RNA to downregulate Raf-1 protein levels. Thesecond is the use of chemical Raf inhibitors such asBAY 43-9006, which has entered Phase I trials afterencouraging preclinical results. The third approachis inactivation of MEK by Raf and PD184322 is adrug that does this effectively in preclinical[r]
sensitivity to the individual components of a treatment regimen once progressionoccurs, which may aid in reserving drugs for which there remains sensitivity for fur-ther use. Unlike the mutational mechanisms that underlie resistance with systemicchemotherapies, resistance to targeted agents probably[r]
9. Kalos M: An integrative paradigm to impart quality to correlative science.J Transl Med 2010, 8:26.10. Greenberg PD, Klarnet JP, Kern DE, Cheever MA: Therapy of disseminatedtumors by adoptive transfer of specifically immune T cells. Prog ExpTumor Res 1988, 32:104-127.11. Walter EA, Greenberg PD, G[r]
Histone deacetylase inhibitors (HDACi) exert multiple cytotoxic actions on cancer cells. Currently, different synthetic HDACi are in clinical use or clinical trials; nevertheless, since both pro-invasive and anti-invasive activities have been described, there is some controversy about the effect of[r]
Chapter 081. Principles of Cancer Treatment (Part 19) Solid Tumors Small-molecule epidermal growth factor (EGF) antagonists act at the ATP binding site of the EGF receptor tyrosine kinase. In early clinical trials, gefitinib showed evidence of responses in a small fraction of patients[r]
from pain, to preserve or regain function, and to enjoy life. The components of a patient's health status or quality of life can include bodily comfort, capacity for physical activity, personal and professional function, sexual function, cognitive function, and overall perception of health. Each of[r]
are those that result in the patient's death. Development of targeted agents should proceed quite differently. While Phase I–III trials are still conducted, molecular analysis of human tumors more precisely defines targets expressed in a patient's tumor and should allow patient selection to e[r]
years of the AIDS (acquired immune deficiencysyndrome) epidemic led to the creation of a newFDA category, treatment investigational new drug(treatment IND), that established new proceduresfor more rapid and flexib le drug approval.The pharmaceutical company Burroughs We ll-come first presented AZT a[r]
It is natural to want to answer more than one question in a clinical trial. But one needs tobe clear which questions are secondary ones, and they need to be distinguished from theprimary question. eir results, whether positive or negative, need to be equally interpretedmore cautiously than i[r]
and nabilone (Cesamet) are usually innocuous when administered as antiemetics to patients with cancer10,82.Moreover,tolerance to the unwanted effects of cannabinoids develops rapidly in humans and laboratory animals81,82.For example,the most frequently reported adverse psychoactive effects of dronab[r]
To improve treatment outcome in patients with esopha- geal cancer, novel strategies have been developed, espe- cially those that are molecularly targeted. Information on molecular characteristics may have novel therapeutic po- tential against esophageal cancer. Furthermore, their prog- nostic or pre[r]
designed, Friedberg et al [7] reported that pharmaceuticalindustry oncology drug company-sponsored trials wereless likely to report unfavorable qualitative conclusionsthan those studies sponsored by non-profit organizations(5% vs. 38%, p = 0.04). Marcia Angell has written exten-sively about t[r]
Immunotherapies have advanced the treatment of metastatic melanoma; however, they are associated with immune-related toxicities. Patients with pre-existing autoimmune comorbidities are commonly excluded from clinical trials investigating immunotherapies in metastatic melanoma.
Research and cancer care are closely intertwined; however, it is not clear whether physicians and nurses believe that clinical trials offer the best treatment for patients and, if so, whether this belief is justified.
identification of several low-molecular-weight compounds that bind to the hydrophobic pockets of either Bcl-2 or Bcl-XL and block their ability to associate with death-inducing BH3-only proteins. These compounds inhibit the antiapoptotic activities of Bcl-2 and Bcl-XL at nanomolar concentrations and[r]
have cumulative effects; perhaps due to these cumulativeeffects, several sessions of NIBS are usually associated withgreater magnitude and duration of behavioural effects[129]. This has been also reported in clinical trials instroke patients, in which stimulation with rTMS for 10days c[r]
Repeated experience and familiarity with a wide variety ofphysiological measures such as blood pressure or forcedexpiratory volume, has allowed clinicians to make mean-ingful interpretation of the results. [9,10] In contrast, themeaning of a change in score of x points on a HRQoL in-strument is less[r]
a finding that suggests that genetic differences are not the primary reason for the disparity. The lowest-risk segment of the population in the Framingham Heart Study is sometimes cited to support the occasionally offered suggestion that only about half of the risk for coronary events results from k[r]