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Article ; Online: Koschei the immortal and anti-aging drugs.

Blagosklonny, M V

2014 Volume 5, Page(s) e1552

Abstract: In Slavic folklore, Koschei the Immortal was bony, thin and lean. Was his condition caused by severe calorie restriction (CR)? CR deactivates the target of rapamycin pathway and slows down aging. But the life-extending effect of severe CR is limited by ... ...

Abstract	In Slavic folklore, Koschei the Immortal was bony, thin and lean. Was his condition caused by severe calorie restriction (CR)? CR deactivates the target of rapamycin pathway and slows down aging. But the life-extending effect of severe CR is limited by starvation. What if Koschei's anti-aging formula included rapamycin? And was rapamycin (or another rapalog) combined with commonly available drugs such as metformin, aspirin, propranolol, angiotensin II receptor blockers and angiotensin-converting enzyme inhibitors.
MeSH term(s)	Aging/drug effects ; Aging/metabolism ; Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Aspirin/pharmacology ; Caloric Restriction ; Exercise ; Folklore ; Gene Expression ; Glucose/metabolism ; Humans ; Insulin Resistance ; Longevity/drug effects ; Longevity/physiology ; Metformin/pharmacology ; Propranolol/pharmacology ; Russia ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Angiotensin-Converting Enzyme Inhibitors ; Metformin (9100L32L2N) ; Propranolol (9Y8NXQ24VQ) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Glucose (IY9XDZ35W2) ; Aspirin (R16CO5Y76E) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2014-12-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2014.520
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Article ; Online: TOR-centric view on insulin resistance and diabetic complications: perspective for endocrinologists and gerontologists.

Blagosklonny, M V

Cell death & disease

2013 Volume 4, Page(s) e964

Abstract: This article is addressed to endocrinologists treating patients with diabetic complications as well as to basic scientists studying an elusive link between diseases and aging. It answers some challenging questions. What is the link between insulin ... ...

Abstract	This article is addressed to endocrinologists treating patients with diabetic complications as well as to basic scientists studying an elusive link between diseases and aging. It answers some challenging questions. What is the link between insulin resistance (IR), cellular aging and diseases? Why complications such as retinopathy may paradoxically precede the onset of type II diabetes. Why intensive insulin therapy may initially worsen retinopathy. How nutrient- and insulin-sensing mammalian target of rapamycin (mTOR) pathway can drive insulin resistance and diabetic complications. And how rapamycin, at rational doses and schedules, may prevent IR, retinopathy, nephropathy and beta-cell failure, without causing side effects.
MeSH term(s)	Aging/genetics ; Aging/metabolism ; Animals ; Diabetes Complications/genetics ; Diabetes Complications/metabolism ; Endocrinology/methods ; Geriatrics/methods ; Humans ; Insulin Resistance/genetics ; Insulin Resistance/physiology ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.1.1)
Language	English
Publishing date	2013-12-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2013.506
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Article ; Online: Linking calorie restriction to longevity through sirtuins and autophagy: any role for TOR.

Blagosklonny, M V

Cell death & disease

2011 Volume 1, Page(s) e12

MeSH term(s)	Animals ; Autophagy ; Caenorhabditis elegans/metabolism ; Caloric Restriction ; Humans ; Longevity ; Sirtuins/metabolism ; TOR Serine-Threonine Kinases/physiology
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2011-03-02
Publishing country	England
Document type	Comment ; News
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2009.17
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Article ; Online: M(o)TOR of aging: MTOR as a universal molecular hypothalamus.

Blagosklonny, Mikhail V

Aging

2013 Volume 5, Issue 7, Page(s) 490–494

Abstract: A recent ground-breaking publication described hypothalamus-driven programmatic aging. As a Russian proverb goes "everything new is well-forgotten old". In 1958, Dilman proposed that aging and its related diseases are programmed by the hypothalamus. This ...

Abstract	A recent ground-breaking publication described hypothalamus-driven programmatic aging. As a Russian proverb goes "everything new is well-forgotten old". In 1958, Dilman proposed that aging and its related diseases are programmed by the hypothalamus. This theory, supported by beautiful experiments, remained unnoticed just to be re-discovered recently. Yet, it does not explain all manifestations of aging. And would organism age without hypothalamus? Do sensing pathways such as MTOR (mechanistic Target of Rapamycin) and IKK-beta play a role of a "molecular hypothalamus" in every cell? Are hypothalamus-driven alterations simply a part of quasi-programmed aging manifested by hyperfunction and secondary signal-resistance? Here are some answers.
MeSH term(s)	Aging/physiology ; Animals ; Gene Expression Regulation/physiology ; Hypothalamus/physiology ; I-kappa B Kinase/genetics ; I-kappa B Kinase/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.1.1) ; I-kappa B Kinase (EC 2.7.11.10)
Language	English
Publishing date	2013-07-19
Publishing country	United States
Document type	Journal Article
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.100580
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Article ; Online: Evaluation of off-label rapamycin use to promote healthspan in 333 adults.

Kaeberlein, Tammi L / Green, Alan S / Haddad, George / Hudson, Johnny / Isman, Anar / Nyquist, Andy / Rosen, Bradley S / Suh, Yousin / Zalzala, Sajad / Zhang, Xingyu / Blagosklonny, Mikhail V / An, Jonathan Y / Kaeberlein, Matt

GeroScience

2023 Volume 45, Issue 5, Page(s) 2757–2768

Abstract: Rapamycin (sirolimus) is an FDA-approved drug with immune-modulating and growth-inhibitory properties. Preclinical studies have shown that rapamycin extends lifespan and healthspan metrics in yeast, invertebrates, and rodents. Several physicians are now ... ...

Abstract	Rapamycin (sirolimus) is an FDA-approved drug with immune-modulating and growth-inhibitory properties. Preclinical studies have shown that rapamycin extends lifespan and healthspan metrics in yeast, invertebrates, and rodents. Several physicians are now prescribing rapamycin off-label as a preventative therapy to maintain healthspan. Thus far, however, there is limited data available on side effects or efficacy associated with use of rapamycin in this context. To begin to address this gap in knowledge, we collected data from 333 adults with a history of off-label use of rapamycin by survey. Similar data were also collected from 172 adults who had never used rapamycin. Here, we describe the general characteristics of a patient cohort using off-label rapamycin and present initial evidence that rapamycin can be used safely in adults of normal health status.
MeSH term(s)	Humans ; Sirolimus/pharmacology ; Off-Label Use ; TOR Serine-Threonine Kinases ; Longevity
Chemical Substances	Sirolimus (W36ZG6FT64) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2023-05-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2886586-8
ISSN	2509-2723 ; 2509-2715
ISSN (online)	2509-2723
ISSN	2509-2715
DOI	10.1007/s11357-023-00818-1
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Article: Target for cancer therapy: proliferating cells or stem cells.

Blagosklonny, M V

Leukemia

2006 Volume 20, Issue 3, Page(s) 385–391

Abstract: Tumor stem cells are quiescent and, therefore, resistant to therapy, yet harbor the capacity to replenish a tumor after therapy. Therefore, it is tempting to explain all therapeutic failures by the persistence of tumor stem cells. Yet, this explanation ... ...

Abstract	Tumor stem cells are quiescent and, therefore, resistant to therapy, yet harbor the capacity to replenish a tumor after therapy. Therefore, it is tempting to explain all therapeutic failures by the persistence of tumor stem cells. Yet, this explanation is relevant only to initial stages of stem-cell-dependent tumors (such as chronic myeloid leukemia) that, actually, are well controlled by therapy. In advanced cancers that poorly respond to therapy, quiescent tumor stem cells play a negligible role. Instead, proliferating cells determine disease progression, prognosis, therapeutic failures, and resistance to therapy. And therapy fails not because it eliminates only proliferating tumor cells, but because it does not eliminate them. With noticeable exceptions, it is the proliferating cell that should be targeted, whereas resting cancer cells including stem and dormant cells need to be targeted only when they 'wake up'. Finally, I discuss a strategy of selectively killing dominant proliferating clones, including proliferating stem-like and drug-resistant cancer cells, while sparing normal cells.
MeSH term(s)	Cell Division ; Cell Line ; Drug Resistance, Neoplasm ; Humans ; Neoplasms/pathology ; Neoplasms/therapy ; Recurrence ; Stem Cell Transplantation
Language	English
Publishing date	2006-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/sj.leu.2404075
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Zs.A 2295: Show issues

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Article: Carcinogenesis, cancer therapy and chemoprevention.

Blagosklonny, M V

Cell death and differentiation

2005 Volume 12, Issue 6, Page(s) 592–602

Abstract: Carcinogenesis and cancer therapy are two sides of the same coin, such that the same cytotoxic agent can cause cancer and be used to treat cancer. This review links carcinogenesis, chemoprevention and cancer therapy in one process driven by cytotoxic ... ...

Abstract	Carcinogenesis and cancer therapy are two sides of the same coin, such that the same cytotoxic agent can cause cancer and be used to treat cancer. This review links carcinogenesis, chemoprevention and cancer therapy in one process driven by cytotoxic agents (carcinoagents) that select either for or against cells with oncogenic alterations. By unifying therapy and cancer promotion and by distinguishing nononcogenic and oncogenic mechanisms of resistance, I discuss anticancer- and chemopreventive agent-induced carcinogenesis and tumor progression and, vice versa, carcinogens as anticancer drugs, anticancer drugs as chemopreventive agents and exploiting oncogene-addiction and drug resistance for chemoprevention and cancer therapy.
MeSH term(s)	Animals ; Carcinogens/adverse effects ; Carcinogens/pharmacology ; Carcinogens/therapeutic use ; Chemoprevention/trends ; Disease Progression ; Drug Resistance, Neoplasm ; Humans ; Neoplasms/drug therapy ; Neoplasms/pathology
Chemical Substances	Carcinogens
Language	English
Publishing date	2005-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1225672-9
ISSN	1350-9047
ISSN	1350-9047
DOI	10.1038/sj.cdd.4401610
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Zs.A 4230: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: M(o)TOR of pseudo-hypoxic state in aging: rapamycin to the rescue.

Leontieva, Olga V / Blagosklonny, Mikhail V

Cell cycle (Georgetown, Tex.)

2014 Volume 13, Issue 4, Page(s) 509–515

Abstract: A groundbreaking publication by Sinclair and coworkers has illuminated the pseudo-hypoxic state in aging and its reversibility. Remarkably, these data also fit the mTOR-centered model of aging. Here we discuss that the mTOR pathway can cause cellular ... ...

Abstract	A groundbreaking publication by Sinclair and coworkers has illuminated the pseudo-hypoxic state in aging and its reversibility. Remarkably, these data also fit the mTOR-centered model of aging. Here we discuss that the mTOR pathway can cause cellular pseudo-hypoxic state, manifested by HIF-1 expression and lactate production under normoxia. We found that rapamycin decreased HIF-1 and lactate levels in proliferating and senescent cells in vitro. This reduction was independent from mitochondrial respiration: rapamycin decreased lactate production in normoxia, hypoxia, and in the presence of the OXPHOS inhibitor oligomycin. We suggest that pseudo-hypoxic state is not necessarily caused by mitochondrial dysfunction, but instead mitochondrial dysfunction may be secondary to mTOR-driven hyperfunctions. Clinical applications of rapamycin for reversing pseudo-hypoxic state and lactate acidosis are discussed.
MeSH term(s)	Aging/drug effects ; Aging/metabolism ; Animals ; Antibiotics, Antineoplastic/pharmacology ; Cell Hypoxia/drug effects ; Cell Line ; Cell Proliferation/drug effects ; Cellular Senescence/drug effects ; Humans ; Hypoxia/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Lactic Acid/biosynthesis ; Mice ; Mitochondria/metabolism ; Oligomycins/pharmacology ; Oxidative Phosphorylation ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Antibiotics, Antineoplastic ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Oligomycins ; Lactic Acid (33X04XA5AT) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2014-01-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.27973
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Zs.A 5881: Show issues

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Article ; Online: Fasting levels of hepatic p-S6 are increased in old mice.

Leontieva, Olga V / Paszkiewicz, Geraldine M / Blagosklonny, Mikhail V

Cell cycle (Georgetown, Tex.)

2014 Volume 13, Issue 17, Page(s) 2656–2659

Abstract: TOR is involved in aging in a wide range of species from yeast to mammals. Here we show that, after overnight fasting, mTOR activity is higher in the livers of 28 months old female mice compared with middle-aged mice. Taken together with previous reports, ...

Abstract	TOR is involved in aging in a wide range of species from yeast to mammals. Here we show that, after overnight fasting, mTOR activity is higher in the livers of 28 months old female mice compared with middle-aged mice. Taken together with previous reports, our data predict that the life-extending effect of calorie restriction (CR) may be diminished, if CR is started in very old age. In contrast, rapamycin is known to be effective, even when started late in life.
MeSH term(s)	Aging/metabolism ; Animals ; Body Weight ; Cellular Senescence ; Fasting/metabolism ; Female ; Health ; Liver/metabolism ; Longevity ; Mice, Inbred C57BL ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2014-12-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/15384101.2014.949150
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Zs.A 5881: Show issues

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Article: Do cells need CDK2 and ... Bcr-Abl?

Blagosklonny, M V

Cell death and differentiation

2004 Volume 11, Issue 3, Page(s) 249–251

MeSH term(s)	Antineoplastic Agents/therapeutic use ; Benzamides ; CDC2-CDC28 Kinases/metabolism ; Cyclin-Dependent Kinase 2 ; Fusion Proteins, bcr-abl/metabolism ; HL-60 Cells ; Humans ; Imatinib Mesylate ; Leukemia, Promyelocytic, Acute/drug therapy ; Models, Biological ; Piperazines/therapeutic use ; Pyrimidines/therapeutic use
Chemical Substances	Antineoplastic Agents ; Benzamides ; Piperazines ; Pyrimidines ; Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; CDC2-CDC28 Kinases (EC 2.7.11.22) ; CDK2 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 2 (EC 2.7.11.22)
Language	English
Publishing date	2004-03
Publishing country	England
Document type	Journal Article
ZDB-ID	1225672-9
ISSN	1350-9047
ISSN	1350-9047
DOI	10.1038/sj.cdd.4401361
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