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Готові списки джерел за темами / Formation of vincristine

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Добірка наукової літератури з теми "Formation of vincristine"

Автор: Grafiati

Опубліковано: 6 вересня 2023

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Статті в журналах з теми "Formation of vincristine"

1

Wawro, Marta Ewelina, Katarzyna Sobierajska, Wojciech Michał Ciszewski, and Jolanta Niewiarowska. "Nonsteroidal Anti-Inflammatory Drugs Prevent Vincristine-Dependent Cancer-Associated Fibroblasts Formation." International Journal of Molecular Sciences 20, no. 8 (2019): 1941. http://dx.doi.org/10.3390/ijms20081941.

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Vincristine is used in the clinical treatment of colon cancer, especially in patients diagnosed in the advanced phase of cancer development. Unfortunately, similar to other agents used during antitumor therapy, vincristine might induce chemoresistance. Studies of this process focus mainly on the analysis of the molecular mechanisms within cancer, usually ignoring the role of stromal cells. Our present findings confirm that vincristine stimulates the secretion of tumor growth factors class beta and interleukin-6 from cancer-associated fibroblasts as a result of paracrine stimulation by cancer c

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2

Moha, Rico. "Chemotherapy medication of Vincristine and Vinblastine." Cancer Research and Cellular Therapeutics 1, no. 1 (2017): 01–02. http://dx.doi.org/10.31579/2640-1053/007.

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Cancers treated with Vincristine and vinblastine include: acute leukemia, Hodgkin's and non- Hodgkin's lymphoma, neuroblastoma, rhabdomyosarcoma, Ewing's sarcoma, Wilms' tumor, multiple myeloma, chronic leukemias, thyroid cancer, brain tumors, non-small cell lung cancer, bladder cancer, melanoma, and testicular cancer andIt is also used to treat some blood disorders. It is given by injection into a vein. Vincristine and vinblastine exhibit differential activity against tumors and normal tissues. In this work, a number of cultured cell lines were assayed for their sensitivity to the antiprolife

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3

Bowman, Laura C., Janet A. Houghton, and Peter J. Houghton. "Formation and stability of vincristine-tubulin complex in kidney cytosols." Biochemical Pharmacology 37, no. 7 (1988): 1251–57. http://dx.doi.org/10.1016/0006-2952(88)90778-2.

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4

Takahashi, Tsutomu, Yoshio Honma, Koshi Kawakami та Junji Suzumiya. "Cotylenin Α, a Fusicoccane Diterpene Glycoside with a Complex Sugar Moiety, and Vincristine Synergistically Inhibit the Growth of Myeloma Cell in Vitro and in Vivo". Blood 124, № 21 (2014): 5721. http://dx.doi.org/10.1182/blood.v124.21.5721.5721.

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Abstract Introduction: Multiple myeloma is still incurable and optimize existing chemotherapeutic strategies and development of novel agents are necessary to improve the outcome of patients. Cotylenin A, a fusicoccane diterpene glycoside with a complex sugar moiety, was isolated as a plant-growth regulator. Cotylenin A modulates the 14-3-3 intracellular signaling pathway and has been shown to inhibit the growth of several cancer cells. Herein, we examined the antitumor effects of cotylenin A to develop a novel treatment against myeloma. Methods: Five human myeloma cell lines, RPMI8226, KMS-11,

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5

Singh, Akannsha, Mariana Zapata, Yong Sung Choi, and Sun-Ok Yoon. "GSI promotes vincristine-induced apoptosis by enhancing multi-polar spindle formation." Cell Cycle 13, no. 1 (2013): 157–66. http://dx.doi.org/10.4161/cc.26951.

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6

Diouf, Barthelemy, Kristine Crews, Glen Lew, et al. "Genome-Wide Association Analyses Identify Susceptibility Loci For Vincristine-Induced Peripheral Neuropathy In Children With Acute Lymphoblastic Leukemia." Blood 122, no. 21 (2013): 618. http://dx.doi.org/10.1182/blood.v122.21.618.618.

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Abstract Introduction Vincristine, a vinca alkaloid, is one of the most widely used and effective medications for acute lymphoblastic leukemia (ALL). Vincristine exerts its cytotoxic effects by interfering with microtubule formation and mitotic spindle dynamics, leading to mitotic arrest and cell death. However its use often causes neuropathy characterized by abdominal pain, sensory and motor dysfunctions. To date, various candidate gene studies have failed to identify consistent genetic variants associated with an increased risk of vincristine-induced neuropathy. Methods Vincristine-induced n

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7

Zhang, Jiandi, Mary C. Reedy, Yusuf A. Hannun, and Lina M. Obeid. "Inhibition of Caspases Inhibits the Release of Apoptotic Bodies: Bcl-2 Inhibits the Initiation of Formation of Apoptotic Bodies in Chemotherapeutic Agent-induced Apoptosis." Journal of Cell Biology 145, no. 1 (1999): 99–108. http://dx.doi.org/10.1083/jcb.145.1.99.

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During apoptosis, the cell actively dismantles itself and reduces cell size by the formation and pinching off of portions of cytoplasm and nucleus as “apoptotic bodies.” We have combined our previously established quantitative assay relating the amount of release of [3H]-membrane lipid to the degree of apoptosis with electron microscopy (EM) at a series of timepoints to study apoptosis of lymphoid cells exposed to vincristine or etoposide. We find that the [3H]-membrane lipid release assay correlates well with EM studies showing the formation and release of apoptotic bodies and cell death, and

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Liedtke, Michaela, Clare Twist, Marcia Bieber, Neelima Bhat, Nelson N. H. Teng, and Steven Coutre. "A Phase I Study of a Novel Human Monoclonal Antibody (mAb216) with Chemotherapy for the Treatment of Patients with Relapsed or Refractory B-Lineage Acute Lymphoblastic Leukemia." Blood 110, no. 11 (2007): 2831. http://dx.doi.org/10.1182/blood.v110.11.2831.2831.

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Abstract BACKGROUND: Despite improvements in front-line therapy for adult ALL, most patients eventually relapse and do not tolerate or respond to reinduction therapy. Novel targeted therapies are needed that have both activity against adult ALL and a toxicity profile distinct from conventional chemotherapy. MAb216 is a naturally occurring human IgM monoclonal antibody derived from the VH4-34 (variable heavy chain) gene. It has shown promise as a novel therapy for B-ALL in preclinical studies. In vitro, mAb216 specifically binds and is cytotoxic to normal human B-lymphocytes and B-progenitor ly

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Shah, Mithun Vinod, Karen S. Flatten, B. Douglas Smith, Allan D. Hess, and Scott H. Kaufmann. "MTH1 Inhibitor-Induced Cytotoxicity in Acute Myeloid Leukemia." Blood 126, no. 23 (2015): 1273. http://dx.doi.org/10.1182/blood.v126.23.1273.1273.

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Abstract BACKGROUND: Acute myeloid leukemia (AML) is an aggressive leukemia with 5-year overall survival of 20-25%. The major reason for treatment failure in AML is resistance to chemotherapy. Thus, there is an urgent need for identification of novel therapeutic agents for AML. Neoplastic cells, including AML, have dysfunctional redox regulation that results in increased reactive oxygen species (ROS). Accumulation of ROS leads to oxidation of free and incorporated nucleotides, leading to DNA damage and cell death. MTH1 is a nudix family hydrolase that sanitizes the oxidized nucleotide pool to

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Fine, R. L., S. Koizumi, G. A. Curt, and B. A. Chabner. "Effect of calcium channel blockers on human CFU-GM with cytotoxic drugs." Journal of Clinical Oncology 5, no. 3 (1987): 489–95. http://dx.doi.org/10.1200/jco.1987.5.3.489.

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Calcium channel blockers (CCBs) such as verapamil and nitrendipine are capable of increasing drug sensitivity in resistant murine and human tumor cells. This finding has potential value in the treatment of acquired drug resistance in human malignancies. Thus, we tested the ability of CCBs of two different structural classes to enhance the toxicity of doxorubicin (DOX), vinblastine (VBL), and vincristine (VCR) for normal myeloid and macrophage colony formation (marrow colony forming units-granulocyte-monocyte [CFU-GM]). Drug effects on colony formation from 35 normal volunteer marrows and from

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