Serum fucosylation changes in oral cancer and oral precancerous conditions: alpha-L-fucosidase as a marker.

Background: The objective of the current study was to investigate the clinical usefulness of serum fucose, fucosylated glycoproteins (fucoproteins), fucosyltransferase (FucT), and alpha-L-fucosidase in oral carcinoma.

Methods: Blood samples were collected from 130 patients with untreated oral cancer (OC), from 75 patients with oral precancerous conditions (OPC), and from 100 healthy controls. Cancer patients were followed after the initiation of anticancer treatments, and 75 follow-up samples were also collected.

TNF-alpha induction of GM2 expression on renal cell carcinomas promotes T cell dysfunction.

Previous studies from our laboratory demonstrated the role of tumor-derived gangliosides as important mediators of T cell apoptosis, and hence, as one mechanism by which tumors evade immune destruction. In this study, we report that TNF-alpha secreted by infiltrating inflammatory cells and/or genetically modified tumors augments tumor-associated GM2 levels, which leads to T cell death and immune dysfunction. The conversion of weakly apoptogenic renal cell carcinoma (RCC) clones to lines that can induce T cell death requires 3-5 days of TNF-alpha pretreatment, a time frame paralleling that needed for TNF-alpha to stimulate GM2 accumulation by SK-RC-45, SK-RC-54, and SK-RC-13.

Effect of renal cell carcinomas on the development of type 1 T-cell responses.

Purpose: We reported that in renal cell carcinoma patients with active disease, T-cell reactions to the tumor-associated antigens MAGE-6 and EphA2 are highly skewed toward TH2-type cytokine responses [interleukin (IL) 5]. Herein, we determined whether tumor-derived products, including gangliosides isolated from renal cell carcinoma patients, participate in the down-regulation of type 1 T-cell responses.

Experimental Design: T cells from healthy volunteers or renal cell carcinoma patients were cultured in the presence and absence of supernatants derived from renal cell carcinoma explants or with gangliosides isolated from those tumor supernatants.

Loss of expression of tropomyosin-1, a novel class II tumor suppressor that induces anoikis, in primary breast tumors.

Suppression of tropomyosins (TMs), a family of actin-binding, microfilament-associated proteins, is a prominent feature of many transformed cells. Yet it is unclear whether downregulation of TMs occur in human tumors. We have investigated the expression of tropomyosin-1 (TM1) in human breast carcinoma tissues by in situ hybridization and immunofluorescence.

A Study of Various Sociodemographic Factors and Plasma Vitamin Levels in Oral and Pharyngeal Cancer in Gujarat, India.

Present study examined various socio-demographic factors, dietary patterns, habit of tobacco consumption and plasma vitamin levels in 56 healthy individuals, 146 patients with oral precancerous conditions (OPC) and 132 untreated oral and pharyngeal cancer patients. The subjects were interviewed with a detailed health, habit and diet questionnaire. Plasma b-carotene, vitamin-A and vitamin-E levels were determined spectrophotometrically.

Vitamin B(12) and Folate Status in Head and Neck Cancer.

Deficiency of vitamin B(12) and folate is associated with causation of certain precancerous conditions and cancer. The present study was carried out on 56 controls, 167 patients with oral precancerous conditions (OPC) and 214 head and neck cancer patients, to evaluate the plasma vitamin B(12) and folate levels to determine their association with tobacco habits and vegetarianism and several sociodemographic factors. The subjects were interviewed using a health habit and diet questionnaire at the time of blood collection.

Suppression of the transformed phenotype of breast cancer by tropomyosin-1.

Changes in the expression of microfilament-associated proteins, such as tropomyosins (TMs), are commonly found in malignantly transformed cells. Previous work from this laboratory has shown that tropomyosin-1 (TM1) expression is consistently abolished in human breast carcinoma cell lines, suggesting that the loss of TM1 could be a common biochemical event in the transformation of mammary epithelium. To investigate whether changes in TM1 expression are causally linked to mammary carcinogenesis, we have tested the hypothesis that TM1 is a tumor suppressor of breast cancer.