The hallmarks of cancer.

抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Atherosclerosis, the principal cause of heart attack, stroke and gangrene of the extremities, is responsible for 50% of all mortality in the USA, Europe and Japan. The lesions result from an excessive, inflammatory-fibroproliferative response to various forms of insult to the endothelium and smooth muscle of the artery wall. A large number of growth factors, cytokines and vasoregulatory molecules participate in this process. Our ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.

The pathogenesis of atherosclerosis: a perspective for the 1990s

http://aiocm.org/member/Immunity,%20Inflammation,%20and%20Cancer.pdf

Immunity, Inflammation, and Cancer

The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms. Work over the past few years has led to the elucidation of a TGF-beta signal transduction network. This network involves receptor serine/threonine kinases at the cell surface and their substrates, the SMAD proteins, which move into the nucleus, where they activate target gene transcription in association with DNA-binding partners. Distinct repertoires of receptors, SMAD proteins, and DNA-binding partners seemingly underlie, in a cell-specific manner, the multifunctional nature of TGF-beta and related factors. Mutations in these pathways are the cause of various forms of human cancer and developmental disorders.

TGF-beta signal transduction.

Thirty-eight urinary bladders from Fischer rats were organ cultured for 7 days in Ham's Medium F12 with varying concentrations of hydrocortisone added. Measurements of cell numbers and relative areas of nuclei and cytoplasm (N/C ratios) were made with an automated image analyzer on 1.5-µm-thick plastic sections of the tissues. Epithelia cultured in the absence of hydrocortisone became hyperplastic and dysplastic and contained approximately 2.5 times as many cells per unit length as uncultured controls. N/C ratios were increased by over 50%, caused mainly by a decrease in the cytoplasmic area. Concentrations of hydrocortisone below 10-7 m had no significant effect on the hyperplasia or N/C ratios. Increasing concentrations above 10-7 m resulted in progressive decreases of both the number of cells per unit length and the N/C ratios. Epithelia cultured in 2 × 10-5 m hydrocortisone were not significantly different from uncultured controls.

N/C ratios from 85 fields with a wide range of values were quantitated both with the image analyzer and a manual point-counting technique. Linear regression analysis revealed a close linear relationship and a correlation coefficient of 0.922. The analyzer provided an efficient, accurate tool for quantitating morphological observations.

Michael B. Sporn

Papers

Quantitation with an Automated Image Analyzer of Nuclear-Cytoplasmic Changes Induced by Hydrocortisone in Bladder Epithelium

Agents for Chemoprevention and Their Mechanism of Action

Vitamin A and its analogs (retinoids) in cancer prevention.

Variables in the high-pressure cation-exchange chromatography of proteins.

Cytokine and Growth Factor Reviews to be published six times a year