells was also demonstrated by glucose deprivation during in vitro bone marrow cell culture and by using a glycolysis inhibitor in the bone marrow cell culture. Taken together, these findings indicate that glucose dependency differs at different B cell developmental stages and that HIF-1alpha plays an important role in B cell development.

Published
2009

50. In Vivo Hypoxic Preconditioning Protects From Warm Liver Ischemia-Reperfusion Injury Through the Adenosine A2B Receptor

Author

Choukèr, Alexander, primary, Ohta, Akio, additional, Martignoni, André, additional, Lukashev, Dmitriy, additional, Zacharia, Lefteris C., additional, Jackson, Edwin K., additional, Schnermann, Jürgen, additional, Ward, Jerrold M., additional, Kaufmann, Ines, additional, Klaunberg, Brenda, additional, Sitkovsky, Michail V., additional, and Thiel, Manfred, additional

Published
2012
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