Prognostic significance of cachexia score assessed by CT in male patients with small cell lung cancer.

To determine the prognostic significance of CT-determined cachexia scores (CSs) in 127 consecutive male small cell lung cancer (SCLC) patients, cross-sectional areas of muscle and fat tissues at the third lumbar vertebra (L3) were retrospectively measured on baseline CT images. CSs were determined based on the presence of sarcopenia and/or adipopenia. According to the presence of sarcopenia (L3 muscle index <55 cm2 /m2 , 86.8%) and adipopenia (L3 fat index <22 cm2 /m2 , 11.8%), CSs were defined as follows: CS2 (sarcopenia and adipopenia, 11.8%), CS1 (sarcopenia only, 74.8%) and CS0 (13.4%). CS2 was significantly related to lower body mass index (p < .001) and poor performance status (p = .002), and patients with CS2 had shorter OS than patients with CS1 or CS0 (median OS, 5.0 months vs. 8.9 months vs. 18.3 months; p = .007). Multivariable analysis revealed that CS was an independent prognostic factor of poor survival (HR, 1.99 for CS1 and 2.59 for CS2, p = .036 and .023, CS0 as a reference), along with extensive stage (p < .001), supportive care only (p < .001) and an elevated lactate dehydrogenase (p = .005). CT-determined CSs, based on the presence of sarcopenia and/or adipopenia, could be used to predict prognosis in male SCLC.

Indole-3-carbinol enhances ultraviolet B-induced apoptosis by sensitizing human melanoma cells.

Indole-3-carbinol (I3C) has been found to act against several types of cancer, while ultraviolet B (UVB) is known to induce the apoptosis of human melanoma cells. Here, we investigated whether I3C can sensitize G361 human melanoma cells to UVB-induced apoptosis. We examined the effects of combined I3C and UVB (I3C/UVB) at various dosages. I3C (200 microM)/UVB (50 mJ/cm(2)) synergistically reduced melanoma cell viability, whereas I3C (200 microM) or UVB (50 mJ/cm(2)), separately, had little effect on cell viability. DNA fragmentation assays indicated that I3C/UVB induced apoptosis. Further results show that I3C/UVB activates caspase-8, -3, and Bid and causes the cleavage of poly(ADP-ribose) polymerase. Moreover, I3C decreased the expression of the anti-apoptotic protein, Bcl-2, whereas UVB increased the translocation of Bax to mitochondria. Thus, an increased Bax/Bcl-2 ratio by I3C/UVB may result in melanoma apoptosis. In conclusion, our study demonstrated that I3C sensitizes human melanoma cells by down-regulating Bcl-2.

Sonography of the stomach: an in vitro study to determine the anatomic cause of inner hyperechoic and hypoechoic layers of the gastric wall.

OBJECTIVE: Sonography of the normal gastric wall delineates five distinct layers: from the luminal side, a first, inner hyperechoic layer; a second, hypoechoic layer; a third, middle hyperechoic layer; a fourth, hypoechoic layer; and a final, outer hyperechoic layer. The anatomic origin of the inner two sonographic layers has been a matter of controversy. To verify the histologic origin of the inner two sonographic layers, we attempted to correlate sonographic and histologic layers of resected gastric specimens. Because we hypothesized that the fluid covering the mucosa and the mucosa may be responsible for the sonographic inner two layers of the stomach, we selected specimens in which the mucosa was sloughed or thickened. MATERIALS AND METHODS: We selected five resected gastric specimens with ulcerative carcinoma in which the mucosa was totally sloughed, one specimen with a mucosal polyp, and two specimens with a polypoid lesion and partial surface ulceration. The gastric specimens were immersed in normal saline and examined with 5-MHz high-resolution sonographic equipment. Sonographic findings were correlated with gross and microscopic pathologic findings. Two phantoms were immersed in normal saline and examined with the same technique to evaluate the thickness of the sonographic interface between water and phantoms. RESULTS: The inner hyperechoic layer was constant in thickness, measuring 1 mm, and covered the surface of the normal areas and the areas where the mucosa was lost or thickened. The hypoechoic layer underlying the hyperechoic layer was obliterated where the mucosa was defective and thickened where the mucosa was thickened. The sonographic interface between water and phantoms was 1 mm thick. CONCLUSION: Our results show that the inner hyperechoic layer of the stomach seen on sonograms is due to echoes arising from the interface between fluid in the gastric lumen and the mucosal surface. The underlying hypoechoic layer is caused by the mucosa itself.