Chemotherapy cisplatin

Megadosage vitamin B6 (pyridoxine) and cisplatin cause sensory neuronopathy. Pyridoxine toxicity, usually the result of inappropriate self-overmedication, kills dorsal root ganglion neurons. Affected individuals become severely ataxic because of loss of proprioceptive afferent input to the cerebellum. A similar syndrome is elicited by cisplatin chemotherapy. Neurotrophin-3 treatment is effective in protecting dorsal root ganglion neurons in experimental animals against these toxins [48,49]. 

Reed FP, Yuspa SH, Zwelhng LA, Ozols RF, Poirier MC. Quantitation of cisplatin-DNA intrastrand adducts in testicular and ovarian cancer patients receiving cisplatin chemotherapy. J Clin Invest 1986 77 545-550. 

Parker RJ, Gill I, Tarone R, et al. Platinum-DNA damage in leukocyte DNA of patients receiving carboplatin and cisplatin chemotherapy measured by atomic absorption spectrometry. Carcinogenesis 1991 12 1253-1258. 

Marcial VA, Paj ak TF, Mohuiddin M, et al. ConComitant cisplatin chemotherapy and radiotherapy in advanced mucosal squamous cell carcinoma of the head and neck. Cancer 1990 66 1861-1868. 

GOG-9804 Phase I/II Study of Extended Field Radiation Therapy With Concurrent Paclitaxel and Cisplatin Chemotherapy in Patients With Previously Untreated Carcinoma of the Cervix Metastatic to the Para-aortic Lymph Nodes. Study Protocol, http //www.cancer.gov/search/clinical trials... 

Shaw EG, McGinnis WL, Jett JR, et al. Pilot study of accelerated hyper-fractionated thoracic radiation therapy plus concomitant cisplatin chemotherapy in patients with unresectable stage M non small cell lung cancer. J Natl Cancer Inst 1993 85 321-323. 

In the 1980s numerous phase II pilot studies combining chemotherapy with radiation were conducted primarily using 5 -FU and cisplatin chemotherapy. In general, the median survival (12-20 mo) and 2-yr survival (35-40%) were improved over historical controls. Despite these encouraging results, randomized studies were needed to determine whether chemoradiation was superior to radiation alone. 

Martinez-Pineiro J, Martin MG, Arocena F, et al. Neoadjuvant cisplatin chemotherapy before radical cystectomy in invasive transitional cell carcinoma of the bladder a prospective randomized phase III study. J Urol 1995 153 964-973. 

Pearcey RG, Brandage MD, Drouin P, et al. Phase III trial comparing radical radiotherapy with and without cisplatin chemotherapy in patients with advance squamous cell cancer of the cervix. J Clin Oncol 2002 20 966-972. 

Tattersall MHN, Larvidhaya V, Vootiprux V, et al. Randomized trial of epirubicin and cisplatin chemotherapy followed by pelvic radiation in locally advanced cervical cancer. Am J Clin Oncol 1995 13 444-451. 

Sakamoto, K., Oka, M., Yoshino, S., hazama, S., Abe, T., Okayama, N. and Hinoda, Y. (2006) Relation between cytokine promoter gene polymorphism and toxicity of 5-fluorouracil plus cisplatin chemotherapy. Oncology Reports, 16, 381-387. 

Following construction, characterization, and scale-up of trastuzumab, phase I testing of the humanized mAh was carried out in patients with HER2-overexpressing metastatic breast cancer. The initial phase I study evaluated the safety and pharmacokinetics of a single, escalating (10-500 mg) intravenous dose of trastuzumab. A subsequent phase I study evaluated the safety and pharmacokinetics of multiple-dose administration, with weekly intravenous doses and similar dose escalation by cohort (10-500 mg). Both studies of 32 patients overall demonstrated that trastuzumab monotherapy was very well tolerated, with no serious adverse events attributable to mAh treatment. A third phase I study included trastuzumab, again via weekly intravenous administration of 10-500 mg, in combination with cisplatin chemotherapy at 50 or 100 mg/m2 per 4-week cycle. Toxicities in this trial were those commonly seen with cisplatin. 

As stated in a recent review [53], the development of efficient cisplatin chemotherapy has brought an unexpected challenge as many patients survive longer, they find themselves at risk of late complication in their anti-neoplasic therapy. Indeed, although unambiguous data on the capacity of cisplatin to induce secondary cancers in humans is still lacking, its carcinogenic properties in rats and mice has been reported [53] [54], Treatment-... 

Effectiveness of antiemetic activity of some drug combinations against emetic episodes in first 24 hours after cisplatin chemotherapy. 

De Wit R, Roberts )T, Wilkinson PM et al. (2001) Equivalence of three or four cycles of bleomycin, etoposide and cisplatin chemotherapy and of a 3- or 5-day schedule in good prognosis germ cell cancer a randomised study of the European Organization for Research and Treatment of Cancer Genitourinary Tract Cooperative Group and the Medical Research Council. Journal of Clinical Oncology 19 1629-1640. 

Chang, B. K., Guthrie, T. H., Hayakawa, K., and Gangerosa, L. P. A pilot study of iontophoretic cisplatin chemotherapy of basal and squamous cell carcinomas of the skin. Arch. Dermatol. 729 425, 1993. 

Conti JA, Scher HI. Acute arterial thrombosis after escalated-dose methotrexate, vinblastine, doxorubicin, and cisplatin chemotherapy with recombinant granulocyte colony-stimulating factor. A possible new recombinant granulocyte colony-stimulating factor toxicity. Cancer 1992 70(ll) 2699-702. 

Samuels BL, Vogelzang NJ, Kennedy BJ. Severe vascular toxicity associated with vinblastine, bleomycin, and cisplatin chemotherapy. Cancer Chemother Pharmacol 1987 19(3) 253-6. 

Rabinowits M, Souhami L, Gil RA, Andrade CA, Paiva HC. Increased pulmonary toxicity with bleomycin and cisplatin chemotherapy combinations. Am J Chn Oncol I990 I3(2) I32-8. 

Gonzalez C, Villasanta U. Life-threatening hypocalcemia and hypomagnesemia associated with cisplatin chemotherapy. Obstet Gynecol 1982 59(6) 732. ... 

Kahn CE Jr, Messersmith RN, Samuels BL. Brachial plexopathy as a complication of intraarterial cisplatin chemotherapy. Cardiovasc Intervent Radiol 1989 12(l) 47-9. 

Schilsky RL, Barlock A, Ozols RF. Persistent hypomagnesemia following cisplatin chemotherapy for testicular cancer. Cancer Treat Rep 1982 66(9) 1767-9. 

Schilsky RL, BarlockA,OzolsRF. Persistent hypomagnesemia following cisplatin chemotherapy fortesticular cancer. CancerTreat Reports 1982 66 1767-9. 

Indications Prevention of nausea and vomiting associated with cancer (cisplatin) chemotherapy ... 

Ross CJ, Ratzov-Eckert M, Dubey MP et al (2009) Genetic variants in TPMT and COMT are associated with hearing loss in children receiving cisplatin chemotherapy. Nat Genet 41 1345-1349... 

Wang, G. Reed, E. Li, Q. Q. Molecular basis of cellular response to cisplatin chemotherapy in non-smaU cell lung cancer [Review]. Oncol. Rep. 2004, 12, 955-965. 

ChevalUer B, Cappelaere P, Splinter T, et al. A double-blind, multicenter comparison of intravenous dolasetron mesylate and metoclopramide in the prevention of nausea and vomiting in cancer patients receiving high-dose cisplatin chemotherapy. Support Care Cancer 1997 5 22-30. 

The clinical use of cisplatin is limited by nephrotoxicity, characterized by a decline in glomerular filtration rate that is in proportion to the number of cycles of cisplatin chemotherapy. Progressive and persistent reductions in glomerular filtration rale and renal blood flow may follow each successive treatment cycle [17]. Renal plasma flow, whole kidney glomerular filtration rate, single nephron glomerular filtration rate, and stop-flow pressure are reduced compared to controls... 

From the animal screens emerged the set of structure-activity relationships enumerated earlier (Section IV.E.l). Both cisplatin and carboplatin conform to these rules, and to date no compounds with demonstrably better antitumor activity have been tested in humans. The decision to move an experimental drug into the clinic is a difficult one, however, and it may be that molecules such as cis-[Pt(NH3)2(4-Br-py)Cl]Cl (see Section V.D.V.c) would be effective for tumors that are refractive to cisplatin chemotherapy. In any case, the foregoing chain of events, from studying the effects of a compound on cells in culture through animal screens and eventually to humans, constitutes the principal route for introducing a new anticancer drug. The process can take more than a decade. 

---