Mikhail V Blagosklonny

Summary

Affiliation: Ordway Research Institute
Country: USA

Publications

  1. ncbi request reprint Cancer and aging: more puzzles, more promises?
    Mikhail V Blagosklonny
    Cell Cycle 7:2615-8. 2008
  2. ncbi request reprint Depletion of mutant p53 and cytotoxicity of histone deacetylase inhibitors
    Mikhail V Blagosklonny
    New York Medical College, Valhalla, New York 12208, USA
    Cancer Res 65:7386-92. 2005
  3. pmc Validation of anti-aging drugs by treating age-related diseases
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, Albany, NY 12208, USA
    Aging (Albany NY) 1:281-8. 2009
  4. pmc Hyper-mitogenic drive coexists with mitotic incompetence in senescent cells
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 11:4642-9. 2012
  5. pmc Elimination of proliferating cells unmasks the shift from senescence to quiescence caused by rapamycin
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, New York, United States of America
    PLoS ONE 6:e26126. 2011
  6. pmc DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 2:924-35. 2010
  7. pmc Yeast-like chronological senescence in mammalian cells: phenomenon, mechanism and pharmacological suppression
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 3:1078-91. 2011
  8. pmc Quantifying pharmacologic suppression of cellular senescence: prevention of cellular hypertrophy versus preservation of proliferative potential
    Zoya N Demidenko
    Oncotarget, Buffalo, NY 14263, USA
    Aging (Albany NY) 1:1008-16. 2009
  9. pmc Selective anti-cancer agents as anti-aging drugs
    Mikhail V Blagosklonny
    Cell Stress Biology Roswell Park Cancer Institute Buffalo, NY USA
    Cancer Biol Ther 14:1092-7. 2013
  10. pmc Resveratrol potentiates rapamycin to prevent hyperinsulinemia and obesity in male mice on high fat diet
    O V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Cell Death Dis 4:e472. 2013

Collaborators

Detail Information

Publications124 found, 100 shown here

  1. ncbi request reprint Cancer and aging: more puzzles, more promises?
    Mikhail V Blagosklonny
    Cell Cycle 7:2615-8. 2008
    ..Here, we discuss the relationship between aging and cancer, the mechanism of metformin action, and the prospects of using this compound for life span extension in humans...
  2. ncbi request reprint Depletion of mutant p53 and cytotoxicity of histone deacetylase inhibitors
    Mikhail V Blagosklonny
    New York Medical College, Valhalla, New York 12208, USA
    Cancer Res 65:7386-92. 2005
    ..In a broader perspective, this shows how selectivity may be achieved by targeting a non-cancer-specific target, such as histone deacetylases, in the presence of a cancer-specific alteration, such as mutant p53...
  3. pmc Validation of anti-aging drugs by treating age-related diseases
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, Albany, NY 12208, USA
    Aging (Albany NY) 1:281-8. 2009
    ..If the group is large, then the anti-aging effect could be validated in a couple of years. Startlingly, retrospective analysis of clinical and preclinical data reveals four potential anti-aging modalities...
  4. pmc Hyper-mitogenic drive coexists with mitotic incompetence in senescent cells
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 11:4642-9. 2012
    ..We conclude that cellular senescence is characterized by futile hyper-mitogenic drive associated with mTOR-dependent mitotic incompetence...
  5. pmc Elimination of proliferating cells unmasks the shift from senescence to quiescence caused by rapamycin
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, New York, United States of America
    PLoS ONE 6:e26126. 2011
    ..This problem also complicates the study of senescence caused by minimal levels of p21 that are capable to arrest a few cells...
  6. pmc DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 2:924-35. 2010
    ..We conclude that induction of p53 does not activate the senescence program in quiescent cells. In cells with induced p53, re-activation of mTOR by serum stimulation causes senescence, as an equivalent of cellular growth...
  7. pmc Yeast-like chronological senescence in mammalian cells: phenomenon, mechanism and pharmacological suppression
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 3:1078-91. 2011
    ..We discuss that although CS does not mimic organismal aging, the same signal transduction pathways that drive CS also drive aging...
  8. pmc Quantifying pharmacologic suppression of cellular senescence: prevention of cellular hypertrophy versus preservation of proliferative potential
    Zoya N Demidenko
    Oncotarget, Buffalo, NY 14263, USA
    Aging (Albany NY) 1:1008-16. 2009
    ..When p21 was switched off, competent cells, by resuming proliferation, became progressively less hypertrophic. Preservation of proliferative potential is a sensitive and quantitative measure of suppression of mTOR-driven senescence...
  9. pmc Selective anti-cancer agents as anti-aging drugs
    Mikhail V Blagosklonny
    Cell Stress Biology Roswell Park Cancer Institute Buffalo, NY USA
    Cancer Biol Ther 14:1092-7. 2013
    ..At low doses, certain agents may decelerate aging and age-related diseases. Importantly, deceleration of aging can in turn postpone cancer, which is an age-related disease...
  10. pmc Resveratrol potentiates rapamycin to prevent hyperinsulinemia and obesity in male mice on high fat diet
    O V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Cell Death Dis 4:e472. 2013
    ..Given distinct mechanisms of action of rapamycin and resveratrol at clinically relevant doses, their combination warrants further investigation as a potential antiaging, antiobesity and antidiabetic modality...
  11. pmc Hypoxia, MTOR and autophagy: converging on senescence or quiescence
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Autophagy 9:260-2. 2013
    ..What is the relationship between autophagy and cellular senescence? Also, can inhibition of MTOR and stimulation of autophagy explain the gerosuppressive effects of hypoxia?..
  12. pmc Rapamycin extends life- and health span because it slows aging
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY, 14263, USA
    Aging (Albany NY) 5:592-8. 2013
    ..Rapamycin affects the same processes in young and old animals: young animals' traits and phenotypes, which continuations become hyperfunctional, harmful and lethal later in life. ..
  13. pmc M(o)TOR of aging: MTOR as a universal molecular hypothalamus
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 5:490-4. 2013
    ....
  14. pmc MTOR-driven quasi-programmed aging as a disposable soma theory: blind watchmaker vs. intelligent designer
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 12:1842-7. 2013
    ..This model is consistent with a view that (1) soma is disposable, (2) aging and menopause are not programmed and (3) accumulation of random molecular damage is not a cause of aging as we know it. ..
  15. pmc Big mice die young but large animals live longer
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 5:227-33. 2013
    ..The concept that aging (and age-related diseases) is an aimless continuation of developmental growth, a hyperfunction driven by the same nutrient-sensing and growth-promoting pathways such as MTOR, may explain this longstanding paradox...
  16. pmc Answering the ultimate question "what is the proximal cause of aging?"
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 4:861-77. 2012
    ..I discuss that these arguments actually support a new theory. Are any questions remaining? And might accumulation of molecular damage still play a peculiar role in aging?..
  17. pmc Rapalogs in cancer prevention: anti-aging or anticancer?
    Mikhail V Blagosklonny
    Department of Cell Stress Biology Roswell Park Cancer Institute Buffalo, NY, USA
    Cancer Biol Ther 13:1349-54. 2012
    ..Can cancer prevention be explained by direct targeting of cancer cells? Or does rapamycin prevent cancer indirectly through slowing down the aging process? Increasing evidence points to the latter scenario...
  18. pmc Once again on rapamycin-induced insulin resistance and longevity: despite of or owing to
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Aging (Albany NY) 4:350-8. 2012
    ..Here I introduce the notion of benevolent diabetes and discuss whether starvation-like effects of chronic high dose treatment with rapamycin are an obstacle for its use as an anti-aging drug...
  19. pmc How to save Medicare: the anti-aging remedy
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 4:547-52. 2012
    ..At the same time this advance could save Medicare as we know it. Here I discuss how anti-aging interventions could solve otherwise intractable political problems without tax increases or curtailment of health care benefits...
  20. pmc Tumor suppression by p53 without apoptosis and senescence: conundrum or rapalog-like gerosuppression?
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 4:450-5. 2012
    ..But can gerossuppression suppress tumors?..
  21. doi request reprint Prospective treatment of age-related diseases by slowing down aging
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA
    Am J Pathol 181:1142-6. 2012
    ..Preclinical and clinical studies demonstrated the therapeutic effects of rapamycin in diverse age-related diseases. One simple reason why a single drug is indicated for so many age-related diseases is that it inhibits the aging process...
  22. pmc Wt p53 impairs response to chemotherapy: make lemonade to spare normal cells
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Oncotarget 3:601-7. 2012
    ..Also, several therapeutic paradigms can be reassessed, including the role of cellular senescence in cancer therapy...
  23. pmc Cell cycle arrest is not yet senescence, which is not just cell cycle arrest: terminology for TOR-driven aging
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 4:159-65. 2012
    ....
  24. pmc NCI's provocative questions on cancer: some answers to ignite discussion
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Oncotarget 2:1352-67. 2011
    ..National Cancer Institute has announced 24 provocative questions on cancer. Here I try to answer some of them by linking the dots of existing knowledge...
  25. doi request reprint Rapamycin-induced glucose intolerance: hunger or starvation diabetes
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 10:4217-24. 2011
    ..If rapamycin is a CR-mimetic, no wonder it may, in certain models, induce "hunger diabetes." But will rapamycin prevent true type II diabetes? Here are some answers...
  26. pmc Molecular damage in cancer: an argument for mTOR-driven aging
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 3:1130-41. 2011
    ..I also discuss how random molecular damage, via rounds of multiplication and selection, brings about non-random hallmarks of cancer...
  27. ncbi request reprint Antagonistic drug combinations that select against drug resistance: from bacteria to cancer
    Mikhail V Blagosklonny
    Ordway Research Institute, Cancer Institute, 150 New Scotland Avenue, Albany, New York 12208, USA
    Cancer Biol Ther 6:1013-4. 2007
    ..This has important application not only for antibacterial therapy but also for cancer therapy: to control cancer with lesser side effects and to eliminate drug-resistant cancer cells, while sparing sensitive normal cells...
  28. ncbi request reprint Aging-suppressants: cellular senescence (hyperactivation) and its pharmacologic deceleration
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Cell Cycle 8:1883-7. 2009
    ..How can growth inhibitors suppress senescence? May these aging-suppressants decelerate organismal aging? To answer these questions, we need to reconsider the meaning of aging...
  29. ncbi request reprint An anti-aging drug today: from senescence-promoting genes to anti-aging pill
    Mikhail V Blagosklonny
    Oncotarget Inc, Albany, NY 12203, USA
    Drug Discov Today 12:218-24. 2007
    ..I also discuss other potential anti-aging agents (calorie restriction, metformin, resveratrol and sirtuins) and their targets, interference with the TOR pathway and combination with antioxidants...
  30. ncbi request reprint Aging: ROS or TOR
    Mikhail V Blagosklonny
    Ordway Research Institute, and Oncotarget, Albany, New York 12208, USA
    Cell Cycle 7:3344-54. 2008
    ..Here I discuss evidence for and against the ROS theory. Remarkably, even supporting evidence has an alternative explanation, consistent with the model that aging is driven by the TOR (target of rapamycin) signaling pathway...
  31. ncbi request reprint Prevention of cancer by inhibiting aging
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, and Oncotarget, Albany, NY 12208, USA
    Cancer Biol Ther 7:1520-4. 2008
    ..Retrospective analysis of clinical data reveals that inhibitors of TOR prevent cancer in humans. This article envisions a potential clinical use of TOR inhibitors in order to slow aging and delay cancer...
  32. ncbi request reprint Aging, stem cells, and mammalian target of rapamycin: a prospect of pharmacologic rejuvenation of aging stem cells
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, 150 New Scotland Avenue, Albany, NY 12208, USA
    Rejuvenation Res 11:801-8. 2008
    ..On the basis of the hypothesis that insensitivity to stimuli is in part due to hyperactivation of the target of rapamycin (TOR), this article suggests a means of pharmacologic rejuvenation of stem cells and wound-healing cells...
  33. ncbi request reprint "Targeting the absence" and therapeutic engineering for cancer therapy
    Mikhail V Blagosklonny
    Ordway Research Institute and Oncotarget Inc, Albany, NY, USA
    Cell Cycle 7:1307-12. 2008
    ..Here I discuss restrictive combinations of currently available drugs that could be tested in clinical trials. Could then these combinations cure cancer today? And what does 'cure' really mean? This article suggests the answer...
  34. ncbi request reprint Program-like aging and mitochondria: instead of random damage by free radicals
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, 150 New Scotland Ave, and Oncotarget, Albany, New York 12208, USA
    J Cell Biochem 102:1389-99. 2007
    ..In theory, pharmacologic inhibitors of the TOR pathway may reverse accumulation of defective mitochondria, while also inhibiting the aging process...
  35. ncbi request reprint Research by retrieving experiments
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, 150 New Scotland Ave, Albany, New York 12208, USA
    Cell Cycle 6:1277-83. 2007
    ..Enormous 'pre-published' databases coupled with Google-like search engines can change the structure of scientific research, and shrinking funding will make this inevitable...
  36. ncbi request reprint Cellular quiescence caused by the Mdm2 inhibitor nutlin-3A
    Lioubov G Korotchkina
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, Buffalo, NY, USA
    Cell Cycle 8:3777-81. 2009
    ..We discuss that Mdm antagonists could be used in combination with chemotherapy to reversibly arrest normal cells, thus protecting them during chemotherapy of cancer (cyclotherapy)...
  37. ncbi request reprint TOR-driven aging: speeding car without brakes
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, Buffalo, NY, USA
    Cell Cycle 8:4055-9. 2009
    ....
  38. ncbi request reprint Calorie restriction: decelerating mTOR-driven aging from cells to organisms (including humans)
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 9:683-8. 2010
    ..Therefore in humans the effect of CR may be somewhat blunted. Still how much does CR extend human lifespan? And could this extension be surpassed by gerosuppressants such as rapamycin?..
  39. pmc Progeria, rapamycin and normal aging: recent breakthrough
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 3:685-91. 2011
    ..Here I discuss four potential scenarios, comparing progeria with both normal and accelerated aging. This reveals further indications of rapamycin both for accelerated aging in obese and for progeria...
  40. pmc Cell cycle arrest is not senescence
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 3:94-101. 2011
    ..Also, the relation between cancer and senescence is distorted. Here I discuss why the link between arrest and senescence is semi-coincidental and how senescence is related to aging and cancer...
  41. ncbi request reprint Increasing healthy lifespan by suppressing aging in our lifetime: preliminary proposal
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 9:4788-94. 2010
    ....
  42. doi request reprint Revisiting the antagonistic pleiotropy theory of aging: TOR-driven program and quasi-program
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 9:3151-6. 2010
    ..Early in life the TOR pathway drives developmental program, which persists later in life as an aimless quasi-program of aging and age-related diseases...
  43. pmc Why men age faster but reproduce longer than women: mTOR and evolutionary perspectives
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 2:265-73. 2010
    ..This quasi-program causes over-activation of female reproductive system, which is very vulnerable to over-activation. Mechanisms of aging and menopause are discussed...
  44. ncbi request reprint Rapamycin and quasi-programmed aging: four years later
    Mikhail V Blagosklonny
    Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 9:1859-62. 2010
    ..One prediction remains to be confirmed: rapamycin will become the cornerstone of anti-aging therapy in our life time...
  45. pmc Why human lifespan is rapidly increasing: solving "longevity riddle" with "revealed-slow-aging" hypothesis
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Buffalo, NY 14263, USA
    Aging (Albany NY) 2:177-82. 2010
    ..I discuss why slow aging is manifested as postponed (healthy) aging, why the rate of deterioration is independent from aging and also entertain hypothetical use of rapamycin in different eras as well as the future of human longevity...
  46. pmc Growth and aging: a common molecular mechanism
    Mikhail V Blagosklonny
    Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 1:357-62. 2009
    ..Thus, the nutrient-sensing and growth-promoting TOR signaling pathway may provide a molecular link between growth and aging that is universal from yeast to human...
  47. pmc Hormesis does not make sense except in the light of TOR-driven aging
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 3:1051-62. 2011
    ..Hormesis B includes ischemic preconditioning and, in part, physical exercise, heat shock, hypoxia and medical interventions...
  48. ncbi request reprint Molecular theory of cancer
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cancer Biol Ther 4:621-7. 2005
    ....
  49. ncbi request reprint The power of chemotherapeutic engineering: arresting cell cycle and suppressing senescence to protect from mitotic inhibitors
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 10:2295-8. 2011
    ..By knowing the mechanisms of cell cycle arrest, death and senescence, we can design "rainbow combinations" that obediently kill or spare desired cells. Knowledge is power...
  50. pmc Impact papers on aging in 2009
    Mikhail V Blagosklonny
    Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 2:111-21. 2010
    ..The emerging message in 2009 is that aging is not random but determined by a genetically-regulated longevity network and can be decelerated both genetically and pharmacologically...
  51. ncbi request reprint Growth stimulation leads to cellular senescence when the cell cycle is blocked
    Zoya N Demidenko
    Oncotarget, Albany, New York, USA
    Cell Cycle 7:3355-61. 2008
    ..Inhibition of TOR partially prevented senescent phenotype caused by DOX. Thus growth stimulation coupled with cell cycle arrest leads to senescence, whereas quiescence (a condition with inactive TOR) prevents senescence...
  52. pmc The choice between p53-induced senescence and quiescence is determined in part by the mTOR pathway
    Lioubov G Korotchkina
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Buffalo, NY 14263, USA
    Aging (Albany NY) 2:344-52. 2010
    ..We conclude that status of the mTOR pathway can determine, at least in part, the choice between senescence and quiescence in p53-arrested cells...
  53. ncbi request reprint Selective killing of adriamycin-resistant (G2 checkpoint-deficient and MRP1-expressing) cancer cells by docetaxel
    Zoya N Demidenko
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York, USA
    Cancer Res 65:4401-7. 2005
    ..We propose a therapeutic strategy to prevent normal cells from entering mitosis while increasing apoptosis selectively in mitotic cancer cells...
  54. pmc Exploring long-term protection of normal human fibroblasts and epithelial cells from chemotherapy in cell culture
    Pasha Apontes
    Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Oncotarget 2:222-33. 2011
    ....
  55. ncbi request reprint Cytostatic activity of paclitaxel in coronary artery smooth muscle cells is mediated through transient mitotic arrest followed by permanent post-mitotic arrest: comparison with cancer cells
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York, USA
    Cell Cycle 5:1574-9. 2006
    ..These in vitro findings suggest a mechanism for the cytostatic activity of PTX in CASMC for the inhibition of restenosis...
  56. pmc Mechanistic or mammalian target of rapamycin (mTOR) may determine robustness in young male mice at the cost of accelerated aging
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3 312, Elm and Carlton Streets, Buffalo, NY 14263, USA
    Aging (Albany NY) 4:899-916. 2012
    ..Our data suggest higher efficacy of rapamycin compared to fasting. Higher sensitivity of females to rapamycin may explain more pronounced life extension by rapamycin observed in females compared to males in several studies...
  57. pmc Hypoxia suppresses conversion from proliferative arrest to cellular senescence
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Proc Natl Acad Sci U S A 109:13314-8. 2012
    ..Thus, in normal and cancer cell lines, hypoxia suppresses geroconversion caused by diverse stimuli. Physiological and clinical implications of the present findings are discussed...
  58. pmc Paradoxical suppression of cellular senescence by p53
    Zoya N Demidenko
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Proc Natl Acad Sci U S A 107:9660-4. 2010
    ..Thus, in spite of its ability to induce cell cycle arrest, p53 can act as a suppressor of cellular senescence...
  59. ncbi request reprint Kinase-addiction and bi-phasic sensitivity-resistance of Bcr-Abl- and Raf-1-expressing cells to imatinib and geldanamycin
    Zoya N Demidenko
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York, USA
    Cancer Biol Ther 4:484-90. 2005
    ..Although Bcr-Abl renders cells hyper-sensitive, an excess of Bcr-Abl results in resistance (due to the remaining activity). We discuss therapeutic approaches to overcome bi-phasic resistance to mechanisms-based agents...
  60. ncbi request reprint Pharmacologic inhibition of MEK and PI-3K converges on the mTOR/S6 pathway to decelerate cellular senescence
    Zoya N Demidenko
    Oncotarget, Albany, NY, USA
    Cell Cycle 8:1896-900. 2009
    ..Taken together this suggests that (a) simultaneous activation of PI-3K and MEK is required to ensure cellular senescence and (b) U0126 and LY294002 suppress senescence via the rapamycin-sensitive pathway...
  61. ncbi request reprint Accumulation of hypoxia-inducible factor-1alpha is limited by transcription-dependent depletion
    Zoya N Demidenko
    Brander Cancer Research Institute, New York Medical College, Valhalla, NY, USA
    Oncogene 24:4829-38. 2005
    ..But under hypoxia, HIF-1alpha accumulates and transcriptionally activates its own degradation that is independent from the PHD/VHL pathway...
  62. ncbi request reprint At concentrations that inhibit mTOR, resveratrol suppresses cellular senescence
    Zoya N Demidenko
    Oncotarget, Albany, NY, USA
    Cell Cycle 8:1901-4. 2009
    ....
  63. ncbi request reprint Rapamycin decelerates cellular senescence
    Zoya N Demidenko
    Oncotarget, Albany, NY, USA
    Cell Cycle 8:1888-95. 2009
    ..During cell cycle arrest, rapamycin transformed the irreversible arrest into a reversible condition. Our data demonstrate that senescence can be pharmacologically suppressed...
  64. ncbi request reprint Weak p53 permits senescence during cell cycle arrest
    Olga V Leontieva
    Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 9:4323-7. 2010
    ..We conclude that low p53 levels during prolonged cell cycle arrest tend to cause senescence, whereas high levels of p53 tend to cause either quiescence or cell death...
  65. ncbi request reprint Paclitaxel induces primary and postmitotic G1 arrest in human arterial smooth muscle cells
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, New York Medical College, Hawthorne, New York, USA
    Cell Cycle 3:1050-6. 2004
    ..These post-mitotic cells were subsequently arrested in G(1) but maintained normal elongated morphology and were viable for at least 21 days. We conclude that in SMC PTX causes post-mitotic cell cycle arrest rather than cell death...
  66. ncbi request reprint Paradoxes of aging
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, 150 New Scotland Ave, Albany, New York 12208, USA
    Cell Cycle 6:2997-3003. 2007
    ....
  67. ncbi request reprint p21 (CDKN1A) is a negative regulator of p53 stability
    Eugenia V Broude
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cell Cycle 6:1468-71. 2007
    ..These results indicate that p21 acts as a negative regulator of p53 stability in different cell types. p53 regulation by p21 may provide a negative regulatory loop that limits p53 induction...
  68. pmc Rapamycin extends lifespan and delays tumorigenesis in heterozygous p53+/- mice
    Elena A Komarova
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 4:709-14. 2012
    ..In addition, rapamycin decreased the incidence of spontaneous tumors. This observation may have applications in management of Li-Fraumeni syndrome patients characterized by heterozygous mutations in the p53 gene...
  69. ncbi request reprint Cell senescence: hypertrophic arrest beyond the restriction point
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, 150 New Scotland Avenue, Albany, NY 12208, USA
    J Cell Physiol 209:592-7. 2006
    ..Prolonged hypertrophic arrest culminates in cell senescence. This review discusses that quiescence and senescence are two opposite, mutually exclusive conditions and that cell senescence can be reversed and prevented...
  70. ncbi request reprint Cancer stem cell and cancer stemloids: from biology to therapy
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, 150 New Scotland Ave, Albany, New York 12208, USA
    Cancer Biol Ther 6:1684-90. 2007
    ..In contrast, true CSCs are not only a difficult, but also an insufficient and perhaps even an unnecessary therapeutic target, especially in advanced malignancies...
  71. pmc Common drugs and treatments for cancer and age-related diseases: revitalizing answers to NCI's provocative questions
    Mikhail V Blagosklonny
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY, USA
    Oncotarget 3:1711-24. 2012
    ..Can we use common existing drugs for cancer prevention and treatment? Can we use some targeted "cancer-selective" agents for other diseases and … aging itself...
  72. pmc Hypoxia and gerosuppression: the mTOR saga continues
    Olga V Leontieva
    Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
    Cell Cycle 11:3926-31. 2012
    ..Therefore, the effects of hypoxia on the oxygen-sensing mTOR pathway and geroconversion are cell type-specific. We also briefly discuss replicative senescence, organismal aging and free radical theory...
  73. ncbi request reprint The purpose of the HIF-1/PHD feedback loop: to limit mTOR-induced HIF-1α
    Zoya N Demidenko
    Department of Cell Stress Biology, Roswell Park Cancer Institute Buffalo NY, USA
    Cell Cycle 10:1557-62. 2011
    ..The failure to limit mTOR-dependent induction of HIF-1 may contribute to age-related macular degeneration and diabetic retinopathy, suggesting rapamycin for prevention of these age-related diseases...
  74. pmc New nanoformulation of rapamycin Rapatar extends lifespan in homozygous p53-/- mice by delaying carcinogenesis
    Maria Comas
    Departments of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA
    Aging (Albany NY) 4:715-22. 2012
    ..Our data demonstrate that water soluble Rapatar micelles represent safe, convenient and efficient form of rapamycin suitable for a long-term treatment and that Rapatar may be considered for tumor prevention...
  75. ncbi request reprint How Avastin potentiates chemotherapeutic drugs: action and reaction in antiangiogenic therapy
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, Albany, New York, NY 12208, USA
    Cancer Biol Ther 4:1307-10. 2005
    ..And this is exactly what Avastin does (by blocking VEGF). While chemotherapy inhibits angiogenesis, Avastin abrogates the reactive resistance, sensitizing both endothelial and cancer cells to therapy...
  76. ncbi request reprint Differential sensitivity of cancer cells to inhibitors of the epidermal growth factor receptor family
    Philippe C Bishop
    Medicine Branch, NCI, NIH, Bethesda, Maryland, MD 20892, USA, and FDA CBER OTRR DCTDA Oncology Branch, HFM 573, Rockville, Maryland, MD 20852, USA
    Oncogene 21:119-27. 2002
    ..We infer that independence from mitogen-mediated signaling confers insensitivity to HER1 inhibitors in a large subset of cancer cell lines...
  77. ncbi request reprint Complementation of two mutant p53: implications for loss of heterozygosity in cancer
    Zoya N Demidenko
    Brander Cancer Research Institute, New York Medical College, Valhalla, NY, USA
    FEBS Lett 579:2231-5. 2005
    ..We suggest that, due to complementation of two mutant p53, cancer cells need to delete the second p53 allele rather than mutate it...
  78. ncbi request reprint Why therapeutic response may not prolong the life of a cancer patient: selection for oncogenic resistance
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cell Cycle 4:1693-8. 2005
    ..Therapy will control cancer if it can selectively suppress proliferating cancer cells and will improve survival as long as acquired resistance can be exploited...
  79. ncbi request reprint Prolonged mitosis versus tetraploid checkpoint: how p53 measures the duration of mitosis
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cell Cycle 5:971-5. 2006
    ..If a cell stays in mitosis too long, (e.g. mitotic arrest caused by Taxol or nocodazole), then p53 accumulates. This explains how p53 can measure mitotic time and perhaps represents the most fundamental function of p53...
  80. ncbi request reprint Mitotic arrest and cell fate: why and how mitotic inhibition of transcription drives mutually exclusive events
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cell Cycle 6:70-4. 2007
    ..Also, I discuss that mitotic depletion of short-lived proteins collaborates with mitotic phosphorylation of p53, Bcl-2 and BclxL. Finally this article clarifies notions of apoptosis-prone and -reluctant cells and mitotic catastrophe...
  81. ncbi request reprint Teratogens as anti-cancer drugs
    Mikhail V Blagosklonny
    Cancer Center, Ordway Research Institute, Albany, New York 12208, USA
    Cell Cycle 4:1518-21. 2005
    ....
  82. ncbi request reprint P53: an ubiquitous target of anticancer drugs
    Mikhail V Blagosklonny
    Medicine Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Int J Cancer 98:161-6. 2002
    ....
  83. pmc Cell senescence and hypermitogenic arrest
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, New York Medical College, Hawthorne, New York 10532, USA
    EMBO Rep 4:358-62. 2003
    ..The concept of hypermitogenic arrest defines cell senescence as a functionally active, stable and conditionally reversible state...
  84. ncbi request reprint Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition
    Mikhail V Blagosklonny
    Cell Cycle 5:2087-102. 2006
    ..Finally, I discuss that extended life span will reveal new causes for aging (e.g., ROS, 'wear and tear', Hayflick limit, stem cell exhaustion) that play a limited role now, when quasi-programmed senescence kills us first...
  85. ncbi request reprint Cyclotherapy: protection of normal cells and unshielding of cancer cells
    Mikhail V Blagosklonny
    Laboratory of Translational Oncology, New York Medical College, Hawthorne, New York 10532, USA
    Cell Cycle 1:375-82. 2002
    ..Following pretreatment with low doses of kinase inhibitors, the chemotherapy that predominantly induces apoptosis in cycling cells (cyclotherapy) will kill cancer cells while sparing normal cells...
  86. ncbi request reprint Histone deacetylase inhibitors all induce p21 but differentially cause tubulin acetylation, mitotic arrest, and cytotoxicity
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Mol Cancer Ther 1:937-41. 2002
    ..We conclude that HDIs have differential effects on non-histone deacetylases and that rapid acetylation of tubulin caused by TSA is a marker of nontranscriptional effects of TSA...
  87. ncbi request reprint Apoptosis, proliferation, differentiation: in search of the order
    Mikhail V Blagosklonny
    Department of Medicine, Brander Cancer Research Institute, New York Medical College, 19 Bradhurst Avenue, Hawthorne, NY 10532, USA
    Semin Cancer Biol 13:97-105. 2003
    ..When depicted in multidimensional axis, this universal model may also include invasiveness, senescence, metastatic and angiogenic responses and even such integral characteristics as malignant transformation...
  88. ncbi request reprint Are p27 and p21 cytoplasmic oncoproteins?
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, 19 Bradhurst Ave, Suite 2400, Hawthorne, New York 10532, USA
    Cell Cycle 1:391-3. 2002
    ....
  89. ncbi request reprint Basic cell cycle and cancer research: is harmony impossible?
    Mikhail V Blagosklonny
    National Cancer Institute Medicine Branch, Building 10, Room 12N226, 10 Center Drive, MSC 1906, Bethesda, Maryland 20892, USA
    Cell Cycle 1:3-5. 2002
  90. ncbi request reprint A new science-business paradigm in anticancer drug development
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, Dept of Medicine, New York Medical College, 19 Bradhurst Ave, Hawthorne, NY 10532, USA
    Trends Biotechnol 21:103-6. 2003
    ..The pharmacological industry could develop low cost, effective therapeutic modalities, by "re-using" already marketed and late-stage products in cancer-selective therapeutic kits...
  91. ncbi request reprint Hormonal and differentiation agents in cancer growth suppression
    Mikhail V Blagosklonny
    Medicine Branch, National Institutes of Health, Bethesda, MD, USA
    Methods Mol Biol 223:505-22. 2003
  92. ncbi request reprint How cancer could be cured by 2015
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, New York Medical College, Hawthorne, New York 10532, USA
    Cell Cycle 4:269-78. 2005
    ..And finally, these strategies will benefit from molecular diagnostics and can be used for chemoprevention...
  93. ncbi request reprint Prospective strategies to enforce selectively cell death in cancer cells
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, New York Medical College, 19 Bradhurst Ave, Hawthorne, Valhalla, NY 10532, USA
    Oncogene 23:2967-75. 2004
    ..In theory, consecutive use of these drug combinations may control cancer...
  94. ncbi request reprint Matching targets for selective cancer therapy
    Mikhail V Blagosklonny
    New York Medical College, 19 Bradhurst Avenue, Suite 2400, Hawthorne, NY 10532, USA
    Drug Discov Today 8:1104-7. 2003
  95. ncbi request reprint Targeting cancer cells by exploiting their resistance
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, New York Medical College, 19 Bradhurst Ave, Hawthorne, NY 10532, USA
    Trends Mol Med 9:307-12. 2003
    ..By abolishing several dose-limiting side effects of chemotherapy, this strategy provides a means to treat selectively most deranged, aggressive and resistant cancers...
  96. ncbi request reprint Cell immortality and hallmarks of cancer
    Mikhail V Blagosklonny
    Brander Cancer Research Institute New York Medical College 19 Bradhurst Ave, Suite 2400 Hawthorne, New York 10532, USA
    Cell Cycle 2:296-9. 2003
    ..In growth-limiting conditions, cells that express telomerase and inactivate tumor suppressors have a selective advantage due to resistance to growth arrest. Accidentally such cells become immortal...