Sentences with phrase «tumor cell apoptosis»

To search for more evidence of tumor cell apoptosis, a TUNEL assay was performed on mice tumor sections.

Claudin - 4 activity in ovarian tumor cell apoptosis resistance and migration.

This class of drug candidates has gathered wide attention as a causal means to induce tumor cell apoptosis [11, 12].

The researchers picked one such experimental drug called RITA — Reactivation of p53 and Induction of Tumor cell Apoptosis — and used it to treat mice for a few days after cardiac injury.

Not exact matches

Goji's are reported to have anti-aging properties and show anti-tumor activities against various types of skin cancer cells by inhibiting tumor growth and inducing apoptosis.

Since the cancer cells in both types of tumors were the same, the researchers compared the noncancerous cells present in the induced and transplanted tumors to explore what might be causing the T cell apoptosis.

Their paper, which appears in Nature Communications, describes how an immune cell recruited to the tumor induces the programmed suicide, or apoptosis, of the killer T cells harnessed by many immunotherapies.

The nanovesicles fuse with tumor cells, causing them to self - destruct by apoptosis.

Giving the mice antibiotics helped gemcitabine kill tumor cells, increasing the number of tumor cells going through a type of cell death called apoptosis from about 15 percent to 60 percent or more.

Using tumor samples from the Women's Healthy Eating and Living clinical trial, researchers identified stem - like tumor cells as being characterized by low levels of the molecule p53 upregulated modulator of apoptosis (PUMA).

«Liver cancer due to chronic inflammation: Tumor growth follows programmed cell death (apoptosis).»

New research shows that microRNA - 486 is a potent tumor - suppressor molecule in lung cancer, and that the it helps regulate the proliferation and migration of lung - cancer cells, and the induction of programmed cell death, or apoptosis, in those cells.

BCL - 2 is present in high amounts in many tumors and helps cancer cells to survive, but when the BCL - 2 gene is blocked by MM41 in mice, the cancer cells succumb to apoptosis and die.»

According to University of Helsinki scientist and Finnish Academy Research Fellow Juha Klefström, PhD, who led the study, «Myc oncoprotein not only boosts tumor cell proliferation but it also makes the cells vulnerable to cell suicide program, apoptosis.

Because it more effectively induces cancer cell apoptosis in p53 - deficient tumors, FL118 is especially effective against late - stage cancers, which usually lose functional p53 and are resistant to DNA - damage drugs.

In addition, they found that epithelial - derived MMP9 suppresses tumors in CAC by activating the MMP9 - Notch1 - ARF - p53 axis pathway, which increases apoptosis, initiates cell cycle arrest and keeps a check on DNA damage.

«Most chemotherapies kill cancer cells through apoptosis, and the cancer cells that escape apoptosis are the root cause of chemotherapy resistance and tumor progression,» said Chi.

That's how the tumor cells may be able to avoid the induced apoptosis,» says Zou.

Myc cancer gene empowers tumor cells to relentlessly divide but simultaneously, provokes a cell suicide process called apoptosis.

When using a well established model of colorectal cancer, the researchers observed that dietary emulsifier consumption was sufficient to make the animals more susceptible to developing colonic tumors because this created and maintained a pro-inflammatory environment associated with an altered proliferation / apoptosis (cell death) balance.

These compounds have been shown to inhibit cancer cell growth, induce cancer cell apoptosis, and reduce tumor volume in mice (14, 15, 16, 17).

In fact, KLF4 blocks senescence and apoptosis by repressing transcription of P53, whereas it can activate P21 - dependent cell - cycle arrest, and therefore, KLF4 can function both as a tumor suppressor and an oncogene (33, 34).

In the study, the biomedical engineers killed the cancerous tumor cells within days, by injecting liposomes armed with TRAIL (Tumor necrosis factor Related Apoptosis - Inducing Ligand) that attach to «natural killer» cells — a type of white blood cell — residing in the lymph ntumor cells within days, by injecting liposomes armed with TRAIL (Tumor necrosis factor Related Apoptosis - Inducing Ligand) that attach to «natural killer» cells — a type of white blood cell — residing in the lymph nTumor necrosis factor Related Apoptosis - Inducing Ligand) that attach to «natural killer» cells — a type of white blood cell — residing in the lymph nodes.

Takeda K, Hayakawa Y, Smyth MJ, Kayagaki N, Yamaguchi N, Kakuta S, Iwakura Y, Yagita H, Okumura K. Involvement of tumor necrosis factor - related apoptosis - inducing ligand in surveillance of tumor metastasis by liver NK cells.

Additional studies are attempting to determine if the transgene expression of various anti-apoptotic genes can protect T cells from tumor - induced apoptosis.

The tumor suppressor p53 is critical in the protection of cells against radiation - induced carcinogenesis, most likely through its ability to trigger apoptosis of radiation - damaged cells (45).

Phosphorylation of Merkel cell polyomavirus large tumor antigen at serine 816 by ATM kinase induces apoptosis in host cells.

Injections of iPSC - EPCs did not however have significant effect on tumor growth or on overall survival, but transducing cells with a baculovirus expressing CD40L, a member of the TNF gene family which can induce apoptosis [6, 7], and injection into the breast cancer lung metastasis, increased levels of pro-apoptotic cytokines in lung tissues, indicating the induction of apoptosis by CD40L carried by the EPCs (See figure).

25: Radaeva S, Sun R, Jaruga B, Nguyen VT, Tian Z, Gao B. Natural killer cells ameliorate liver fibrosis by killing activated stellate cells in NKG2D - dependent and tumor necrosis factor - related apoptosis - inducing ligand - dependent manners.

Tumor - associated B7 - H1 promotes T - cell apoptosis: a potential mechanism of immune evasion.

Conversely, they have found that interfering with survivin expression in tumor cells is sufficient to trigger apoptosis, to enhance the efficacy of conventional anti-tumor treatment, and to exert potent anti-tumor activity in vivo.

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.

In addition to a critical role in cell division, it is also clear that survivin has a function in protecting cells from apoptosis and that this pathway is followed in nearly every human tumor.

In a xenograft KMT2D - mutated T - lymphoma model, dual treatment with chidamide and decitabine significantly retarded tumor growth and induced cell apoptosis through modulation of the KMT2D / H3K4me axis.

The restriction of cellular growth by p53 has been reported to result in cell cycle arrest or apoptosis [6], and targeting p53 and restoring p53 function to limit tumor growth has been intensively researched for cancer therapy [7].

They include its effects on endothelial cell «differentiation» to yield tubular - like structures, endothelial and tumor cell proliferation, apoptosis, and migration, as well as its effects on extracellular matrix remodelling enzyme activities of matrix metalloproteinase - 2 (MMP - 2) and urokinase - type plasminogen activator (uPA).

Topotecan works by trapping Top1ccs in tumor cells, resulting in the DNA damage that triggers apoptosis.

The King Lab has pioneered the use of selectin proteins to deliver apoptosis death signals to tumor cells in flowing blood, and to deliver therapeutic cargo (e.g., siRNA, chemotherapeutics) encapsulated in nanoscale liposomes.

In addition, ActD has been shown to mimic nutlin - 3 in the activation of p53 - dependent transcription, induction of a reversible protective growth arrest in normal cells, and enhancement of the activity of the chemotherapeutic drugs, melphalan and etoposide, resulting in apoptosis of p53 positive human tumor cells [14].

It is widely believed that cellular senescence is a tumor suppressor mechanism; however, it has not been understood why it is advantageous for organisms to retain mutant cells is a postmitotic state rather than simply eliminating them by apoptosis.

Interestingly, fluid shear stress also modulates how tumor cells respond to apoptosis death signals in the bloodstream.

Elephants have 20 copies of the gene p53, a tumor suppressor famous for being involved in apoptosis or «assisted suicide» for cells with damaged DNA, for example.

Stephen Alexander, UK - Cannabinoid receptors, transporters, endocannabinoid turnover, hydrogen sulphide turnover Arthur Christopoulos, Australia (GPCRs Liaison)- G protein - coupled receptors; analytical pharmacology; allosteric modulation; biased agonism; drug discovery; neuropharmacology John Cidlowski, USA (NHRs Liaison)- Glucocorticoid receptor signaling; apoptosis and the immune system Anthony P. Davenport, UK (Chair Evolving Pharmacology, GPCRs Liaison) Doriano Fabbro, Switzerland - Kinases and their biology, kinase inhibitors, drug discovery, pharmacology of drugs (kinase inhibitors) in the indication oncology, biology of oncology Kozo Kaibuchi, Japan Yoshikatsu Kanai, Japan - Transporters, amino acid signals, epithelial function, cancer biology Francesca Levi - Schaffer, Israel - eosinophils and mast cells as effector cells in allergic inflammation: characterization of new receptors / ligands, hypoxia / angiogenesis and eosinophils, asthma, atopic dermatitis, allergic rhinitis, immunopharmacological modulation of allergic diseases by bispecific recombinant antibodies, bacteria interactions with eosinophils and mast cells, the allergic effector unit, mast cell derived tumors: new antibody based treatment, the allergic inflammation and the resolvome, non IgE - mediated mast cell activation in diseases Eliot H. Ohlstein, USA (Editor)- Drug discovery and development, urogenital biology, cardiovascular / metabolic medicine John A. Peters, UK (LGICs Liaison) Alex Phipps, UK - Oncology, Clinical Pharmacology, Biologics and Immunotherapy Joerg Striessnig, Austria (VGICs Liaison)- Physiology, pharmacology and pathophysiological role of voltage-gated calcium channels

In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].

TGFβ inhibits tumor initiation and progression by inducing cell cycle arrest and apoptosis; however epithelial tumorigenesis may escape this common antitumor mechanism by inducing aberrations in TGFβ signaling resulting in enhanced development and progression of human carcinomas.

Melanoma Differentiation Associated Gene - 7 / Interleukin - 24 Promotes Tumor Cell - Specific Apoptosis through Both Secretory and Nonsecretory Pathways

All CM members have research interests in basic cancer mechanisms, including the normal functions of oncogenes and tumor suppressor genes; regulators of cell cycle and apoptosis; regulators of angiogenesis and metastasis; and stem cells and blood formation.

When introduced into the MDA - MB - 231 cells, the Δ2A mutant did not induce apoptosis of these cells whereas WT LARP7 readily impaired cell survival, supporting the model that the ability of LARP7 to assemble 7SK snRNP and suppress P - TEFb is necessary for its tumor suppressor potential.

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).

In cells from certain brain tumors, in stomach cancer, and in colorectal cancer lines, vitamin K halts the reproductive cell cycle and induces apoptosis.