• Cellular processes like genome duplication and cell division stop. (wikipedia.org)
  • In this manuscript, we report the in vitro mutagenicity of waterpipe smoke condensate (WSC), the alteration in cellular parameters of lung alveolar cells in response to WSC exposure and discuss the implication of cellular responses in the pathophysiology of chronic obstructive pulmonary disease (COPD). (nih.gov)
  • However, WSC induced cell cycle arrest and cellular senescence mediated by the p53-p21 pathway. (nih.gov)
  • The data reported here represent the first in vitro demonstration of the effect of waterpipe smoke on cellular parameters providing evidence of the potential involvement of WPS in the pathogenesis of COPD through impairing cellular growth and inducing inflammation. (nih.gov)
  • Because age-related cellular senescence and type 2 diabetes (T2D) have been recognised as risk factors for CRC development, the recent finding that type 2 diabetic patients present an elevated circulating volume of senescent cells raises the question whether type 2 diabetes facilitates the process of CRC tumorigenesis by inducing premature cell senescence. (frontiersin.org)
  • In this review, we will discuss the mechanisms according to which T2D induces cellular senescence and the role of type 2 diabetes-induced cellular senescence in the pathogenesis and progression of colorectal cancer. (frontiersin.org)
  • More recently, cellular senescence has been considered as an additional cause of age-related tumorigenesis. (frontiersin.org)
  • Senescence is a stress-response cellular state characterised by proliferative arrest but active metabolism ( 7 ). (frontiersin.org)
  • However, cellular senescence is not exclusive to ageing. (frontiersin.org)
  • Age-related and metabolic diseases such as type 2 diabetes (T2D) represent a source of cellular stress due to their disruptive effect on normal physiological processes and, therefore, can induce premature senescence ( 10 ). (frontiersin.org)
  • The INK and CIP/KIP families of cyclin dependent kinase inhibitors (CDKis) protect cells from oncogenic signals-initiated cellular transformation. (sigmaaldrich.com)
  • INK4a and INK4b are induced by oncogenic Ras and are involved in cell cycle G1 arrest and cellular senescence. (sigmaaldrich.com)
  • Cellular senescence, which recently has gained broad attention, is thought to be an important player in the onset and development of diabetic nephropathy. (hindawi.com)
  • In this issue, we generally review the mechanisms of cellular senescence in diabetic nephropathy, which involve telomere attrition, DNA damage, epigenetic alterations, mitochondrial dysfunction, loss of Klotho, Wnt/ β -catenin signaling activation, persistent inflammation, and accumulation of uremic toxins. (hindawi.com)
  • Moreover, we highlight the potential therapeutic targets of cellular senescence in diabetic nephropathy and provide important clues for clinical strategies. (hindawi.com)
  • Recently, the emerging role of cellular senescence in DN has attracted a broad attention. (hindawi.com)
  • In the present review, we will focus on the role of cellular senescence and its related mechanisms in DN. (hindawi.com)
  • Furthermore, we will explore the potential therapeutic targets of cellular senescence and provide important clues for clinical strategies in the management of DN. (hindawi.com)
  • Cellular aging or cellular senescence is the critical factor for the process of aging. (hindawi.com)
  • Several hallmarks of cellular senescence, such as cell cycle arrest, expression of cyclin-dependent kinase inhibitors, DNA damages, and senescence-associated secretory profile were evaluated. (aging-us.com)
  • Etoposide-induced senescence model may help investigate the initiation of cellular senescence in chondrocytes, and provide a useful model to develop therapeutic approaches to target senescence in OA. (aging-us.com)
  • Cellular senescence has been described as one of the major drivers of aging [ 6 ] and has been implicated in the pathogenesis of many age-related diseases [ 7 ]. (aging-us.com)
  • Recently, cellular senescence has emerged as a new target to treat OA [ 8 ]. (aging-us.com)
  • Because a specific marker for cellular senescence has yet to be identified, a combination of markers should be used to identify SnCs [ 14 ]. (aging-us.com)
  • Considering the role of cellular senescence in age-related diseases including OA, the therapeutic potential of senolytic (drugs that induced SnCs death) and senomorphic (drugs that modulate the SASP) compounds have been contemplated with growing interest [ 15 ]. (aging-us.com)
  • The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
  • Researchers began to wonder whether cellular aging was a barrier to iPS cell conversion. (biologists.com)
  • Cellular senescence, which is morphologically characterized by an enlarged and flattened cell shape, was first described by Hayflick [ 9 ]. (hindawi.com)
  • Cellular senescence refers to active cells that eventually enter a state of irreversible growth arrest. (hindawi.com)
  • Moreover, replicative senescence of MSCs exhibits reduced functionality, and cellular senescence might impair the regenerative potential of MSCs [ 10 ]. (hindawi.com)
  • The mechanisms underlying the cellular senescence of MSCs are still poorly understood. (hindawi.com)
  • Studies show that replicative senescence or cellular senescence is induced by intrinsic or extrinsic environmental factors [ 11 ]. (hindawi.com)
  • Cellular senescence is a complex process, and its molecular mechanisms are unknown. (hindawi.com)
  • Additionally, Abedin and King showed that FGF-2 suppresses the cellular senescence of human MSCs [ 17 ]. (hindawi.com)
  • Plasmid driven short hairpin RNA approach was employed to validate the role of HSP70-2 in cellular proliferation, senescence, migration, invasion and tumor growth. (biomedcentral.com)
  • Depletion of HSP70-2 in MDA-MB-231 and MCF7 cells resulted in a significant reduction in cellular growth, motility, onset of apoptosis, senescence, cell cycle arrest as well as reduction of tumor growth in the xenograft model. (biomedcentral.com)
  • We also report that HSP70-2 plays an important role in cellular growth, migration and invasion of breast cancer cells and tumor growth of breast cancer xenograft. (biomedcentral.com)
  • Cellular senescence was first identified as a type of irreversible cell cycle arrest that occurs when cells reach the end of their replicative potential ( Hayflick and Moorhead, 1961 ). (rupress.org)
  • Senescent cells also undergo dramatic changes in their morphology and in the organization and architecture of their cellular compartments. (rupress.org)
  • Irreversible cell cycle arrest is one of the phenomena that characterize cellular senescence. (dojindo.com)
  • The activation/upregulation of these proteins are used as indicators of cellular senescence. (dojindo.com)
  • Doxorubicin (DOX) is known as an anticancer drug that acts in the G2/M phase of the cell cycle to arrest cell proliferation and induce cellular senescence (see the upper left figure). (dojindo.com)
  • Cellular senescence is controlled by various factors such as cell type and physiological conditions, such as oxidative stress. (dojindo.com)
  • Therefore, it is desirable to determine and confirm cellular senescence using multiple indicators. (dojindo.com)
  • Common detection indicators for assessing cellular senescence include features related to cell cycle progression (DNA synthesis, p16/p21 expression, etc.), features related to morphology (of the cell, nucleus, nucleolus, etc. (dojindo.com)
  • Cellular senescence was reported by Hayflick in 1981. (dojindo.com)
  • Subsequent studies have revealed that cellular senescence is caused not only by telomere length reduction, but also by external factors such as oncogene activation, oxidative stress, and DNA damage. (dojindo.com)
  • The induction and control mechanisms of cellular senescence - in which genetic and external factors are intricately involved - have yet to be fully elucidated. (dojindo.com)
  • Research into apoptosis, necrosis, autophagy, and cellular senescence is very important for understanding the intracellular functions that control cell survival and death. (dojindo.com)
  • Recently, various fields have given particular attention to cellular senescence due to the recent discoveries of SASP (a known cancer-causing factor) and senescence-related phenomena in stem cell research. (dojindo.com)
  • 13 Thus, the application of radiation therapy following surgery appears to prevent keloid scar recurrence by decreasing fibroblast proliferation, arresting the cell cycle and inducing premature cellular senescence. (jcadonline.com)
  • MAPK pathways refer to various cellular functions, including cell proliferation, differentiation and migration. (springer.com)
  • Cellular senescence is a multifaceted process that arrests the proliferation of cells that are at risk of neoplastic transformation. (nature.com)
  • There is now substantial evidence that cellular senescence is a barrier to malignant tumorigenesis in vivo . (nature.com)
  • There is also mounting evidence that cellular senescence contributes to ageing. (nature.com)
  • Proliferating cells can initiate an additional response by adopting a state of permanent cell-cycle arrest that is termed cellular senescence. (nature.com)
  • Understanding the causes and consequences of cellular senescence has provided novel insights into how cells react to stress, especially genotoxic stress, and how this cellular response can affect complex organismal processes such as the development of cancer and ageing. (nature.com)
  • Campisi, J. Cellular senescence as a tumor-suppressor mechanism. (nature.com)
  • We hypothesize that cellular senescence plays a role in the onset of cognitive problems following chemotherapy. (nki.nl)
  • Cellular senescence is a state of cell cycle arrest that is accompanied by secretion of inflammatory cytokines, immune modulators, growth factors and proteases. (nki.nl)
  • In this study we aim to determine the cellular mechanisms underlying the therapy-induced cognitive problems and work towards the identification of drugs that can attenuate these effects to improve cognition. (nki.nl)
  • In this study, we investigated how higher-order chromatin structure modulates differential expression of the human INK4b-ARF-INK4a locus during progenitor cell differentiation, cellular ageing and senescence of cancer cells. (biomedcentral.com)
  • We currently tested whether Berberine can affect premature, stress-induced cellular senescence caused by mitoxantrone. (aging-us.com)
  • In view of the evidence that BRB localizes in mitochondria, inhibits respiratory electron chain and activates AMPK, the observed attenuation of the replication stress-induced cellular senescence most likely is mediated by AMPK that leads to inhibition of mTOR signaling. (aging-us.com)
  • The encoded protein responds to diverse cellular stresses to regulate expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. (cubebiosystems.com)
  • Deciphering the purpose, causes, and consequences of cellular senescence will provide us with a better understanding of the role they may play in a wide variety of diseases and how we can use therapies to remove them to improve human health. (sens.org)
  • This term might be the most unfamiliar to you, so let's take a deeper dive into the causes and consequences of cellular senescence. (sens.org)
  • In reality, senescent cells are highly metabolically active which means that there are still many cellular processes happening within the cytoplasm. (sens.org)
  • These signals can help recruit immune cells to clear up cellular damage and these molecules can also support tissue repair and remodeling. (sens.org)
  • So far, it seems like cellular senescence is a great mechanism to have in our bodies, but as is the case with many cellular processes, too much of a good thing can become a bad thing. (sens.org)
  • Lille, France, Febuary 12, 2022 - StarkAge Therapeutics (SATX), a pioneering discovery-stage biotechnology company focusing on cellular senescence-related diseases, announced today it has established its Scientific Advisory Board (SAB) comprised of leading international independent experts. (starkagetx.com)
  • Dr. David Bernard is a cell and molecular biologist by training with strong expertise in cellular senescence. (starkagetx.com)
  • Currently heading up the Cellular Senescence, Cancer and Aging team at The Cancer Research Center of Lyon (CRCL) , Dr. Bernard's team is developing several research projects focused on new mechanisms and actors of cellular senescence they have identified in regulating cancer, age-related alterations, for example, fibrosis and inflammation, and aging. (starkagetx.com)
  • Dr. D'Adda di Fagagna discovered the engagement of DDR factors in the maintenance of telomeres and demonstrated that cellular senescence, a form of cell aging, is the outcome of DDR activation caused by the direct recognition of critically short or damaged telomeres. (starkagetx.com)
  • Dr. Ana O'Loghlen is an expert in cellular senescence in a variety of contexts such as aging, cancer, and age-related diseases. (starkagetx.com)
  • The focus of her Epigenetics & Cellular Senescence lab at the Blizard Institute of the Queen Mary University of London is understanding the basic mechanisms regulating cellular senescence and its influence on the microenvironment, and the understanding and identification of new components of the Senescence Associated Secretory Phenotype (SASP) and investigating their role with the microenvironment in the context of aging and cancer. (starkagetx.com)
  • Less clear, however, is whether these stress-related effects extend to additional hallmarks of biological aging, including cellular senescence, a stable state of cell cycle arrest. (cdc.gov)
  • The present study aimed to investigate associations between psychosocial stress and two markers of cellular aging-leukocyte telomere length (LTL) and cellular senescence signal p16(INK4a). (cdc.gov)
  • Blood samples were used to assess markers of cellular aging: LTL and gene expression of senescent cell signal p16(INK4a) (CDKN2A). (cdc.gov)
  • Findings also support the hypothesis that chronic stress is associated with accelerated aging by inducing cellular senescence, a common correlate of age-related diseases. (cdc.gov)
  • Senescence can be induced by DNA DAMAGE or other cellular stresses, such as OXIDATIVE STRESS. (bvsalud.org)
  • Cellular senescence during AGING or due to extended passages of normal cells in culture and that is triggered by the DNA damage-response to TELOMERE SHORTENING or by repeated exposure to stress signals. (bvsalud.org)
  • In addition, we studied the effect of WSC on the proliferation and cell cycle of alveolar type II cells and vascular endothelial cells. (nih.gov)
  • Oncogene-induced senescence (OIS) is a tumor suppression mechanism that blocks cell proliferation in response to oncogenic signalling. (nih.gov)
  • In fact, many studies have demonstrated the oleuropein and its derivative have proved pharmacological activity against proliferation of cancer cells and several tumor cell lines by different mechanisms such arrest cell cycle and cause apoptosis in cancerous cells, by modulation of miRNA expression and upregulation and downregulation of several genes. (springer.com)
  • Our study demonstrates that survivin and APE1/Ref-1 are significantly higher in human prostate cancer specimens compared to noncancerous controls and that APE1/Ref-1 redox-specific inhibition with small molecule inhibitor, APX3330 and a second-generation inhibitor, APX2009, decreases prostate cancer cell proliferation and induces cell cycle arrest. (oncotarget.com)
  • Senescence is defined as an irreversible cell proliferation arrest and occurs in response to various stresses, including activation of oncogenes, shortened telomeres, DNA damage, oxidative stress and mitochondrial dysfunction. (biologists.com)
  • In addition, their osteogenic differentiation potential was increased, and genes involved in cell adhesion, FGF-2 signalling, cell cycle, stemness, cell differentiation, and cell proliferation were upregulated, compared to that of the MSCs cultured on uncoated plates. (hindawi.com)
  • Although senescent cells repress proliferation-promoting genes, they also induce the gene program necessary for the implementation of senescence. (rupress.org)
  • It was discovered when pulmonary fibroblasts slowed down their proliferation and eventually ended in cell death after cell passaging had been performed for more than 8 months. (dojindo.com)
  • Genes involved in cell proliferation and extracellular matrix production are down-regulated while genes promoting apoptosis are upregulated. (jcadonline.com)
  • Developmentally regulated EZH2 levels are one of the factors that can determine the higher order chromatin structure and expression pattern of the INK4b-ARF-INK4a locus, coupling human progenitor cell differentiation to proliferation control. (biomedcentral.com)
  • Development and homeostasis require the coordinate regulation of cell proliferation and differentiation. (biomedcentral.com)
  • catenin signaling and influences CRC cell proliferation and experiments in CRC cell lines and an tumor xenograft model. (immune-source.com)
  • The oncoprotein murine double minute 2 (MDM2) promotes cell survival, proliferation, invasion, and therapeutic resistance in many types of cancer. (villajoyosacf.info)
  • AKI603 inhibited cell proliferation and colony formation capacities in imatinib-resistant CML cells by inducing cell cycle arrest with polyploidy accumulation. (scite.ai)
  • Instead of devolving into unchecked proliferation, it undergoes a permanent arrest of the cell cycle which could prevent cancers from growing rapidly. (sens.org)
  • Activated ERK2 and ERK1 promote cell proliferation. (molecularcircuit.com)
  • Oddly enough the AP24534 power of oncogenic to induce premature senescence depends upon the Raf-MEK-ERK pathway that mediates cell proliferation (36). (molecularcircuit.com)
  • miRNAs regulate target genes through biological processes, such as cell growth, proliferation, differentiation and apoptosis. (biomedcentral.com)
  • In response to mito- pendence between the key mecha- gens, cell proliferation is triggered by nistic characteristics. (who.int)
  • H - Ras cell proliferation are also linked with haematopoietic cel s. (who.int)
  • Although the conventional activities of p53 such as cell cycle arrest, senescence, and apoptosis are well accepted as the major checkpoints in stress responses, accumulating evidence implicates the importance of other tumor suppression mechanisms. (nature.com)
  • Is p53-dependent ferroptosis sufficient for tumor suppression in the absence of cell cycle arrest, senescence, and apoptosis? (nature.com)
  • To date, various mechanisms have been suggested to explain the powerful tumor-suppressive effect of p53, including the induction of cell cycle arrest, senescence, and apoptosis. (nature.com)
  • Although the senescent cells remain viable, they show typical changes with enlarged and flattened cell bodies, apoptosis resistance, increased activity of senescence-associated β -galactosidase (SA- β -gal), and upregulation of cyclin-dependent kinase (CDK) inhibitors including p16 INK4A , ARF proteins, and p21 [ 13 - 16 ]. (hindawi.com)
  • Further, we studied the effect of HSP70-2 protein ablation on signaling cascades involved in apoptosis, cell cycle and Epithelial-Mesenchymal-Transition both in culture as well as in-vivo human breast xenograft mouse model. (biomedcentral.com)
  • In addition, we have examined the putative role of HSP70-2 in apoptosis, cell cycle arrest and epithelial-mesenchymal transition (EMT) in-vitro and in-vivo xenograft mouse model using gene silencing approach. (biomedcentral.com)
  • Akt pathways have effects on apoptosis, protein synthesis, metabolism and cell cycle. (springer.com)
  • Oxaliplatin causes cell-cycle arrest promotes accelerated senescence and induces apoptosis in Bexarotene (LGD1069) cancer cells7 8 9 The p53 protein is involved in many biological processes the best known of which are cell-cycle arrest and DNA repair10 11 p53 also regulates apoptosis after exposure to hypoxia and cytotoxic drugs and is one of the most commonly mutated genes in many types of cancer12. (immune-source.com)
  • induces growth arrest or apoptosis depending on the physiological circumstances and cell type. (cubebiosystems.com)
  • LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. (cubebiosystems.com)
  • induce apoptosis (cell death) of rapidly proliferating parasites and cancer cells! (cures.news)
  • In response to severe DNA damage, cells undergo apoptosis to prevent transformation into over here tumour cells. (smadsignaling.com)
  • The best option would be for a cell to successfully repair any damage that occurs, but when this isn't possible (and the damage hasn't reached a critical level of inducing apoptosis) a cell will become senescent to try and avoid becoming cancerous. (sens.org)
  • Inhibition of mammalian target of rapamycin signaling by everolimus induces senescence in adult T-cell leukemia-lymphoma and apoptosis in peripheral T-cell lymphomas. (edu.lb)
  • Everolimus specifically induced oncoprotein Tax degradation and senescence in ATL cells and cell cycle arrest and apoptosis in HTLV-I-negative malignant T-cells. (edu.lb)
  • Everolimus-mediated apoptosis was also associated with an upregulation of p53 upregulated modulator of apoptosis (PUMA-α) proteins, an increase in Bax proteins and downregulation of Bcl-x(L) proteins in all tested HTLV-I-positive and -negative malignant cell lines. (edu.lb)
  • Activation of p53 will increase miR-34a creation, and about-expression of miR-34a induces cell cycle arrest, senescence and apoptosis. (signsin1dayinc.com)
  • Cada célula está programada para realizar determinado número de divisiones celulares y, al finalizar dicho tiempo, la proliferación se interrumpe y la célula entra en un estado de inactividad tras el cual se produce la MUERTE CELULAR a través del proceso de APOPTOSIS. (bvsalud.org)
  • What's more, the converted cells showed no signs of premature aging and appeared "rejuvenated" - iPS cells converted from nearly senescent donor cells regained their replicative potential and, when re-differentiated to fibroblasts, by all accounts resembled young proliferative cells. (biologists.com)
  • Initially, they took fibroblasts from a 74-year-old man and induced them into replicative senescence by serial passaging. (biologists.com)
  • lt;div class="textblock">Oncogenic Ras induces two products of the INK4a/ARF tumor suppressor locus (p16(INK4a) and p19(ARF)) in primary human and rodent fibroblasts, ultimately leading to a permanent state of cell cycle arrest resembling replicative senescence. (ku.dk)
  • We demonstrate that PLL provides favourable microenvironment for MSC culture by reversing the replicative senescence. (hindawi.com)
  • Unlike embryonic stem cells, adult stem cells (MSCs) have a limited lifespan and stop proliferating during in vitro culture due to replicative senescence [ 8 ]. (hindawi.com)
  • A classic paper that describes the limited replicative lifespan of normal human cells. (nature.com)
  • Over lifetime, due to the action of several stressors such as DNA damage and telomere shortening, senescent cells accumulate in the organism and release a variety of pro-inflammatory cytokines responsible for low-grade inflammation. (frontiersin.org)
  • Furthermore, senescent cells, with the secretory features known as the senescence-associated secretory phenotype (SASP), could produce proinflammatory cytokines, such as tumor necrosis factor- α (TNF- α ), interleukin-6 (IL-6), and monocyte chemoattractant protein1 (MCP-1), to greatly affect the neighboring cells [ 17 , 18 ]. (hindawi.com)
  • Senescent cells (SnCs) have been described to accumulate in osteoarthritis (OA) joint tissues in response to injury, thereby participating in OA development and progression. (aging-us.com)
  • Indeed, senescent cells (SnCs) are described to accumulate in joint tissues in response to injury and during aging, thereby participating in its development and progression [ 8 - 10 ]. (aging-us.com)
  • Conversion of somatic cells to iPS cells occurs at very low frequency in any given cell population, but because older individuals have a higher number of senescent cells it has proved to be difficult to convert cells from older-aged donors. (biologists.com)
  • However, the accumulation of senescent cells can have detrimental consequences, such as in age-related pathologies. (rupress.org)
  • Scientists have discovered that, in the absence of resident stem cells, senescent cells can instruct neighboring somatic cells to reprogram. (dojindo.com)
  • None of the individual biomarkers that have been identified so far have been deemed to be specific to senescent cells. (dojindo.com)
  • The development of drugs that eliminate senescent cells in the body (senolytic drugs) is also attracting the attention of researchers as a possible strategy to extend healthy life expectancy. (dojindo.com)
  • Figure 5: Potential deleterious effects of senescent cells. (nature.com)
  • Researchers have found that senescent cells accumulate in our body as we age. (sens.org)
  • As the interest in defining senescent cells has grown, so has the interest in deciphering why they exist in the first place. (sens.org)
  • The leading hypothesis for why senescent cells exist is that they serve as a preventative measure against cancer. (sens.org)
  • Because they are no longer dividing, it might sound like senescent cells are inactive and prevent cancer by completely shutting down. (sens.org)
  • Senescent cells secrete various proteins and molecules that cause inflammation. (sens.org)
  • Senescent cells are great for the initial prevention of cancer, but remember the SASP I just mentioned? (sens.org)
  • Although senescent cells start out as helpers that prevent cancer, too many of them can become a detriment to human health. (sens.org)
  • Researchers have found that senescent cells accumulate around the body as we age, so conditions such as Alzheimer's disease, heart disease, and liver fibrosis may be significantly worsened by the increased inflammation that comes with the accumulation of senescent cells. (sens.org)
  • There is still a lot to be discovered about how senescent cells work and scientists are very interested in understanding what other roles they might be playing in a wide variety of diseases. (sens.org)
  • This has also prompted many research groups to investigate how we might be able to remove senescent cells around the body with drugs or cell therapies which could help improve the health of many individuals. (sens.org)
  • These findings extend previous work on the impact of stress on biological aging by linking chronic stress exposure and daily stressful experiences to an accumulation of senescent cells. (cdc.gov)
  • introduced a new concept of CKD-associated secretory phenotype (CASP), which indicates that senescent renal cells could secrete SASP components of various cytokines such as IL-1, IL-6, and TNF- α [ 19 , 20 ]. (hindawi.com)
  • SnCs exhibit irreversible growth arrest accompanied by increased expression of cyclin-dependent kinase inhibitors (CDKi) such as p16 INK4a , and p21 Cip1 , accumulation of DNA damages, and secretion of diverse bioactive molecules known as the senescence-associated secretory phenotype (SASP). (aging-us.com)
  • The senescence-associated secretory phenotype (SASP) is a hallmark of senescence with an important physiological impact, but how it is established is unclear. (rupress.org)
  • Downregulation of UCK2 induced cell cycle arrest and activated the TNFα/NFκB signalling pathway-related senescence-associated secretory phenotype to modify the tumour microenvironment. (biomedcentral.com)
  • Downregulated UCK2 induced a secretory phenotype, which could improve the microenvironment, and decreased UCK2 remodelling metabolism could lower the resistance of tumour cells to T-cell-mediated killing. (biomedcentral.com)
  • In the present study, we found that knockdown of UCK2 induced cell cycle arrest through dual mechanisms in HCC and that targeting UCK2 promoted the secretory features involved in the senescence-associated secretory phenotype (SASP) and inflammasomes. (biomedcentral.com)
  • Senescence-associated secretory phenotype (SASP) can be induced by telomere dysfunction. (oaepublish.com)
  • These secreted factors are collectively referred to as the senescence-associated secretory phenotype or the SASP. (sens.org)
  • Numerous studies have revealed the critical role of premature senescence induced by various cancer treatment modalities in the pathogenesis of aging-related diseases. (oaepublish.com)
  • Telomeric DNA damage-induced mitochondrial dysfunction and increased reactive oxygen species production are hallmarks of premature senescence. (oaepublish.com)
  • Growing evidence demonstrates that various cancer treatment modalities, including chemotherapy, radiation therapy, targeted therapy, immunotherapy, hormone therapy, stem cell or bone marrow transplant, and surgery [ 3 - 5 ] , cause premature senescence, as reviewed elsewhere [ 6 - 8 ] . (oaepublish.com)
  • In primary mammalian cells oncogenic induces premature senescence depending on an active MEK-extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) pathway. (molecularcircuit.com)
  • Therefore oncogenic provokes premature senescence by activating the MEK-ERK and MKK3/6-p38 pathways in normal primary cells sequentially. (molecularcircuit.com)
  • These studies have got described the molecular occasions inside the signaling cascade that result in premature senescence and therefore have provided brand-new insights into how confers oncogenic change in major cells. (molecularcircuit.com)
  • It continues to be unclear how activation from the mitogenic Raf-MEK-ERK pathway by can stimulate premature senescence and exactly how this harmful growth influence of is certainly bypassed in tumors. (molecularcircuit.com)
  • Ectopic expression of MEKK3 a MAPKKK that activates p38 induced G1 arrest and reversed induces premature senescence through sequential activation of the MEK-ERK pathway and the MKK3/6-p38 pathway in primary human fibroblasts. (molecularcircuit.com)
  • Oncogenic Ras induces p19ARF and growth arrest in mouse embryo fibroblasts lacking p21Cip1 and p27Kip1 without activating cyclin D-dependent kinases. (ku.dk)
  • It was also shown that inhibition of the p16 tumour suppressor gene delays growth arrest and therefore senescence of MSC [ 16 ]. (hindawi.com)
  • Genes necessary for cell cycle progression, such as E2F-dependent genes, are incorporated into the SAHF and are thereby silenced, contributing to the stability of the growth arrest. (rupress.org)
  • Two powerful tumour suppressor pathways, controlled by the p53 and retinoblastoma (pRB) proteins, are important for establishing and maintaining the senescence growth arrest. (nature.com)
  • Process by which cells irreversibly stop dividing and enter a state of permanent growth arrest without undergoing CELL DEATH. (bvsalud.org)
  • Since then, many research teams have become interested in determining the hallmarks of cell senescence, the factors that induce it, and the effect of senescence on other cells and the body as a whole. (sens.org)
  • Clinical hallmarks of VHL disease include the development of retinal and central nervous system (CNS) hemangioblastomas (blood vessel tumors), pheochromocytomas , multiple cysts in the pancreas and kidneys, and an increased risk for malignant transformation of renal cysts into renal cell carcinoma. (medscape.com)
  • Abaza L, Talorete TP, Yamada P, Kurita Y, Zarrouk M, Isoda H (2007) Induction of growth inhibition and differentiation of human leukemia HL-60 cells by a Tunisian gerboui olive leaf extract. (springer.com)
  • The differentiation of mesenchymal stem cells (MSCs) into multiple cell lineages can be exploited as an attractive strategy for cell-based therapy and regenerative medicine [ 1 ]. (hindawi.com)
  • The ECM provides structural and biochemical support to the cells and has various other functions including cell adhesion, cell to cell communication, and differentiation [ 17 , 18 ]. (hindawi.com)
  • We found that INK4b and INK4a , but not ARF , are upregulated following the differentiation of haematopoietic progenitor cells, in ageing fibroblasts and in senescing malignant rhabdoid tumour cells. (biomedcentral.com)
  • During progenitor cell differentiation and ageing, PcG silencer EZH2 attenuates, causing loss of PRC binding and transcriptional activation of INK4b and INK4a . (biomedcentral.com)
  • Due to the role of oncogenic transcriptional activators NFĸB and STAT3 in survivin protein expression, and APE1/Ref-1 redox activity regulating their transcriptional activity, we assessed selective inhibition of APE1/Ref-1's redox function as a novel method to halt prostate cancer cell growth and survival. (oncotarget.com)
  • Immortalized rodent fibroblast cell lines that lack INK4a/ARF function, ARF alone, or p53 are resistant to the growth inhibitory effects of oncogenic Ras and instead continue to proliferate and undergo morphological transformation. (ku.dk)
  • Primary mouse embryo fibroblasts lacking Cip1 and Kip1 genes encoding inhibitors of cyclin-dependent kinase-2 were used to further explore the effects of oncogenic Ras on arrest of the cell division cycle. (ku.dk)
  • Although early passage primary fibroblast strains that lack both p21(Cip1) and p27(Kip1) fail to assemble cyclin D-dependent kinases, oncogenic Ras retained its ability to induce p19(ARF), but not p16(INK4a), protecting Cip/Kip-null cells from proliferating and undergoing transformation. (ku.dk)
  • Therefore, in the absence of p16(INK4a), p21(Cip1), and p27(Kip1), oncogenic Ras affects the functions of genes required for completion of the cell cycle. (ku.dk)
  • Contact inhibition is a method of arresting cells when neighboring cells come into contact with each other. (wikipedia.org)
  • Because APE1/Ref-1 is expressed and elevated in prostate cancer, we sought to characterize APE1/Ref-1 expression and activity in human prostate cancer cell lines and determine the effect of selective reduction-oxidation (redox) function inhibition on prostate cancer cells in vitro and in vivo . (oncotarget.com)
  • The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. (cancerindex.org)
  • Oxaliplatin treatment upregulates p53 and activated p53 enhances growth inhibition in CRC cells treated with oxaliplatin. (immune-source.com)
  • This study is the first to report that inhibition of oxaliplatin-induced cell growth may be dependent on p53 and may involve increased expression of cytochrome enzymes (CYP2S1) in CRC cells. (immune-source.com)
  • Results Inhibition of CRC cell growth by oxaliplatin is usually associated with Bexarotene (LGD1069) the presence of wild-type p53 To investigate the cytotoxicity of the anticancer agent oxaliplatin in CRC cells CCK8 assays were performed using HCT116 SW480 and HT29 cells treated with various concentrations of oxaliplatin for 24?h. (immune-source.com)
  • Body 1 Inhibition of colorectal tumor cell development by oxaliplatin. (immune-source.com)
  • Surprisingly, inhibition of AurA by AKI603 induced leukemia cell senescence in both BCR-ABL wild type and T315I mutation cells. (scite.ai)
  • Senescence was confirmed by FACS analysis showing cell cycle arrest, increase in molecular markers characteristic of senescence, and formation of SAHF. (biologists.com)
  • The defining characteristic of senescence is a highly stable cell cycle arrest, triggered by the up-regulation of cyclin-dependent kinase inhibitors such as p16 INK4a and p21 CIP1a . (rupress.org)
  • They further link to the activation of protein kinase C- (PKC-) induced generation of reactive oxygen species (ROS) [ 6 , 7 ], which further mediates the activation of downstream transcription factor nuclear factor kappa-light-chain enhancer of activated B cells (NF- κ B). Thus, the main treatments of DN refer to modulate glycemic and blood pressure through insulin and RAS inhibitors. (hindawi.com)
  • Furthermore, the induction of senescence was associated with enhancing reactive oxygen species (ROS) level. (scite.ai)
  • DNA harm is induced by environmental variables, like ionizing radiation,but additionally by intrinsic agents, like metabolically produced reactive oxygen species. (smadsignaling.com)
  • Given that some of the mechanisms below of inducing cell cycle arrest involve damaging the DNA, this allows investigation into how the cell responds to damage of its genetic material. (wikipedia.org)
  • This pitfall may be due to the lack of understanding of the mechanisms underlying chondrocyte senescence. (aging-us.com)
  • Chronic exposure to IL-1β induces only partial expression of senescence markers and does not allow us to conclude on its ability to induce senescence in chondrocytes. (aging-us.com)
  • M: A mutant screen of budding yeasts with mitotic arrest identified CDC16, CDC23, and CDC27 as key genes that, when mutated, cause arrest in mitosis. (wikipedia.org)
  • We also assessed the effect of WSC on the expression of genes involved in cell cycle arrest and inflammation. (nih.gov)
  • Prior to senescence, mutant RasV12 activation in primary human fibroblasts compromised mitosis, associated with abnormal expression of mitotic genes that enter M-phase. (nih.gov)
  • Although the mechanism of how these factors induced pluripotency in somatic cells is not completely understood, it is clear that the endogenous pluripotency genes OCT4 , SOX2 and NANOG were activated and, in turn, re-activated the autoregulatory loop that could maintain the pluripotent state independent of the transgenes. (biologists.com)
  • In a recent paper published the November issue of Genes in Development, entitled "Rejuvenating senescent and centenarian human cells by reprogramming through the pluripotent state," Lapasset and colleagues from the Institute of Functional Genomics in France report that they have overcome this barrier and generated iPS cells from human donors as old as 101 years. (biologists.com)
  • In contrast silencing p53 significantly decreases the inhibitory effects of oxaliplatin suggesting an important role for p53 in this process13 14 The p53 protein regulates a group Bexarotene (LGD1069) of cytochrome P450 (CYP) genes in human and mouse liver cells and influences the efficacy of chemotherapeutic treatment regimens15 16 However a role for p53 in regulating CYP450 genes in the intestinal tract has not yet been reported. (immune-source.com)
  • Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. (cubebiosystems.com)
  • While there are ongoing research projects to define new markers or causes of senescence, we do know that senescence can be induced by damage to DNA, shortening of telomeres (which are the protective caps at the end of DNA molecules), mitochondrial damage, and something called epigenetic factors, which refers to changes to our chromosomes that affect the way DNA is packaged and genes are expressed. (sens.org)
  • The use of serum deprivation - partially or completely removing the serum and its nutrients - has been shown to arrest and synchronize cell cycle progression in G0 phase, for example in neonatal mammalian astrocytes and human foreskin fibroblasts. (wikipedia.org)
  • In mammalian organisms, cells that express markers of senescence have been shown to accumulate with age and at sites of certain age-related pathologies. (nature.com)
  • In this submission, we explored the effect of the mammalian target of rapamycin (mTOR) complex-1 (mTORC1) inhibitor everolimus (RAD001) on ATL and HTLV-negative malignant T-cell lines. (edu.lb)
  • Once activated, p53 coordinates multiple downstream pathways, thereby maintaining the homeostasis of the host cell or organism (if the stress is mild, transient, and repairable) or eliminating damaged cells (if the stress is acute, prolonged, and difficult to resist). (nature.com)
  • Common features of senescence include activation of the p53/p21 and p16 / pRb pathways and formation of senescence-associated heterochromatic foci (SAHF). (biologists.com)
  • These marker proteins are known to be tumor suppressors and regulate the cell cycle mainly through two pathways (p16Ink4a-RB and p53-p21CIP1). (dojindo.com)
  • NF-κB pathways are associated with immunity, inflammation and cell survival. (springer.com)
  • These pathways respond to somewhat different stimuli but interact and cooperate to control the senescence response. (nature.com)
  • Figure 4: Senescence controlled by the p53 and p16-pRB pathways. (nature.com)
  • Dr. Fabrizio d'Adda di Fagagna is a cell and molecular biologist at IFOM in Milan and CNR in Pavia (Italy) who studies the involvement of the DNA damage response (DDR) pathways in physiologically relevant processes such as aging and cancer. (starkagetx.com)
  • Sager, R. Senescence as a mode of tumor suppression. (nature.com)
  • On the other hand, etoposide treatment reliably induces DNA damage-related senescence in human articular chondrocytes evidenced by loss of proliferative capacity, DNA damage accumulation, and expression of some SASP components. (aging-us.com)
  • these cells can remain metabolically active, resulting in the secretion of pro-inflammatory factors to result in SASP [ 14 ]. (biomedcentral.com)
  • Well, it turns out that some of those inflammatory proteins and molecules that make up the SASP can have negative effects on other cells and tissues. (sens.org)
  • Frog egg cell extracts have been used extensively in cell cycle research because they are relatively large, reaching a diameter of 1mm, and so contain large amounts of protein, making protein levels more easily measurable. (wikipedia.org)
  • p27Kip1 protein levels are elevated in arresting cells. (wikipedia.org)
  • It is a catalytic subunit of the protein kinase complex that is important for cell cycle G1 phase progression. (thermofisher.com)
  • UCK2 promoted cell cycle progression of HCC by preventing the degradation of mTOR protein and maintaining the stability of PDPK1 mRNA. (biomedcentral.com)
  • The ablation of Epithelial splicing regulatory protein 1 (ESRP1), a major regulator of CD44 mRNA splicing, resulted in the shift from CD44v+ to CD44v- cells in KYSE520. (bvsalud.org)
  • By using a direct in vivo shRNA screen, we show that liver cancer cells that have mutations in the gene encoding the tumor suppressor protein p53 (Trp53 in mice and TP53 in humans) and that are driven by the oncoprotein NRAS become addicted to MYC stabilization via a mechanism mediated by aurora kinase A (AURKA). (scite.ai)
  • mRNA and protein expression comparison We calculated the fold transform in level of mRNAs and proteins transcripts in CD30hi cells in comparison to CD30lo cells in semi quantitative method. (smadsignaling.com)
  • for proteomics data, fold change was calculated by taking the ratio of imply sum of XCorr of that protein in CD30hi to CD30lo cells. (smadsignaling.com)
  • The foamy stromal cells between the capillaries stain positive for glial fibrillary acid protein and neuron-specific enolase. (medscape.com)
  • DeMarini, and Chapter 20, by Rice and cell death determine the size protein in several signal ing path- and Herceg). (who.int)
  • While in G1 the cell synthesizes messenger RNA (mRNA) and proteins in preparation for subsequent steps of interphase leading to mitosis. (wikipedia.org)
  • The proto-oncogene family members encodes little GTP binding proteins that transduce development indicators from cell surface area receptors in response to extracellular stimuli (1 6 37 Prior studies have recommended that aberrant activation of is certainly a crucial stage during tumorigenesis. (molecularcircuit.com)
  • Lastly, we will explore the current therapeutic approaches and challenges in targeting senescence. (frontiersin.org)
  • Mesenchymal stem cells (MSCs) possess great therapeutic potential. (hindawi.com)
  • Studies investigating MSC senescence are therefore crucial for successful therapeutic application of MSCs. (hindawi.com)
  • Our experiments confirm and extend the involvement of CYP2S1 as a potential therapeutic target for enhancing oxaliplatin efficacy in colorectal epithelial cells. (immune-source.com)
  • These results support a therapeutic role for everolimus, particularly as long-term maintenance therapy in patients with ATL and other HTLV-I-negative peripheral T-cell lymphomas. (edu.lb)
  • Microparticles Induce Cell Cycle Arrest Through Redox-Sensitive Processes in Endothelial Cells: Implications in Vascular Senescence. (ohri.ca)
  • Responsible for such pivotal processes, p53 can deliver considerable damage if mutated, thus becoming "the guardian of the cancer cell" [ 8 ] . (encyclopedia.pub)
  • MDM2 can inhibit both p53 and NBS1 to regulate multiple physiological processes and/or induce genomic instability, in which ATM plays a central phosphorylation regulatory role. (villajoyosacf.info)
  • PknD sensor-coated microspheres appear to be largely Bioactive Compound Library order enveloped by actin processes (arrows) indicating that PknD-induced uptake by host cells may be an active process. (hsdpathway.com)
  • Simultaneously, RasV12 activation enhanced survival of damaged mitoses, culminating in extended mitotic arrest and aberrant exit from mitosis via mitotic slippage. (nih.gov)
  • ERK-dependent transcriptional up-regulation of Mcl1 was responsible for enhanced slippage of cells with mitotic defects and subsequent cell survival. (nih.gov)
  • CYP2S1 knockdown conferred a cell survival advantage after oxaliplatin treatment to cells harboring wild-type p53 and cytotoxicity and antitumor activity. (immune-source.com)
  • P53 deficiency results in reduced repair activity and decreased cell survival after UV-induced DNA damage, suggesting the involvement of p53 in nucleotide excision repair (NER) (Smith et al. (villajoyosacf.info)
  • In presence of DNA damage, the tumour suppressor p53 plays a crucial purpose inside the selection among survival and death of your cell. (smadsignaling.com)
  • Hayflick, L. The limited in vitro lifetime of human diploid cell strains. (nature.com)
  • The concept of senescence was first discovered in the 1960's by two scientists named Leonard Hayflick and Paul Moorhead. (sens.org)
  • Induced cell cycle arrest is the use of a chemical or genetic manipulation to artificially halt progression through the cell cycle. (wikipedia.org)
  • The cells can be induced to arrest as they arrive (at different time points) at a certain phase, so that when the arrest is lifted (for instance, rescuing cell cycle progression by introducing another chemical) all the cells resume cell cycle progression at the same time. (wikipedia.org)
  • Mimosine is a plant amino acid that has been shown to reversibly inhibit progression beyond G1 phase in some human cells, including lymphoblastoid cells. (wikipedia.org)
  • This miRNA functions as a tumor suppressor and dysregulation or loss of the host gene from which this miRNA is processed is associated with cancer progression in numerous cell types. (cancerindex.org)
  • As a result, changes in SA-ß-Gal expression, cell cycle progression, and mitochondrial membrane potential were observed. (dojindo.com)
  • Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. (cubebiosystems.com)
  • They were able to induce a pluripotent state in differentiated cells by introducing four transcription factors, OCT4, SOX2, c-MYC, and KLF4 by retroviral infection, hence the name "induced pluripotent stem cells (iPSCs). (biologists.com)
  • Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. (cubebiosystems.com)
  • Conversely, intact damage can lead to transcription and replication arrest, leading to cell death and senescence (Hoeijmakers, 2009). (villajoyosacf.info)
  • catenin signaling and cytochromeP450 enzymes (CYP51A1) were correlated to oxaliplatin sensitivity in 21 colorectal cancer cell lines24. (immune-source.com)
  • However, MSCs need to be expanded in vitro in order to obtain sufficient cells for clinical trials since they are extremely rare in various tissues. (hindawi.com)
  • Furthermore, ZEB1 overexpression induced EMT and increased the levels of CD133- and BMI1-positive GRPs in vitro and gefitinib resistance in vivo. (bvsalud.org)
  • It is an artificial activation of naturally occurring cell cycle checkpoints, induced by exogenous stimuli controlled by an experimenter. (wikipedia.org)
  • Many stimuli elicit a senescence response. (nature.com)
  • It is thought that activation from the MAPK pathway provides cells with constitutive mitogenic indicators indie of extracellular stimuli (7). (molecularcircuit.com)
  • Some epigenetic imprinting remained, the telomeres length was not fully restored, and the descendants of these cells entered senescence prematurely. (biologists.com)
  • Its proposed mechanism of action is an iron/zinc chelator that depletes iron within the cell. (wikipedia.org)
  • Other reports also show that DN is highly associated with accelerated aging in various types of cells such as tubular cells, podocytes, mesangial cells, and endothelial cells [ 21 - 23 ]. (hindawi.com)
  • They extensively tested whether the iPS cells retained marks of aging similar to cells they originated from. (biologists.com)
  • iPS cells showed many characteristics of human embryonic stem cells (hESCs) such as expression of pluripotency markers, reactivation of telomerase and the ability to form teratomas, demonstrating a potential to redifferentiate into descendants of all three embryonic lineages. (biologists.com)
  • Individual clones were able to differentiate into cells expressing markers of all three germ layers as well as form teratomas with organ-like structures typical of all three embryonic lineages. (biologists.com)
  • All these markers of senescence were distinctly diminished, in a concentration-dependent manner, by Berberine. (aging-us.com)
  • CD44v+ and CD44v- cells showed the expression of epithelial and mesenchymal markers, respectively. (bvsalud.org)
  • In addition, pyrimidine metabolites can induce epithelial to mesenchymal transition to promote tumour metastasis, playing a non-proliferative role in pyrimidine metabolism in cancer [ 7 ]. (biomedcentral.com)
  • Single-cell sorting of CD44v+ and CD44v- cells revealed both cells gave rise to cell populations consisting of CD44v+ and CD44v- cells, indicating CD44v+ epithelial-like and CD44v- mesenchymal-like cells can generate counterparts, respectively. (bvsalud.org)
  • BACKGROUND: Zinc-finger E-box-binding homeobox 1 (ZEB1) is an important regulator of epithelial-mesenchymal transition (EMT) and is involved in the maintenance of cancer stem cells (CSCs) via miR-200c and BMI1 pathway. (bvsalud.org)
  • Recent studies have suggested that epithelial-mesenchymal transition (EMT) of alveolar epithelial cells influences development of pulmonary fibrosis, which is mediated by transforming growth factor ß (TGF-ß). (bvsalud.org)
  • E. Wells containing endothelial cells with microspheres were analyzed for fluorescence. (hsdpathway.com)
  • [ 2 ] Diagnosed in 50% of patients with VHL disease, these hemangiomas are composed of endothelial cells and pericytes. (medscape.com)
  • G2: Fission yeast expressing some mutant forms of CDC2 unable to arrest in G2 in response to DNA damage, indicating the gene product is involved in G2 arrest. (wikipedia.org)
  • The initiation and development of tumor cell is accompanied by elevated stresses, such as oncogene activation, DNA damage, genome instability, and reprogrammed tumor metabolism. (nature.com)
  • This study used etoposide, to induce DNA damage-related senescence or chronic exposure to IL-1β to entail inflammation-related senescence in human OA chondrocytes. (aging-us.com)
  • Cells continually experience stress and damage from exogenous and endogenous sources, and their responses range from complete recovery to cell death. (nature.com)
  • Telomeric DNA damage response induced by some cancer treatments can persist for months, possibly accounting for long-term sequelae of cancer treatments. (oaepublish.com)
  • Throughout our lives, the cells in our bodies can experience external damage from the sun or chemicals in our environment. (sens.org)
  • Normally, our cells are pretty good at repairing and coping with damage that occurs. (sens.org)
  • There are a few different things that can happen once cell damage occurs. (sens.org)
  • Ideally, the damage gets repaired, and the cell goes right back to its normal function. (sens.org)
  • Taken together, our data demonstrate that the small molecule AurA inhibitor AKI603 may be used to overcome drug resistance induced by BCR-ABL-T315I mutation in CML. (scite.ai)
  • The DDR brings about temporal cell cycle arrest, when the degree of DNA harm is low, Docetaxel Microtubule Formation inhibitor so the cell can restore it. (smadsignaling.com)
  • patients with type E (AD) tumor had higher incidence of nodal metastasis at MGCD0103 cell line TGF-beta inhibitor mediastinal lymph node than did patients in tumor groups, and all mediastinal positive nodes existed in lower mediastinal area. (hsdpathway.com)
  • Importantly, mitotic slippage and oncogene signalling synergistically induced senescence and key senescence regulators p21 and p16. (nih.gov)
  • Braig, M. & Schmitt, C. A. Oncogene-induced senescence: putting the brakes on tumor development. (nature.com)
  • Can ferroptosis be specifically induced in tumors but not in normal tissues? (nature.com)
  • For example CYP2S1 which is usually most highly expressed in intestinal tract epithelial cells may be involved in metabolizing aromatic hydrocarbons and other xenobiotic substrates20 21 Madanayake also identified that human CYP2S1 is an important enzyme in the metabolism of COX-derived prostaglandins at nanomolar concentrations and the authors suggested that CYP2S1 may play an important role in modulating the inflammatory process23. (immune-source.com)
  • We demonstrate that, at clinically achievable concentrations, long-term treatment with everolimus resulted in a dramatic inhibitory effect on the growth of HTLV-I-positive and -negative malignant T-cells, while normal resting or activated T-lymphocytes were resistant. (edu.lb)
  • The INK4b-ARF-INK4a tumour suppressor locus controls the balance between progenitor cell renewal and cancer. (biomedcentral.com)
  • The INK4b-ARF-INK4a tumor suppressor locus (Figure 1A ) plays a central role in controlling the equilibrium between progenitor cell renewal and cancer risk [ 1 - 8 ]. (biomedcentral.com)
  • Immune cell infiltration level and immune-related functional scores were evaluated to assess the link between tumour microenvironment and UCK2. (biomedcentral.com)
  • Scientists working in basic, translational, and clinical cancer metabolism research are invited to join the Academy in New York on April 17th to discuss the intersection between cell signaling and metabolism. (nyas.org)
  • HIF-1 is included in angiogenesis, invasion, metastasis, glucose uptake and rate of metabolism in most cancers cells[17]. (signsin1dayinc.com)