Sentences with phrase «known as apoptosis»

The study team discovered that GSE targets colorectal cancer through inducing oxidative stress that leads to the programmed cell death known as apoptosis.

Instead, they turned on genes that promote the death of cancer cells (known as apoptosis) and the growth of healthy, normal cells!

Cancer patients who increase eating raspberries create the potential to destroy malignant growths through a process known as Apoptosis, a systematic cell death via a biochemical reaction.

This disease - fighting nutrient can slow the growth and development of new blood vessels that nourish tumors, increase a type of programmed cancer cell death known as apoptosis and reduce the proliferation of new cancer cells.

Estrogen does this by activating a gene known as Bcl - 2 that slows the process of cell death, known as apoptosis.

The drugs reduce pain and inflammation by inhibiting the cyclooxygenase (COX) enzymes, which are involved not only with inflammation but also with certain processes involved in cancer, such as blood supply to the tumor and programmed cell death (known as apoptosis).

Ideally, they should die by the process known as apoptosis, but as we age, more and more frequently they don't.

Bcl - 2 proteins play a key role in cell survival by protecting against a form of cell suicide known as apoptosis.

Survivin belongs to a class of proteins that prevent cells from self - destructing, a process known as apoptosis.

However, in developing brain cells, the researchers found TLR3 activation also influences 41 genes that add up to a double whammy in this model — diminished stem cell differentiation into brain cells and increased cell suicide, a carefully controlled process known as apoptosis.

MAPK regulates cell functions, including proliferation, gene expression, differentiation, cell division and a form of cell suicide known as apoptosis.

The scientists discovered that dinaciclib, by interfering with UPR activation, caused multiple myeloma and myeloid leukemia cells to initiate a form of cell suicide known as apoptosis when exposed to agents that induced ER stress.

Not exact matches

If this fails, the UPR instructs the cell to self - destruct, a process known as programmed cell death or apoptosis.

ABT - 737 targets proteins known as B - cell lymphoma 2 (Bcl - 2) and Bcl - xL, which prevent apoptosis, a form of cell suicide, in cancer cells.

They know from previous studies that apoptosis begins with the activation of what are known as Bax proteins.

The drug, known as HRX9, works by preventing the cancer cells from avoiding apoptosis — the natural process by which unhealthy and damaged cells close themselves down and die.

Earlier research had shown that cells surrounding an HIV - infected cell die as a result of apoptosis, or programmed cell suicide, and scientists knew that Nef had a hand in starting that process.

Similarly, Bernaudin et al. [43] found increased expression of 18 genes in the neonatal rat brain following hypoxia (8 % O2 for 3 h) including several known hypoxia inducible genes such as MAP kinase phosphatase - 1 (MKP - 1), several HIF - 1 target genes including VEGF and GLUT - 1, genes implicated in apoptosis, signal transduction molecules, and transcription factors.

Members of a family that includes the apoptosis regulator APAF1 (apoptotic - protease - activating factor 1), mammalian NOD - LRR proteins (also known as NACHT - LRR proteins or CATERPILLERs) and plant disease - resistance gene products.

Human pluripotent stem cells (hPSCs), including human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs), are known to be vulnerable to apoptosis upon various technical manipulation, such as single cell dissociation, freezing and thawing, etc., which hinder their use for clonal isolation in gene transfer, differentiation and FACS cell sorting.

The Altieri laboratory is interested in how tumor cells evade apoptosis — also known as programmed cell death — which is the process that normally causes dysfunctional cells to self - destruct.

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.

Approximately 50 % of PTCL are unclassifiable and categorized as PTCL, not otherwise specified (PTCL - NOS).1 Using gene expression profiling, PTCL - NOS lymphocytes can be distinguished from normal T lymphocytes, with deregulation of genes involved in apoptosis, proliferation, cell adhesion, and transcription regulation.2 Two subgroups of PTCL - NOS have been identified, which are characterized by high expression of either GATA3 or TBX21 / T - bet transcription factors and downstream target genes.3 However, actionable biomarkers closely related to the pathogenic mechanism need to be further investigated and may become potential therapeutic targets of PTCL - NOS. 4, 5

The plates contained genes associated with proliferation and apoptosis, to confirm our in vitro findings that no changes occurred, as well as genes known to identify / enrich for CSC and those involved in CSC signaling.

Many mechanisms of MDR have been described, such as the overexpression of MDR1 (also known as P - glycoprotein or ABCB1) or other ATP - dependent transporters that pump drugs out of the cancer cells, amplification of drug - inactivating enzymes, mutations or modifications of drug targets, alterations in DNA repair machinery, and increased resistance to apoptosis (1 — 3).

Estradiol promotes the onco (cancer) gene, Bcl - 2, while progesterone promotes the protective gene known as p53 which slows cell apoptosis.

Unlike their healthy counterparts, cancer cells lack the mechanism that tells them to stop multiplying, as well as the process known as programmed cell death (aka «apoptosis»), which gets rid of unneeded cells.