Objective evaluation of nutritional status using the prognostic nutritional index during and after chemoradiotherapy in Japanese patients with head and neck cancer: a retrospective study.

Objectives: The incidence of severe mucosal damage due to low nutritional status is high in patients receiving concurrent chemoradiotherapy (CCRT) for head and neck cancer. Objective assessments do not exist for discharge criteria after completion of CCRT. Although the prognostic nutritional index (PNI) is an objective indicator of postoperative outcomes in patients undergoing cancer surgery, the prognostic impact of the PNI in patients with head and neck cancer receiving CCRT is unexplored.

[Three Cases of Augmented Chemotherapy-Induced Peripheral Neuropathy after Changing from mFOLFOX6 to FOLFIRI Therapy in Patients with Colorectal Cancer].

We had cases in which peripheral neuropathy was augmented after changing from mFOLFOX6, a chemotherapy for colorectal cancer, to FOLFIRI and comparatively examined disease status and trends. There were no shared points with respect to patient characteristics, timing of peripheral neuropathy augmentation, drug dosage, etc. It appeared that the change in chemotherapy itself had an effect on neuropathic symptoms.

Statins induce apoptosis through inhibition of Ras signaling pathways and enhancement of Bim and p27 expression in human hematopoietic tumor cells.

Recently, statins have been demonstrated to improve cancer-related mortality or prognosis in patients of various cancers. However, the details of the apoptosis-inducing mechanisms remain unknown. This study showed that the induction of apoptosis by statins in hematopoietic tumor cells is mediated by mitochondrial apoptotic signaling pathways, which are activated by the suppression of mevalonate or geranylgeranyl pyrophosphate biosynthesis.

The sensitivity of head and neck carcinoma cells to statins is related to the expression of their Ras expression status, and statin-induced apoptosis is mediated via suppression of the Ras/ERK and Ras/mTOR pathways.

Statins induce apoptosis of tumour cells by inhibiting the prenylation of small G-proteins. However, the details of the apoptosis-inducing mechanisms remain poorly understood. The present study showed that the induction of apoptosis by statins in four different human head and neck squamous cell carcinoma (HNSCC) cell lines, HSC-3, HEp-2, Ca9-22, and SAS cells was mediated by increased caspase-3 activity.

Statins improve survival by inhibiting spontaneous metastasis and tumor growth in a mouse melanoma model.

Metastatic melanoma is a life-threatening disease for which no effective treatment is currently available. In melanoma cells, Rho overexpression promotes invasion and metastasis. However, the effect of statins on spontaneous metastasis and tumor growth remains unclear.

Inhibition of the tumour necrosis factor-alpha autocrine loop enhances the sensitivity of multiple myeloma cells to anticancer drugs.

Several autocrine soluble factors, including macrophage inflammatory protein-1α and tumour necrosis factor-alpha (TNF-α), promote the survival and growth of multiple myeloma (MM) cells. We hypothesised that inhibition of the TNF-α autocrine loop may enhance the cytotoxic effect of anticancer drugs in MM cell lines. In the present study, a TNF-α-neutralizing antibody suppressed cell proliferation and enhanced the cytotoxic effect of anticancer drugs on MM cells.