Search PubMedSearch

PubMed · 3109538

The flow cytometer.

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A H Wyllie. 1987-01-17. The flow cytometer.. https://doi.org/10.1136/bmj.294.6565.139

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Human lung carcinomas express Fas ligand.

To reach a clinically detectable size, neoplasms must be able to suppress or evade a host immune response. Activated T cells may enter apoptosis in the presence of Fas ligand (FasL) (1), and tissue expression of FasL has been shown to contribute to immune privilege in the eye and testis (2, 3). We have demonstrated that all human lung carcinoma cell lines tested (16 of 16) express a Mr 38,000 protein consistent with FasL by immunoblotting, whereas the majority of resected tumors (23 of 28) show positive staining for FasL by immunohistochemistry. DNA sequencing of reverse transcription-PCR products from lung cancer cells and resected lung tumors confirms the presence of human FasL mRNA in these neoplastic tissues. Furthermore, lung carcinoma cells are capable of killing a Fas-sensitive human T cell line (Jurkat) in coculture experiments; this killing was inhibited by a recombinant form of the soluble portion of the Fas receptor (FasFc). FasL expression by neoplastic cells represents a potential mechanism for peripheral deletion of tumor-reactive T-cell clones.

DNA, Neoplasm

GSTM1 gene polymorphism as a possible marker for susceptibility to head and neck cancers among Japanese smokers.

Increased risk of lung cancer has been reported in individuals with glutathione S-transferase M1 (GSTM1) gene deletion, with limited evidence for head and neck (HN) cancer. Here, we report the results of a case-control study in Japanese HN cancer patients (n = 158) and community controls (n = 174). GSTM1 null genotype (GSTM1(-)) was distributed more in smoker patients than in control subjects (56.7% vs. 48.5%) but not in non-smoker patients (48.3%). In smokers, GSTM1(-) was detected at increased frequency in non-larynx cancer (62.7%, odds ratio 1.77, 95% CI 1.04-3.01) but not in larynx cancer (48.1%). In larynx cancer GSTM1(-) was presented at higher frequency in patients < 60 years old than in those > or = 60 years old (78.6% vs. 36.8%). These findings suggest that the GSTM1 gene polymorphism potentially modifies the risk for HN cancer depending on smoking history, the region of cancer and age.

DNA, Neoplasm