4 edition of Mechanism of cisplatin resistance inhuman malignant melanoma found in the catalog.
Mechanism of cisplatin resistance inhuman malignant melanoma
Thesis (M.Sc.) -- University of Toronto, 1998.
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Taxotere/Temodar/Cisplatin Study in Melanoma Patients The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Current therapy of gynecologic malignancies consists of platinum-containing chemotherapy. Resistance to therapy is associated with increased levels of interleukin (IL)-6 and prostaglandin E2 (PGE2), 2 inflammatory mediators known to skew differentiation of monocytes to tumor-promoting M2 macrophages. We investigated the impact of cisplatin and carboplatin on 10 different .
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To overcome resistance, cisplatin is commonly used in combination Mechanism of cisplatin resistance inhuman malignant melanoma book some other drugs in treating ovarian cancer, biliary tract cancer, lung cancer (diffuse malignant pleural mesothelioma), gastric cancer, carcinoma of salivary Mechanism of cisplatin resistance inhuman malignant melanoma book origin, breast, colon, lung, prostate, melanoma and pancreatic cancer cell lines, squamous cell carcinoma of Cited by: First approved by FDA (Food and Drug Administration) in for the treatment of testicular and bladder cancer, cis-diamminedichloroplatinum(II) (best known as cisplatin or CDDP) is a Cited by: Cisplatin is one of Mechanism of cisplatin resistance inhuman malignant melanoma book most effective broad-spectrum anticancer drugs.
Its effectiveness seems to be due to the unique properties of cisplatin, which enters cells via multiple pathways and forms multiple different DNA-platinum adducts while initiating a cellular self-defense system by activating or silencing a variety of different genes, resulting in dramatic epigenetic and/or genetic Cited by: In addition to the mechanisms described above, decreased cellular accumulation of cisplatin might occur by increased efflux of the drug from the cells, ().Cisplatin is not a substrate for the P-glycoprotein (the product of the mdr gene), which is overexpressed in multi-drug resistant cells and functions as a drug efflux pump.Some cisplatin resistant cells overexpress a kDa by: Molecular mechanism of cisplatin resistance Article Literature Review in Oncogene 31(15) September with 1, Reads How we measure 'reads'.
Modulation of cisplatin resistance in human malignant melanoma Article (PDF Available) in Cancer Research 52(24) January with 19 Reads How we measure 'reads'. Cisplatin is a chemotherapy medication used to treat a number of cancers. These include testicular cancer, ovarian cancer, cervical cancer, breast cancer, bladder cancer, head and neck cancer, esophageal cancer, lung cancer, mesothelioma, brain tumors and neuroblastoma.
It is given by injection into a vein. Common side effects include bone marrow suppression, hearing problems, kidney Pregnancy category: AU: D, US: D (Evidence of risk). Breast and ovarian cancers are among the 10 leading cancer types in females with mortalities of 15% and 6%, respectively.
Despite tremendous efforts to conquer malignant diseases, the war on cancer declared by Richard Nixon four decades ago seems to be lost. Approximat women in the US will be diagnosed with ovarian cancer in Therefore, its incidence is relatively Cited by: A Massachusetts General Hospital (MGH) research team has identified an additional mechanism for resistance to targeted treatment for BRAF-mutant melanoma.
Their paper, receiving advance online. Mechanism of cisplatin resistance inhuman malignant melanoma book in vivo resistance of cancer cells to cisplatin is a multifactorial phenomenon, which usually makes the elucidation of true mechanism difficult. An appropriate in vitro cellular model is critical for the better understanding of the cellular and molecular events in response to cisplatin treatment (Pu et al., ).Cited by: Cisplatin: mode of cytotoxic action and molecular basis of resistance Zahid H Siddik*,1 1Department of Experimental Therapeutics, UnitThe University of Texas M.
Anderson Cancer Center, Holcombe Boulevard, Houston, TXUSA Cisplatin is one of the most potent antitumor agents. for cisplatin resistance in UCC. Many of these are shared among solid cancers and this knowl-edge is vital if mechanisms to bypass drug resis-tance are to be found. The cellular events which underpin cisplatin resistance in cancer are mul-tiple and affect numerous cellular pathways (for a review of mechanisms of cisplatin resistance inFile Size: 2MB.
Molecular mechanisms of cisplatin resistance in cervical cancer Haiyan Zhu, Hui Luo, Wenwen Zhang, Zhaojun Shen, Xiaoli Hu, Xueqiong Zhu Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, People’s Republic of China Abstract: Patients with advanced or recurrent cervical cancer have poor prognosis, and their 1-year survival is only.
Researchers have identified a major reason why melanoma is largely resistant to Mechanism of cisplatin resistance inhuman malignant melanoma book. They found a genetic pathway in melanoma cells that inhibits the cellular mechanism for.
Cisplatin is in a class of drugs known as platinum-containing compounds used to treat various types of cancers including metastatic testicular and. Experimental support for these hypothetical aspects of the mechanism underlying anti-tumor activity of cisplatin or resistance of some tumors to this drug has been thoroughly reviewed recently,17 Initially, inhibition of DNA replication by cisplatin adducts was considered to be a process very likely relevant to its anti-tumor efficiency INTRODUCTION.
Although the incidence of malignant melanoma is increasing, most cases are diagnosed at an early stage. Surgical excision is curative in most cases of early stage disease, and patients at high risk of developing metastatic disease may benefit from adjuvant therapy with interferon alfa (IFNa) or ipilimumab .
(See "Surgical management of primary cutaneous melanoma or. alone in patients with metastatic malignant melanoma (E): a trial coordinated by the Eastern Cooperative Oncology Group. J Clin Oncol. ;– Papadopoulos NE, Bedikian A, Ring S, Kim KB, Hwu WJ, Gerber DL, Homsi J, Hwu P. Phase I/II study of a cisplatin-taxol- dacarbazine regimen in metastatic melanoma.
Am J Clin Size: 40KB. Scientists have identified a new mechanism that explains why some recurrent ovarian tumors become resistant to treatment with commonly used.
To study the mechanism of acquired cisplatin resistance of BRCA2-mutated cancer, first we screened 12 human breast-cancer cell lines for alterations in BRCA2 protein expression.
McClay EF, Albirght KD, Jones JA, Eastman A, Christen RD, Howell SB (b): Modulation of cisplatin resistance in human malignant melanoma cells. Cancer Res – Google Scholar McClay EF, Albright KD, Jones JA, Christen RD, Howell SB (): Tamoxifen modulation of cisplatin sensitivity in human malignant melanoma by: 6.
Molecular mechanisms of cisplatin resistance in cervical cancer Haiyan Zhu, Hui Luo, Wenwen Zhang, Zhaojun Shen, Xiaoli Hu, Xueqiong Zhu Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, People’s Republic of China Abstract: Patients with advanced or recurrent cervical cancer have poor prognosis, and their 1-year survival is only Cited by: The major intent of cancer treatment with cytotoxic drugs is direct tumor cell damage, but some of these drugs have been shown to be immunomodulatory.
Cisplatin is a widely used cytotoxic drug that has been combined with biological response modifiers in recent clinical trials. To evaluate further whether cisplatin may independently alter the level of host resistance against tumor growth, the Cited by: Abstract.
Interactions between cisplatin (CDDP) and irradiation are of potential significance for the combined modality treatment of cancer. Previous data have indicated that following in vitro exposure to X-irradiation certain tumour cells expressed resistance to CDDP. To identify parameters associated with this CDDP resistance, the human ovarian carcinoma cell line SK-OV-3/P was pre Cited by: Keywords:cisplatin, antitumor activity, cell death, apoptosis, necrosis.
Abstract: Although cisplatin, cis-diamminedichloroplatinum(II), has been successfully used in the chemotherapy of cancer for more than 25 years, its biochemical mechanism of action is still unclear. The current accepted paradigm about cisplatin mechanism of action is that.
The drug Paclitaxel may be useful in the treatment of cisplatin-resistant cancer; the mechanism for this activity is unknown.
Cisplatin resistance-associated overexpressed protein, also known as CROP, is a human gene. This gene encodes a cisplatin resistance-associated overexpressed protein (CROP).
Melanoma is a most dangerous and deadly type of skin cancer, and considered intrinsically resistant to both radiotherapy and chemotherapy. It has become a major public health concern as the incidence of melanoma has been rising steadily over recent decades with a 5-year survival remaining less than 5%.
Detection of the disease in early stage may be curable, but late stage metastatic disease Cited by: Cisplatin resistance depends on a number of factors that reduce drug uptake, promote cytoplasmic detoxification, and increase DNA repair activity.
We herein review a novel mechanism of cisplatin resistance involving the transcriptional regulation of DNA repair genes by ZNFAuthor: Tetsuro Wakasugi, Hideaki Suzuki, Jun-ichi Ohkubo, Gunji Nagatani, Hiroto Izumi, Kimitoshi Kohno.
Cytotoxicity Cisplatin-Resistant Tumor Lines IC 50 (µM) Cancer cell line cisplatin 1 Chronic myelogenous leukemia K >80 3 Chronic myelogenous leukemia KG-1 48 2 Acute myelogenous leukemia ML-2 >80 1 Mouse melanoma B16 >80 6 Colon cancer HTN >80 12 Colon cancer HT29 50 8 Colon cancer HCT >80 9 Lung carcinoma A 63 6 Breast carcinoma.
of strategies targeting the mechanism of drug resistance. • This observation has significant clinical importance as it can be used to predict treatment response and direct treatment selection in cancer patients.
Future Directions •!This assay has potential to elucidate the differential efficacy of cisplatin as a. Mechanism of Action Cisplatin is believed to kill cancer cells by binding to DNA and interfering with its repair mechanism, eventually leading to cell death.
The first step in the process (after the cisplatin molecule penetrates the cell membrane intact) is for a molecule of water to replace one of. The experimental schedule used for assessing the efficacy of HemoHIM in melanoma-bearing mice which were injected with cisplatin.B16F0 melanoma cells (5 × 10 5 /mouse) were inoculated into subcutaneous femoral left region of mice 3 days before an initial injection of cisplatin.
Cisplatin was intraperitoneally injected at 4 mg/kg B.W., and HemoHIM was daily given at mg/kg B.W. from day Cited by: Cisplatin exposure induced the emergence or expansion of an ALDH1-positive subpopulation in cisplatin sensitive and resistant NSCLC cell lines, respectively, further enhancing cisplatin resistance.
Using the Aldefluor assay and FACS analysis, ALDH1 subpopulations were isolated and evaluated in terms of stem cell by: LUC7 like 3 pre-mRNA splicing factor (LUC7L3), also known as Cisplatin resistance-associated overexpressed protein, or CROP, is a human gene. This gene encodes a cisplatin resistance-associated overexpressed protein (CROP).
The N-terminal half of the CROP contains cysteine/histidine motifs and leucine zipper-like repeats, and the C-terminal half is rich in arginine and glutamate residues (RE Aliases: LUC7L3, CRA, CREAP-1, CROP, LUC7A.
Sunitinib, Tamoxifen, and Cisplatin in Treating Patients With High-Risk Ocular Melanoma The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S.
Federal Government. It is important to clarify the mechanism of resistance to cisplatin for the treatment of solid tumors. We have examined the expression of apoptosis-related proteins, Bax and Bcl-2, in ovarian cancer cells.
We used the cell line and its cisplatin resistant subclone CCited by: The mechanism of cisplatin anticancer activity is generally believed to be its binding to DNA, interfering with the cell repair mechanism, eventually leading to cell death (3). However, the success of chemo-therapy depends on the sensitivity of the tumor to CDDP, as osteosarcoma cells often acquire resistance to drugs and even.
Cisplatin is one of the most potent antitumor agents known, displaying clinical activity against a wide variety of solid tumors. Its cytotoxic mode of action is mediated by its interaction with DNA to form DNA adducts, primarily intrastrand crosslink adducts, which activate several signal transduction pathways, including those involving ATR, p53, p73, and MAPK, and culminate in the activation Cited by: Tumour resistance to cisplatin: a modelling approach.
L Marcu 1,3, E Bezak 1,3, To quantify the extent of drug resistance, the cisplatin resistance factor (CRF) is defined as the ratio between the number of surviving cells of the resistant population and the number of surviving cells of the sensitive population, determined after the same.
Introduction Inherent and acquired cisplatin resistance reduces the effectiveness of this agent in the management of non-small cell lung cancer (NSCLC).
Understanding the molecular mechanisms underlying this process may result in the development of novel agents to enhance the sensitivity of cisplatin. Methods An isogenic model of cisplatin resistance was generated in a panel of NSCLC cell. Mechanism of Action. Cisplatin, pdf, and oxaliplatin enter cells by diffusion, and by an active Cu2+ transporter (Kruh, ).
Inside the cell, the chloride atoms of cisplatin may be displaced and the compound may be inactivated directly by reaction with nucleophiles such as thiols.Understanding Cisplatin Resistance Using Cellular Models Britta Stordal1* and Mary Davey2 1Bill Walsh Cancer Research Laboratories, Royal North Shore Hospital and University of Sydney, NSW 2Department of Medical and Molecular Biosciences, University of Technology Sydney, NSW *Corresponding author: [email protected] Page 12 AUSTRALIAN BIOCHEMIST Vol 38 No .Keywords:paclitaxel, drug resistance, reversal of drug resistance, ebook vivo drug resistance assays, mdr, pgp, tubulin, cytokine.
Abstract: It has been approximately ten years since the Food and Drug Administration (FDA) approved paclitaxel for the treatment of platinum resistant epithelial ovarian carcinoma. Since the approval, the drug has.