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N C Munshi - One of the best experts on this subject based on the ideXlab platform.

  • Arsenic Trioxide: an emerging therapy for multiple myeloma.
    The oncologist, 2001
    Co-Authors: N C Munshi
    Abstract:

    Arsenic Trioxide can inhibit proliferation and induce apoptosis in multiple myeloma (MM) cells in vitro and in vivo. In addition to affecting tumor growth, Arsenic Trioxide has been shown to inhibit angiogenesis, suggesting that it may have significant potency in the treatment of MM. Based on these observations, the clinical efficacy of Arsenic Trioxide was evaluated in patients with advanced refractory MM using a fixed-dose intravenous infusion given daily for a maximum of 60 days. Nine patients were evaluable. All nine had extensive prior therapy; seven had two or more high-dose chemotherapy cycles with autologous stem cell support. All nine patients had cytogenetic abnormalities, and six had chromosome 13 deletions. Of the four patients who completed more than 30 days of Arsenic Trioxide infusion, two had >50% reduction in myeloma paraprotein, one had stable disease, and one progressed. Of the five patients with 50% paraprotein reduction). The regimen was well tolerated except for development of cytopenia, which responded to G-CSF, and a grade III pulmonary complication in one patient. In summary, Arsenic Trioxide has activity in end-stage, high-risk myeloma and deserves further evaluation in earlier-stage disease.

  • Arsenic Trioxide: An Emerging Therapy for Multiple Myeloma
    The Oncologist, 2001
    Co-Authors: N C Munshi
    Abstract:

    Arsenic Trioxide can inhibit proliferation and induce apoptosis in multiple myeloma (MM) cells in vitro and in vivo. In addition to affecting tumor growth, Arsenic Trioxide has been shown to inhibit angiogenesis, suggesting that it may have significant potency in the treatment of MM. Based on these observations, the clinical efficacy of Arsenic Trioxide was evaluated in patients with advanced refractory MM using a fixed-dose intravenous infusion given daily for a maximum of 60 days. Nine patients were evaluable. All nine had extensive prior therapy; seven had two or more high-dose chemotherapy cycles with autologous stem cell support. All nine patients had cytogenetic abnormalities, and six had chromosome 13 deletions. Of the four patients who completed more than 30 days of Arsenic Trioxide infusion, two had >50% reduction in myeloma paraprotein, one had stable disease, and one progressed. Of the five patients with 50% paraprotein reduction). The regimen was well tolerated except for development of cytopenia, which responded to G-CSF, and a grade III pulmonary complication in one patient. In summary, Arsenic Trioxide has activity in end-stage, high-risk myeloma and deserves further evaluation in earlier-stage disease. The Oncologist 2001;6(suppl 2):17-21

Lin Ying - One of the best experts on this subject based on the ideXlab platform.

  • Recent Advances in Arsenic Trioxide Against Malignant Tumor
    Journal of Qilu Oncology, 2002
    Co-Authors: Lin Ying
    Abstract:

    Long term clinical trials have indicated the Arsenic Trioxide is very effective in treatment of acute promyelocytic leukemia.The efficacy in treatment of other types of leukemia and solid tumor and the mechanism in how Arsenic Trioxide targets the tumor cells are,however,not clearly understood.This paper reviews the current research situation of the Arsenic Trioxide against malignant tumor;exploring the possibilities for the efficacy and mechanism in treatment of malignant tumor,provide the reference for developing a new field in Arsenic Trioxide against malignant tumor.

Zhong-ying Shen - One of the best experts on this subject based on the ideXlab platform.

  • The alteration of mitochondria is an early event of Arsenic Trioxide induced apoptosis in esophageal carcinoma cells.
    International journal of molecular medicine, 2000
    Co-Authors: Zhong-ying Shen, W.j. Cai, J Shen, C Hong, Minghao Zheng
    Abstract:

    It is accepted that inorganic Arsenic Trioxide is an inducer of apoptosis for many types of cancer. Our previous studies have demonstrated that Arsenic Trioxide induces apoptosis of esophageal carcinoma cells. Administration of Arsenic Trioxide results in the inhibition of growth and survival of tumor cells. Esophageal carcinoma cells treated with Arsenic Trioxide for 3 days demonstrated a typical morphological appearance of apoptosis. To further examine molecular mechanism of Arsenic Trioxide induced apoptosis of esophageal carcinoma cells, we have investigated the early changes of the apoptotic cell induced by Arsenic Trioxide. Our results indicated that Arsenic Trioxide induced apoptosis of esophageal carcinoma cells occurs as early as 2 h after treatment. Annexin-v staining has further proved that the phosphatidylserine is exposed at 2 h. The early morphological change of Arsenic Trioxide treated cells was in the mitochondria. Arsenic Trioxide treated cells displayed aggregated mitochondria. It induces accumulation of high electron-density amorphous substances, swollen and disruption of mitochondria in oesophageal carcinoma cells after 2 h treatment. The alteration of mitochondria induced by Arsenic Trioxide seems to occur before the condensation of chromatin. Thus, our data demonstrated that the primary target of Arsenic Trioxide induced apoptosis of esophageal carcinoma cells may be the mitochondria. It is possible that Arsenic Trioxide is a mitochondriotoxic agent.

  • Arsenic Trioxide induces apoptosis of oesophageal carcinoma in vitro.
    International journal of molecular medicine, 1999
    Co-Authors: Zhong-ying Shen, L.j. Tan, W.j. Cai, J Shen, C. Chen, X.m. Tang, Ming Zheng
    Abstract:

    The Arsenic compounds in traditional Chinese medicine have been recorded to have therapeutic effects on the treatment of psoriasis, syphilis, rheumatosis and a number of malignant tumours. Recent studies showed that Arsenic Trioxide can induce clinical remission in patients with acute promyelocytic leukemia, including those who have relapsed after retinoic acid treatment. however, the mechanism of how Arsenic Trioxide targets tumour cells is not clearly understood. We have examined the effects of Arsenic Trioxide on oesophageal carcinoma cell line EC8712. Our results demonstrated that the growth and survival of tumour cells were markedly inhibited by Arsenic Trioxide. The half dose effect (ED50) was at the concentration of 1 microM. Electron microscopic study demonstrated that EC8712 tumour cells treated with Arsenic Trioxide display a typical morphological appearance of apoptosis, including chromatin condensation and fragmentation of the nuclei. In contrast, no apoptotic features were observed in tumour cells without Arsenic Trioxide treatment. TUNEL assay also showed the biological features of apoptosis in cells treated with Arsenic Trioxide. Flow cytometry analyses showed that apoptotic peak was identified in Arsenic Trioxide treated cells but not in the control. Apoptotic cells in Arsenic Trioxide treated group account for 35% of total cell populations after three days treatment at a dose of 3 microM. In short, our results suggested that the anticancer effect of Arsenic Trioxide is due, at least in part, to the induction of apoptosis in cancer cells.

Chih-hsin Yang - One of the best experts on this subject based on the ideXlab platform.

Guo Hong-rong - One of the best experts on this subject based on the ideXlab platform.

  • Mechanisms of Arsenic Trioxide induced apoptosis in malignant tumor cells
    Journal of Modern Oncology, 2007
    Co-Authors: Guo Hong-rong
    Abstract:

    The proven efficacy of Arsenic Trioxide in the treatment of acute promyelocytic leukemia(APL) and the emerging importance of Arsenic Trioxide in other diseases prompted extensive studies of the mechanisms of action of Arsenic Trioxide in APL and in other malignant solid tumors.In this review we will focus on downstream events in Arsenic Trioxide-induced apoptotic pathways with an emphasis on the role of permeability transition pore(PTP),human telomerase reversetranscriptase(hTERT) and some other factors in Arsenic Trioxide-induced apoptosis.