Neoadjuvant and concomitant chemotherapy and radiation therapy in patients with advanced head and neck carcinoma.

Unlabelled: Our study evaluated the effectiveness of neoadjuvant chemotherapy and concomitant chemotherapy with radiotherapy compared to standard surgery and radiation therapy in patients with resectable stage III/IV head and neck squamous cell carcinoma. Forty-two eligible patients received neoadjuvant chemotherapy (cisplatin 100 mg/m2 intravenously day 1, and 5-fluorouracil 1 g/m2 /day continuous infusion days 1-5 every 3 weeks for 3 courses) followed by radiotherapy (65-70 Gy in 32-39 fractions to the primary site and lymph nodes; 50 Gy in 25-28 fractions to areas at risk) and concomitant chemotherapy (cisplatin 80 mg/m 2 intravenously every 3 weeks starting on day 1 of radiotherapy). Neoadjuvant therapy induced grade 4 cytopenias (12/42 patients) and grade 4 gastrointestinal toxicities (7/42 patients).

Expression of vascular endothelial growth factor and HER2/neu in stage II colon cancer and correlation with survival.

Monoclonal antibody-directed therapy has been used as an effective treatment for some cancers that overexpress HER2/neu and vascular endothelial growth factor (VEGF). Overexpression of the HER2/neu oncogene and VEGF has been reported to occur in adenocarcinomas of the colon. Assessing whether HER2/neu and VEGF overexpression could serve as prognostic indicators for stage II colon cancer may provide insight into optimal treatment following surgery.

Hematopoietic protection by dexamethasone or granulocyte-macrophage colony-stimulating factor (GM-CSF) in patients treated with carboplatin and ifosfamide.

Based on preclinical studies, the authors undertook a pilot study to determine the hematologic and biologic effects of pretreatment with dexamethasone (Dex) or granulocyte-macrophage colony-stimulating factor (GM-CSF) in patients receiving carboplatin and ifosfamide. Patients (n = 28) with metastatic solid tumors were randomized to receive pretreatment with Dex or GM-CSF or no pretreatment prior to courses 1 or 2 of carboplatin and ifosfamide. No alteration in dose of chemotherapy was allowed between course 1 and 2.

Effects of endotoxin on proliferation of human hematopoietic cell precursors.

In examining the effects of corticosteroids on hematopoiesis in vitro, we observed that results were highly dependent on the lot of commercial fetal calf serum (FCS) utilized. We hypothesized that this variability correlated with the picogram (pg) level of endotoxin contaminating the FCS. Randomly obtained commercial lots of FCS contained 0.

Corticosteroids alter hematopoiesis in vitro by enhancing human monocyte secretion of granulocyte colony-stimulating factor.

The mechanism of corticosteroid alteration of hematopoiesis is not completely elucidated. Employing an endotoxin free system, we examined the mechanisms by which hydrocortisone succinate (HCS) enhanced human bone marrow (BM) colony forming unit granulocyte-macrophage (CFU-GM) proliferation. Interleukin-1beta (IL-1) (1 ng/mL), granulocyte-macrophage colony-stimulating factor (GM-CSF) (1 ng/mL), or the combination, induced minimal CFU-GM proliferation unless HCS was added to the cultures (10-25 vs.

Reduction in carboplatin hematopoietic toxicity in tumor bearing mice: comparative mechanisms and effects of interleukin-1 beta and corticosteroids.

Increasing clinical evidence suggests that treatment of certain cancers is more effective with high dose chemotherapy compared to standard dose chemotherapy. Efforts at reduction of high dose chemotherapy hematotoxicity have focused on post-chemotherapy administration of hematopoietic growth factors or stem cells. A pretreatment strategy to induce hematopoietic resistance has not been extensively examined experimentally or clinically.

Corticosteroid alteration of carboplatin-induced hematopoietic toxicity in a murine model.

Corticosteroids exhibit extensive hematopoietic effects both in vitro and in vivo. Some of the previously studied effects suggested that corticosteroids may alter hematopoietic toxicity of chemotherapeutic agents. In this study, we examined (1) the optimum dose and schedule of cortisone acetate (CA) to reduce hematopoietic toxicity of carboplatin (CB) and (2) possible mechanisms involved in this protective effect.

Corticosteroid modulation of interleukin-1 hematopoietic effects and toxicity in a murine system.

Interleukin-1 (IL-1) has been shown to ameliorate the hematopoietic toxicities of antitumor chemotherapeutic agents in both mice and humans. However, IL-1 toxicity in humans is considerable and is similar to the systemic inflammatory toxicities induced by IL-3, IL-6, and other cytokines with pleiotropic biologic activities, eg, fever, nausea, malaise, and hypotension. We hypothesized that corticosteroids may reduce IL-1 toxicity without reducing IL-1 hematopoietic effects in vivo.