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4 results on '"Kristin Koenig"'

1. P492: SAFETY AND EFFICACY OF LP-108 AS MONOTHERAPY AND COMBINED WITH AZACITIDINE IN PATIENTS WITH RELAPSED/REFRACTORY MYELODYSPLASTIC SYNDROMES, CHRONIC MYELOMONOCYTIC LEUKEMIA, OR ACUTE MYELOID LEUKEMIA

Author

Kristin Koenig, Juan Miguel Bergua Burgues, Pau Montesinos, Alison Walker, Dale Bixby, Patrick Burke, Naval Daver, Marina Konopleva, Stephen Anthony, Fenlai Tan, Yi Chen, Yu Chen, Yue Shen, and Emily Curran

Subjects
Diseases of the blood and blood-forming organs, RC633-647.5
Published
2023
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2. Longitudinal Functional Study of Murine Aging: A Resource for Future Study Designs

Author

Daniel S Evans, Monique N O'Leary, Ryan Murphy, Minna Schmidt, Kristin Koenig, Michael Presley, Brittany Garrett, Ha‐Neui Kim, Li Han, Emmeline C Academia, Matt J Laye, Daniel Edgar, Christopher A Zambataro, Tracey Barhydt, Colleen M Dewey, Jarrott Mayfield, Joy Wilson, Silvestre Alavez, Mark Lucanic, Brian K Kennedy, Maria Almeida, Julie K Andersen, Pankaj Kapahi, Gordon J Lithgow, and Simon Melov

Subjects
AGING, BONE, MICRO COMPUTED TOMOGRAPHY (mCT), OSTEOBLASTS, OSTEOCLASTS, Orthopedic surgery, RD701-811, Diseases of the musculoskeletal system, RC925-935
Abstract

ABSTRACT Aging is characterized by systemic declines in tissue and organ functions. Interventions that slow these declines represent promising therapeutics to protect against age‐related disease and improve the quality of life. In this study, several interventions associated with lifespan extension in invertebrates or improvement of age‐related disease were tested in mouse models to determine if they were effective in slowing tissue aging in a broad spectrum of functional assays. Benzoxazole, which extends the lifespan of Caenorhabditis elegans, slowed age‐related femoral bone loss in mice. Rates of change were established for clinically significant parameters in untreated mice, including kyphosis, blood glucose, body composition, activity, metabolic measures, and detailed parameters of skeletal aging in bone. These findings have implications for the study of preclinical physiological aging and therapies targeting aging. Finally, an online application was created that includes the calculated rates of change and that enables power and variance to be calculated for many clinically important metrics of aging with an emphasis on bone. This resource will help in future study designs employing novel interventions in aging mice. © 2021 The Authors. JBMR Plus published by Wiley Periodicals LLC. on behalf of American Society for Bone and Mineral Research.

Published
2021
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3. Supplementary Figures S1 - S10, Tables S1 - S2 from Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse

Author

Judith Campisi, Hyman Muss, Norman E. Sharpless, Daohong Zhou, Simon Melov, Brian K. Kennedy, Alain de Bruin, Boshi Wang, Alexis Valdovinos, Sumner Kilmarx, Emmeline C. Academia, Shani Alston, Allison M. Deal, Natalia Mitin, Catherine Le, Kristin Koenig, Fatouma Alimirah, Su Liu, Lijian Shao, Jianhui Chang, Monique N. O'Leary, and Marco Demaria

Abstract

Supplementary Figures S1 - S10, Tables S1 - S2

Published
2023

4. Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse

Author

Natalia Mitin, Judith Campisi, Alexis Valdovinos, Norman E. Sharpless, Jianhui Chang, Boshi Wang, Hyman B. Muss, Shani Alston, Kristin Koenig, Allison M. Deal, Brian K. Kennedy, Alain de Bruin, Sumner Kilmarx, Fatouma Alimirah, Catherine H. Le, Simon Melov, Monique N. O’Leary, Lijian Shao, Emmeline C. Academia, Daohong Zhou, Su Liu, Marco Demaria, Damage and Repair in Cancer Development and Cancer Treatment (DARE), and Restoring Organ Function by Means of Regenerative Medicine (REGENERATE)

Subjects
BIOMARKER, EXPRESSION, 0301 basic medicine, Senescence, DOXORUBICIN, CLEARANCE, medicine.medical_treatment, Oncology and Carcinogenesis, Antineoplastic Agents, Breast Neoplasms, Mice, Transgenic, Biology, Systemic inflammation, THERAPY, FATIGUE, Transgenic, Article, Proinflammatory cytokine, Mice, 03 medical and health sciences, P16(INK4A), medicine, Animals, Humans, Doxorubicin, Senolytic, IN-VIVO, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Cell Proliferation, Chemotherapy, Cancer, medicine.disease, Neoplasm Recurrence, 030104 developmental biology, Local, Oncology, Bone marrow suppression, CELLS, Immunology, SECRETION, Female, Neoplasm Recurrence, Local, medicine.symptom, medicine.drug
Abstract

Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a proinflammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating cells nonspecifically, often with adverse reactions. In accord with prior work, we show that several chemotherapeutic drugs induce senescence of primary murine and human cells. Using a transgenic mouse that permits tracking and eliminating senescent cells, we show that therapy-induced senescent (TIS) cells persist and contribute to local and systemic inflammation. Eliminating TIS cells reduced several short- and long-term effects of the drugs, including bone marrow suppression, cardiac dysfunction, cancer recurrence, and physical activity and strength. Consistent with our findings in mice, the risk of chemotherapy-induced fatigue was significantly greater in humans with increased expression of a senescence marker in T cells prior to chemotherapy. These findings suggest that senescent cells can cause certain chemotherapy side effects, providing a new target to reduce the toxicity of anticancer treatments. Significance: Many genotoxic chemotherapies have debilitating side effects and also induce cellular senescence in normal tissues. The senescent cells remain chronically present where they can promote local and systemic inflammation that causes or exacerbates many side effects of the chemotherapy. Cancer Discov; 7(2); 165–76. ©2016 AACR. This article is highlighted in the In This Issue feature, p. 115

Published
2017

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