哇,与路透社(Reuters)的新闻擦肩而过

留住孩子们成长的快乐时光。
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研究经费的多少是美国政府的财政状况的晴雨表。去年因大学老板没有拿到研究经费,俺不得不为生计而放弃了十多年的研究,去一家公司为五斗米折腰。(见“十二年的“博士后”终于走到了尽头”)

人走了,但茶还是没有凉。除了把工作移交给学生,还在周末抽点时间去帮老板解决一些学生面临的实际问题。半年后,终于把数据整理完毕,加上学生后面的一些数据,写成文章,匆忙送到了一家一般化的杂志,就是想赶快发表,让老板有机会拿到NIH的研究经费。俺人走了,开年会的机会也只好让给学生了。

“有意栽花花不发,无意插柳柳成荫”。本来以为一本普通的杂志,不会引起同行的多少兴趣。却没想文章先是入选Faculty of 1000 Biology,而送到美国内分泌协会年会的文章也被挑出来,作Press release。前两天见到大学的老板,他乐呵呵的:“Have you seen the news about your paper? I am still writing grant. However, the Endocrine Society gave me some money for one year. So I am not going to be bankruptted for now......”

在美国作了十多年研究,这也算是一种回报吧。今天把新闻给女儿看,女儿还是替老爸骄傲一把,让穷酸书生的老爸多少有些安慰。只是路透社的新闻却没有老爸的名字。:(。

 

New inhibitors of breast cancer cells identified

By Megan Rauscher/> Wednesday, Jun. 18, 2008; 3:33 AM

NEW YORK (Reuters Health) - A team of U.S. scientists has identified a new family of compounds that block the ability of estrogen to stimulate the growth of breast cancer cells.

"The lead inhibitor is quite effective in breast cancer cells that are resistant to tamoxifen," Dr. David J. Shapiro noted at the Endocrine Society's annual meeting underway in San Francisco.

"We are hopeful that as we proceed with further development that these compounds may ultimately lead to therapeutics that are clinically useful against some breast cancers that are resistant to current therapies," added Shapiro, a biochemist at the University of Illinois at Urbana-Champaign.

Currently available treatment for breast cancer driven by estrogen either interfere with estrogen production (e.g., aromatase inhibitors such as letrozole) or block estrogen's ability to bind to estrogen receptors on breast cancer cells (e.g., tamoxifen).

"We targeted a different step in the pathway of estrogen action," Shapiro said, "one that is not targeted by current therapeutics" -- namely, the expression of genes within cell that are controlled by estrogen receptor activity and that contribute to cancer growth.

The researchers found that a compound called TPBM blocked the estrogen-dependent growth of human breast cancer cells that carried estrogen receptors -- even cells resistant to tamoxifen treatment. If cells did not carry estrogen receptors (i.e., ER negative), they were not affected.

"Even at very high concentrations, TPBM has no effect on ER-negative cells, so it is not toxic to these cells at all," Shapiro said. "This gives us a lot of confidence as we go to animal studies that TPBM will not damage human cells."

He noted that while tamoxifen therapy is effective initially, "in essentially all patients, the tumors eventually become resistant to tamoxifen and resume their growth." This fact "underscores the importance of identifying new classes of therapeutic agents that will act outside of the hormone-binding pocket on the estrogen receptor."

 

(7/2/2008)

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