Carboplatin shares some of the therapeutic advantages of cisplatin, but without a significant incidence of the dose-limiting neurotoxicity and nephrotoxicity which is experienced with cisplatin. However, its use is associated with dose-limiting bone marrow suppression.

Clinical pharmacokinetics and dose optimisation of carboplatin

Cancer is a disorder that rigorously affects the human population worldwide. There is a steady demand for new remedies to both treat and prevent this life-threatening sickness due to toxicities, drug resistance and therapeutic failures in current conventional therapies. Researchers around the world are drawing their attention towards compounds of natural origin. For decades, human beings have been using the flora of the world as a source of cancer chemotherapeutic agents. Currently, clinically approved anticancer compounds are vincristine, vinblastine, taxanes, and podophyllotoxin, all of which come from natural sources. With the triumph of these compounds that have been developed into staple drug products for most cancer therapies, new technologies are now appearing to search for novel biomolecules with anticancer activities. Ellipticine, camptothecin, combretastatin, curcumin, homoharringtonine and others are plant derived bioactive phytocompounds with potential anticancer properties. Researchers have improved the field further through the use of advanced analytical chemistry and computational tools of analysis. The investigation of new strategies for administration such as nanotechnology may enable the development of the phytocompounds as drug products. These technologies have enhanced the anticancer potential of plant-derived drugs with the aim of site-directed drug delivery, enhanced bioavailability, and reduced toxicity. This review discusses mechanistic insights into anticancer compounds of natural origins and their structural activity relationships that make them targets for anticancer treatments.

/pdf/a-review-on-mechanistic-insight-of-plant-derived-anticancer-2rrctczq.pdf

A Review on Mechanistic Insight of Plant Derived Anticancer Bioactive Phytocompounds and Their Structure Activity Relationship

This study characterized a panel of NSCLC cell lines as well as a stably transfected cell model expressing wild-type and mutated EGFR variants in terms of response to the EGFR-targeting drugs, gefitinib and cetuximab The examinations support the notion that response to gefitinib is neither exclusive nor strictly determined by the presence of EGFR kinase mutations Yet, cells expressing EGFR kinase domain mutations tended to generally respond better to treatments with gefitinib compared to those with wild-type EGFR On the other hand, preliminary studies suggesting that cellular sensitivity to cetuximab is determined by factors other than EGFR kinase domain mutations could be substantiated through a robust set of data Moreover, several promising candidate genes differentially expressed in gefitinib sensitive and resistant NSCLC cell lines were revealed by a global mRNA expression analyses In addition, though statistically questionable, several biologically interesting genes that are possibly involved in determining in vitro response of NSCLC cells to cetuximab have been postulated In this work, four cancer cell models, which are long-term exposed to gefitinib or cetuximab were established and characterized in terms of gain-of-resistance towards EGFR-targeting compounds, as well as in regard to biological and molecular alterations caused by long-term treatments It was found that gefitinib long-term treatment of primary sensitive A431 cells confered growth-resistance to this TKI, but not to cetuximab This observation may have clinical implications for patients that relapsed on gefitinib as it suggests that they might still profit from cetuximab therapy On the other hand long-term exposure of A431 cells to cetuximab did not render cells resistant to neither the antibody nor gefitinib in regard to in vitro growth-inhibition Furthermore, it appeared that long-term gefitinib-treated A431 cells downregulate overall EGFR levels, while long-term cetuximab exposed cells displayed decreased EGFR surface levels but constant overall expression In addition, a candidate-based approach identified genes that are differentially expressed in cancer cells with primary or secondary resistance to gefitinib or cetuximab Finally, this study for the first time provided evidence that cetuximab may block metastasis-facilitating epithelial-mesenchymal-transition (EMT) in an epithelial cell line Moreover, it was suggested that activation of the HGFR may compensate for cetuximab-mediated blockage of EGFR This was also reflected by an increased response of this population towards treatment with HGFR inhibitors

Molecular analyses of resistance and sensitivity mechanisms to anti-EGFR directed tumor therapy

A phase II trial aiming to verify the effectiveness of a regimen including carboplatin and vindesine was performed. From November 1989 to September 1990, nineteen patients with advanced small cell lung cancer entered this study. Polychemotherapy treatment included: carboplatin 400 mg/sm, on day 1 and vindesine 3 mg/sm, on days 1 and 15, repeated every 4 weeks, as an outpatient regimen. Observed toxicity was mild; myelodepression, and nausea and vomiting were the main adverse events. No objective response was obtained; 14 no changes in the disease and 4 progressions were detected. The low objective response rate observed in this study is strongly influenced by a set of unfavourable prognostic factors. The median overall survival time [32 weeks] is comparable with the results of other studies.

Non small cell lung cancer treatment with carboplatin and vindesine: a phase II study.

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Non small cell lung cancer treatment with carboplatin and vindesine: a phase II study.