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 n
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 n
Tumor 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.