China
Africa
Explore chapters and articles related to this topic
A Pharmacological Appraisal of Antimalarial Plant Species
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Mahwahwatse J. Bapela, Precious B. Ramontja, Mcebisi J. Mabuza
Recrudescent infections as a result of resistant strains of the parasite tend to have higher gametocyte carriage rates, with higher infectivity, than primary infections. Gametocytes are therefore an important mechanism for resistance and drugs that could block transmission by eliminating the gametocytes are much needed to counteract resistance (Richter et al., 2016). Antimalarial drug resistance is complicated by cross-resistance, which mostly occurs among groups of drugs that belong to a similar chemical family or which have the same mode of action. Furthermore, multiple drug resistance of P. falciparum has been observed when the parasite is resistant to more than two operating antimalarial compounds of different chemical classes and mechanisms of action (Sinha et al., 2014). The prevalence of resistance to the well-established antimalarial drugs has resulted in the expansion of antimalarial drug discovery efforts.
Total Body Irradiation
Published in W. P. M. Mayles, A. E. Nahum, J.-C. Rosenwald, Handbook of Radiotherapy Physics, 2021
The American College of Radiology/American Society for Radiation Oncology (ACR-ASTRO) Practice Parameter (ACR 2017) identifies a number of advantages of TBI as part of conditioning for bone marrow transplants: A homogeneous dose is delivered to the whole body (with the option to spare particular organs as required) independently of the blood supply to a particular area. In consequence, there are no sanctuary sites.The dose can be precisely controlled and is not subject to physiological influences.There is less likelihood of cross-resistance with other chemotherapeutic agents.
Clinical Implications of the Phenomenon of Drug Resistance
Published in Nicholas Bruchovsky, James H. Goldie, Drug and Hormone Resistance in Neoplasia, 2019
Providing one keeps in mind what the objectives are in combination chemotherapy, it should be possible to design appropriate and rational drug treatment sequences whose exact form will be dictated by the number and variety of agents available. Because it appears that the requirement for complete lack of cross-resistance can be significantly relaxed, then protocol design which involves the retention of the most active of a series of agents in each treatment block is entirely feasible. Likewise there need be no concern about the continuous application of essentially nontoxic agents such as steroid hormones to the chemotherapy. Although contributing to “cross-resistance”, the quantitative effect of these additional agents will more than counterbalance this effect.
Emerging peptide therapeutics for the treatment of ovarian cancer
Published in Expert Opinion on Emerging Drugs, 2023
Ana C. Veneziani, Eduardo Gonzalez-Ochoa, Amit M. Oza
Primary or acquired treatment resistance has been a major clinical challenge, and subsequent treatment options are limited, leading to broad cross-resistance. For example, in platinum-resistant EOC, response rates to single-agent chemotherapy are as low as 10–15%, and median overall survival (OS) is estimated at only 12 months [8]. Hence, there is an urgent need to identify novel therapeutic approaches, which may be effective in this setting for EOC. Proteomic technologies, such as mass spectrometry and protein array analysis, have significantly advanced our ability to understand molecular signaling events and proteomic profiles [23]. Proteomic analysis of ovarian cancer and its adaptive responses to therapy can reveal new therapeutic options that have the potential to mitigate drug resistance and improve patient outcomes.
Understanding drug resistance mechanisms in cholangiocarcinoma: assisting the clinical development of investigational drugs
Published in Expert Opinion on Investigational Drugs, 2021
Jose JG Marin, Rocio IR Macias
The marked heterogeneity of CCA [4] contributes to the difficulty of understanding the failure of treating these patients with anticancer agents. The reasons why some characteristics allow CCA cells to survive by escaping the cytotoxic effect of drugs, as well as the identification and subsequent attack by immune cells, are relevant, but still unanswered questions with critical clinical impact. Thus, tumor growth that occurs after an initial response to the treatment may be due to small subpopulations of cells (minimal residual disease) that overcome the pharmacological pressure and proliferate when the predominant population of cancer cells has been destroyed. Tumor heterogeneity is therefore associated with the so-called primary or intrinsic pharmacological resistance, which can become more complex during therapy because some tumor cells that are initially sensitive to drugs can rapidly develop secondary or acquired resistance due to either changes in the expression of certain proteins or to the generation of mutations that permit them to resist the effect of anticancer drugs. Moreover, these changes may also be effective against other drugs that share completely, partially, or not at all their mechanisms of action (cross-resistance). The situation becomes critical because the toxicity caused by the administration of antitumor drugs often leads to limiting the dose or discontinuing the treatment for a period of time in some patients, which may favor tumor growth and the development of more effective MPRs.
Mechanisms of antimicrobial resistance in Stenotrophomonas maltophilia: a review of current knowledge
Published in Expert Review of Anti-infective Therapy, 2020
Teresa Gil-Gil, José Luis Martínez, Paula Blanco
One important element to be taken into consideration is the fact that mutation-driven resistance to one antibiotic can result in cross-resistance to other drugs. This feature seems to be particularly relevant in the case of S. maltophilia because a single mutation, leading to the overexpression of an efflux pump can confer simultaneously resistance to several of the antibiotics of choice for treating S. maltophilia infections. When co-trimoxazole resistance is due to the acquisition of resistance genes, the introduction of a second antibiotic (a quinolone or a beta-lactam) is not necessarily problematic. However, the situation is not the same when resistance is due to the over-expression of an efflux pump. It is relevant to remark that S. maltophilia is the only known bacteria in which high-level quinolone resistance is due to the overexpression of MDR efflux pumps [54,83,84,127,128], mainly SmeDEF and, in occasions, SmeVWX [51,81,127]. Notably, these efflux systems can extrude quinolones, co-trimoxazole, and tigecycline, meaning that selection of a resistant mutant by one of these antibiotics, will produce resistance to all of them [52,86].