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Antineoplastic Therapy (antineoplastic + therapy)
Selected AbstractsChronic Pain in the Cancer Survivor: A New FrontierPAIN MEDICINE, Issue 2 2007Allen W. Burton MD ABSTRACT Objective., This monograph is intended to clarify the clinical problem of chronic pain in cancer patients. Design., A pertinent literature review on chronic pain syndromes in cancer patients was undertaken using Medline. Further, the treatment strategies for cancer versus chronic pain are contrasted and clarified. Results., With increasing cancer survivorship come new challenges in patient care. In the United States, the cancer-related death rate has dropped by 1.1% per year from 1993,2002. Seventy-five percent of children and two out of three adults will survive cancer, whereas 50 years ago just one out of four survived. The net effect of these trends and opportunities is a large and rapidly growing population of persons living longer with cancer and/or as cancer survivors. While agreement exists on the best strategies for assessment and treatment of most acute cancer pain syndromes, little consensus exists on the treatment of chronic pain in the patient with slowly progressive cancer or the cancer survivor. Conclusions., The landscape of "cancer pain" is shifting quickly into a chronic pain situation in many instances, thereby blurring previous lines of distinction in treatment strategies most suited for "chronic" versus "malignant" pain. Adopting chronic pain treatment strategies including pharmacologic and other pain control techniques, rehabilitation care, and psychological coping strategies may lead to optimal outcomes. Lastly, as cancer evolves into a chronic illness, with co-morbid conditions, recurrent cancer, and treatment toxicities from repeated antineoplastic therapies, pain management challenges in the oncologic patient continue to increase in complexity. [source] The use of molecular markers of bone turnover in the management of patients with metastatic bone diseaseCLINICAL ENDOCRINOLOGY, Issue 6 2008Markus J. Seibel Summary Biochemical markers of bone turnover are widely used in clinical practice. These indices have been shown to be associated with the occurrence, prognosis and therapeutic response of malignant bone lesions. For example, markers of bone resorption are often elevated in patients with established bone metastases and while this may point to a role of these markers in the diagnostic workup of cancer patients, the available evidence does not permit any final conclusions as to the accuracy and validity of the presently used markers in the early diagnosis of bone metastases. Many bone turnover markers appear to respond to antiresorptive and antineoplastic therapies, and recent evidence from prospective trials suggests that the aim of bisphosphonate therapy should be to normalize rates of bone remodelling to optimize therapeutic and prognostic outcomes. However, it remains unknown whether the use of bone markers in the routine clinical setting has any defined beneficial effects on overall outcome in cancer patients. Clearly, bone turnover markers have insufficient diagnostic or prognostic value to be used in isolation; however, the combination of these markers with other diagnostic techniques may improve clinical assessment of patients with bone-seeking cancers. This article reviews the available evidence (as of August 2007) on the clinical use of bone turnover markers in the management of patients with metastatic bone disease. [source] Silencing MAT2A gene by RNA interference inhibited cell growth and induced apoptosis in human hepatoma cellsHEPATOLOGY RESEARCH, Issue 5 2007Quanyan Liu Aims:, A switch in gene expression from MAT1A to MAT2A was found in liver cancer, suggesting that MAT2A plays an important role in facilitating cancer growth. MAT2A is an interesting target for antineoplastic therapy. The molecular mechanisms of silencing MAT2A by RNA interference inhibited cell growth and induced apoptosis in hepatoma cells was studied. Methods:, We investigated the effects of MAT2A on S-adenosyl-methionine (SAM) production, cell growth and apoptotic cell death in hepatoma cell lines (Bel-7402, HepG2, and Hep3B) using an RNA interference approach. Results:, The treatment of three hepatoma cell lines with small interfering RNA (siRNA) targeting to the MAT2A gene resulted in reducing the MAT II activity, facilitating SAM production, increasing SAM : SAH ratio, inhibiting cell growth and inducing cell apoptosis in hepatoma cells. In addition, silencing MAT2A gene resulted in the stimulation of MAT1A mRNA production, which was blocked by 3-deazaadenosine and l -ethionine, but not d -ethionine, suggesting that such effect was specific and mediated by upregulation of SAM level and SAM : S-adenosylethionine (SAH) ratio. Conclusion:, Silencing MAT2A by sequence-specific small interfering RNA caused a switch of MAT gene expression from MAT2A to MAT1A, which led the content of SAM to change to a higher steady-state level that resulted in the inhibition of cell growth and the induction of apoptotic cell death in human hepatoma cells. These results also suggested that MAT2A may hold potential as a new target for liver cancer gene therapy. [source] Etiology and outcome of extreme leukocytosis in 758 nonhematologic cancer patientsCANCER, Issue 17 2009A retrospective, single-institution study Abstract BACKGROUND: To the authors' knowledge, the literature regarding extreme leukocytosis in solid tumor patients is sparse, consisting of a few case reports and small case series. METHODS: A total of 3770 consecutive solid tumor patients with a white blood cell count>40,000/,L were retrospectively identified over a 3-year period (2005-2008). Those patients without a secondary cause of their leukocytosis were defined as having a paraneoplastic leukemoid reaction. RESULTS: A total of 758 (20%) patients with solid tumors and extreme leukocytosis were identified. The etiology of the leukocytosis was hematopoietic growth factors in 522 (69%) patients, infection in 112 (15%) patients, high-dose corticosteroids in 38 (5%) patients, newly diagnosed leukemia in 9 (1%) patients, and paraneoplastic leukemoid reaction in 77 (10%) patients. The patients diagnosed with a paraneoplastic leukemoid reaction typically had neutrophil predominance (96%) and radiographic evidence of metastatic disease (78%), were clinically stable, and had a poor prognosis; 78% either died or were discharged to hospice within 12 weeks of their initial extreme leukocyte count. All of the 8 (10%) patients who survived>1 year received effective antineoplastic therapy. CONCLUSIONS: Infection was an uncommon cause of extreme leukocytosis in patients with solid tumors. Patients with paraneoplastic leukemoid reactions typically were clinically stable despite having large tumor burdens. However, clinical outcomes were poor unless effective antineoplastic treatment was received. Cancer 2009. © 2009 American Cancer Society. [source] Zoledronic acid delays the onset of skeletal-related events and progression of skeletal disease in patients with advanced renal cell carcinomaCANCER, Issue 5 2003Allan Lipton M.D. Abstract BACKGROUND The objective of this study was to assess the efficacy and safety of zoledronic acid in patients with bone metastases secondary to renal cell carcinoma (RCC). METHODS A retrospective subset analysis of patients with RCC enrolled in a multicenter, randomized, placebo-controlled study of zoledronic acid was performed. Patients were randomized to receive zoledronic acid (4 or 8 mg as a 15-minute infusion) or placebo with concomitant antineoplastic therapy every 3 weeks for 9 months. The primary efficacy analysis was the proportion of patients with one or more skeletal-related events (SREs), which were defined as pathologic fracture, spinal cord compression, radiation therapy, or surgery to bone. Secondary analyses included time to first SRE, skeletal morbidity rate (events per year), disease progression, and multiple event analysis. RESULTS In this subset of 74 patients with RCC, zoledronic acid (4 mg) was found to significantly reduce the proportion of patients with an SRE (37% vs. 74% for placebo; P = 0.015). Similarly, zoledronic acid significantly reduced the mean skeletal morbidity rate (2.68 vs. 3.38 for placebo; P = 0.014) and extended the time to the first event (median not reached vs. 72 days for placebo; P = 0.006). A multiple event analysis demonstrated that the risk of developing an SRE was reduced by 61% compared with placebo (hazard ratio of 0.394; P = 0.008). The median time to progression of bone lesions was significantly longer for patients who were treated with zoledronic acid (P = 0.014 vs. placebo). Zoledronic acid appeared to be well tolerated; the most common adverse events in all treatment groups included bone pain, nausea, anemia, and emesis. CONCLUSIONS Zoledronic acid (4 mg as a 15-minute infusion) demonstrated significant clinical benefit in patients with bone metastases from RCC, suggesting that further investigation of zoledronic acid in this patient population is warranted. Cancer 2003;98:962,9. © 2003 American Cancer Society. DOI 10.1002/cncr.11571 [source] | ||||||||||