পৃষ্ঠা 1 থেকে 864 ফলাফল
In addition to suppressing breast cancer cell growth, retinoids potentiate growth inhibition in human breast cancer when tested in vitro and in vivo with tamoxifen and/or interferon. The purpose of this study was to ascertain the biologic effects of all-trans-retinoic acid (ATRA) administered alone
OBJECTIVE
Our previous work had shown that retinoic acid (RA) inhibits cell growth and induces apoptosis in estrogen receptor-positive (ER-positive) MCF-7 and T-47D human breast carcinoma cells, but not in ER-negative human breast carcinoma cells MB-231 and MB-453. The purpose of this work was to
The membrane receptor Fas (Apo-1/CD95) is an important initiator of programmed cell death induced by anti-Fas antibody or Fas ligand. MCF-7 human breast cancer cells have low levels of Fas receptor (FasR) and are resistant to anti-FasR antibody mediated apoptosis, however two naturally occurring
The relapse of cancer is mostly due to the proliferation of cancer stem cells which could not be eliminated by a standard chemotherapy. A new kind of all-trans retinoic acid stealth liposomes was developed for preventing the relapse of breast cancer and for treating the cancer in combination with a
Using established breast cancer cell lines in a cell culture model we studied the growth effect of retinoic acid (RA) alone or in combination with the antiestrogen 4-hydroxytamoxifen (OHT). Cytoplasmic 3HRA binding sites were determined by sucrose density gradient centrifugation analysis. Of the
Retinoic acid (all-trans and 9-cis) isomers represent important therapeutic agents for many types of cancers, including human breast cancer. Changes in protein composition of the MCF-7 human breast cancer cells were induced by all-trans retinoic acid, 9-cis retinoic acid, and their combination and
BACKGROUND
A growing body of evidence supports the hypotheses that the retinoic acid receptor beta2 (RAR-beta2) gene is a tumor suppressor gene and that the chemopreventive effects of retinoids are due to induction of RAR-beta2. RAR-beta2 expression is reduced in many malignant tumors, and we
The effect of the differentiating agent all-trans-retinoic acid on the expression of components of the milk fat globule membrane and HLA-DR by breast cancer cell lines has been examined. Effects on proliferation were also considered, to determine whether any cell surface changes were related to or
This work aimed to provide, in one isolation and separation step, an overview of the content of proteins with different solubility after treatment with all-trans retinoic acid, which is considered to be an important therapeutic agent, predominantly in acute promyelocytic leukemia. Breast, ovarian,
The ability of retinoids to inhibit breast cancer cell growth correlates with estrogen receptor (ER) alpha status, as shown by the antiproliferative effects of retinoids in ERalpha-positive breast cancer cells and their use as chemopreventive agents in premenopausal women. The discovery of ERbeta,
We studied the effect of 13-cis-retinoic acid (13-cRA) alone and in combination with interferons (IFNs) and tamoxifen (TAM) in two established human breast cancer cell lines: the estrogen-sensitive CG-5 and the estrogen-insensitive MDA-MB-453 cells. 13-cRA (10(-9)-10(-5) M) significantly reduced the
All-trans retinoic acid (ATRA), one of vitamin A derivatives, shows greater growth inhibition of breast cancer cell for ER-positive than ER-negative cells, while triple negative breast cancer cell such as MDA-MB-231 cell is poorly responsive to ATRA treatment. In this study, we found that
Both retinoic acid (RA) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) elicit a number of common biochemical and toxic responses including teratogenic effects in mice and inhibition of cell proliferation of numerous cell lines. In mice, RA plus TCDD interact synergistically as teratogens, suggesting
Epigenetic silencing of retinoic acid receptor-beta2 (RARbeta2) and estrogen receptor-alpha (ERalpha) expressions have been revealed to be important in the development of approaches for diagnosis and therapy of breast cancer. We aimed to explore the correlation of some potential factors with the
The chemotherapeutic drug paclitaxel induces microtubular stabilization and mitotic arrest associated with increased survivin expression. Survivin is a member of the inhibitor of apoptosis (iap) family which is highly expressed in during G2/M phase where it regulates spindle formation during