A5044029265- Telomeres, Telomerase, and Senescence
- Skin Protection and Aging
- melanin and skin pigmentation
- Cancer-related cognitive impairment studies
- PARP inhibition in cancer therapy
- Neuroinflammation and Neurodegeneration Mechanisms
- Immune cells in cancer
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Advanced biosensing and bioanalysis techniques
- Nanoplatforms for cancer theranostics
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Cancer Research and Treatments
- Occupational and environmental lung diseases
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
Buck Institute for Research on Aging
2016-2020
Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a proinflammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating nonspecifically, often with adverse reactions. In accord prior work, we show that several chemotherapeutic drugs induce of primary murine and human cells. Using transgenic mouse permits tracking eliminating senescent cells, therapy-induced (TIS) persist contribute to local...
Senescent cells accumulate in human tissues during ageing and contribute to age-related pathologies. The mechanisms responsible for their accumulation are unclear. Here we show that senescent dermal fibroblasts express the non-classical MHC molecule HLA-E, which interacts with inhibitory receptor NKG2A expressed by NK highly differentiated CD8
Accumulation of senescent cells is associated with the progression pulmonary fibrosis, but mechanisms accounting for this linkage are not well understood. To explore issue, we investigated whether a class biologically active profibrotic lipids, leukotrienes (LT), part senescence-associated secretory phenotype. The analysis conditioned medium (CM), lipid extracts, and gene expression LT biosynthesis enzymes revealed that secreted LT, regardless origin or modality senescence induction....
Abstract Cellular senescence entails an irreversible growth arrest that evolved in part to prevent cancer. Paradoxically, senescent cells secrete proinflammatory and growth-stimulatory molecules, termed the senescence-associated secretory phenotype (SASP), which is correlated with cancer cell proliferation culture xenograft models. However, at what tumor stage how SASP act on endogenous vivo unknown. To understand role of etiology, we subjected p16-3MR transgenic mice, permit identification...
Abstract Squamous cell carcinoma (SCC) is the second most common non-melanoma skin cancer, and has a high rate of recurrence metastasis. Systemic genotoxic chemotherapeutic drugs such as doxorubicin (Doxo) can be used to treat SCC, but these agents have deleterious long-term side effects, including fueling development more aggressive cancers. Some adverse effects chemotherapies might due their ability induce cellular senescence. Cellular senescence tumor suppressive mechanism that entails...
<div>Abstract<p>Cellular senescence entails an irreversible growth arrest that evolved in part to prevent cancer. Paradoxically, senescent cells secrete proinflammatory and growth-stimulatory molecules, termed the senescence-associated secretory phenotype (SASP), which is correlated with cancer cell proliferation culture xenograft models. However, at what tumor stage how SASP act on endogenous <i>in vivo</i> unknown. To understand role of etiology, we subjected...
<div>Abstract<p>Cellular senescence entails an irreversible growth arrest that evolved in part to prevent cancer. Paradoxically, senescent cells secrete proinflammatory and growth-stimulatory molecules, termed the senescence-associated secretory phenotype (SASP), which is correlated with cancer cell proliferation culture xenograft models. However, at what tumor stage how SASP act on endogenous <i>in vivo</i> unknown. To understand role of etiology, we subjected...
<p>Supplementary Data supporting the manuscript.</p>
<p>Supplementary Data supporting the manuscript.</p>
<p>Supplementary Figures S1 - S10, Tables S2</p>
<p>Supplementary Figures S1 - S10, Tables S2</p>
<div>Abstract<p>Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a proinflammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating nonspecifically, often with adverse reactions. In accord prior work, we show that several chemotherapeutic drugs induce of primary murine and human cells. Using transgenic mouse permits tracking eliminating senescent cells, therapy-induced (TIS)...
<div>Abstract<p>Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a proinflammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating nonspecifically, often with adverse reactions. In accord prior work, we show that several chemotherapeutic drugs induce of primary murine and human cells. Using transgenic mouse permits tracking eliminating senescent cells, therapy-induced (TIS)...