Gene therapy shrinks melanoma tumors



(MCT)

NEW YORK - Doctors wiped out melanoma by reengineering patients' own cells, marking the first time gene therapy has worked successfully against a cancer and raising hopes that the treatment can eradicate other forms of the disease.

Government scientists took healthy immune cells from patients with advanced forms of the skin cancer and taught the cells to recognize and destroy the cancer cells. Doctors then fed patients the tailor-made fighter cells intravenously, and their tumors gradually shrank.

Just two of the 17 patients in the study are still disease-free a year and a half after the treatment. But doctors said the research proved that the technique could help patients battling many forms of cancer.

"We can now convert normal lymphocytes into cells that can recognize very common cancers like breast, lung, ovary, prostate and so on. We haven't treated those patients yet, but this represents proof that this kind of approach can work," said study author Dr. Steven Rosenberg, chief of surgery at the National Cancer Institute.

The other 15 patients in the study, published in Friday's issue of the journal Science, grew low levels of the reengineered immune cells for at least two months. Since the trial began in December 2004, scientists have developed more advanced gene therapy techniques that could improve the results, Rosenberg said.

"It is totally intriguing," said Dr. Anna Pavlick, director of the NYU Cancer Institute's melanoma program.

But it's too soon to call the therapy a cure, she said.

"They didn't look at survival and they wouldn't be able to in this small group of patients. That's why it's a little bit premature to know how effective this is going to be, but nonetheless it is a treatment that needs to be studied in a larger number of patients," said Dr. Howard Kaufman, director of the tumor immunotherapy program at New York Presbyterian Hospital Columbia.

Melanoma is one of the deadliest and fastest-growing cancers in the United States. An estimated 62,190 people will develop the disease this year, and 7,910 will die of it, according to the American Cancer Society.

---

http://www.duluthsuperior.com/mld/duluthsuperior/news/nation/15414535.htm

Okay thanks.

Article Preview
Researchers' data from the United Kingdom, Germany and United States advance cancer treatment research

Vaccine Weekly - Sep. 13, 2006
2006 SEP 13 - (NewsRx.com) -- Data on cancer treatment are outlined in reports from the United Kingdom, Germany and United States.

Study 1: A new anticancer glycolipid monoclonal antibody, SC104, directly induces tumor cell apoptosis.

According to recent research from England, "A novel monoclonal antibody was raised by immunization of mice with colorectal tumor cell lines. The fusion was screened by immunohistochemistry for binding to primary colorectal tumors. Subsequent analysis on primary disaggregated colorectal tumors show that the antibody recognizes a cell surface antigen expressed by the majority of colorectal tumors."

"Antigen characterization has shown that the antibody ...

http://www.therapeuticsdaily.com/news/article.cfm?contentValue=1078531&contentType=sentryarticle&channelID=28


EIRX THERAPEUTICS PLC ("EIRX")

POTENTIAL NEW THERAPIES FOR COLORECTAL & OTHER CANCERS


Cork, Ireland, 10th January, 2006 EiRx Therapeutics plc (AIM: ERX), the drug discovery company developing targeted therapies for cancer, is pleased to announce the filing of patent applications describing a novel class of drug candidates with potential value as treatments for a range of cancers including colorectal and breast tumours. This class of molecule is structurally dissimilar to the class of molecules for which patent applications were made in August 2005, thus ensuring a deeper pipeline of development for the treatment of colorectal and breast cancer.

Exploiting the insight afforded to them through their ALIBITM genomics platform, EiRx scientists developed EnPADTM technology to target APC-b-catenin signalling, a cellular control pathway known to play a major role in the majority of cases of colorectal cancer, as well as in several other tumour types. A custom-designed EnPADTM cell line was used to screen a focused library of drug-like, kinase inhibitor compounds, resulting in the discovery of a series of related compounds with selective activity against transformed cell types including colorectal and breast cancer cell lines. The EnPADTM technology development programme was funded in part by the Marie Curie Transfer Of Knowledge grant.

Commenting on the discovery, EiRxs Chief Scientific Officer Prof Tom Cotter said: The company's EnPADTM technology has again proven its ability to identify novel classes of molecules with selective biological activity. The class of molecules filed in the current patent applications are structurally quite different to those that were the subject of the earlier patent applications in August 2005. As a result we are in the enviable position of moving two chemical scaffolds through preclinical with the potential to treat these socio-economically important diseases.

EiRx Chairman John Pool said: Not only does filing a second class of molecule with activity against colorectal and breast cancer endorse our EnPADTM approach in drug discovery; it also demonstrates that EiRx has set its sights firmly on the identification and development of novel molecules to treat cancer. Having two series of molecules in preclinical development, both with the potential to treat colorectal and breast cancer, demonstrates that EiRx has the potential to rapidly become a key player in these very considerable therapeutic markets.

expect news this week, big news!!!

colon cancer

Protein May Help Targeting for Anti-Tumor Drugs
21:35:11 EDT Oct 12, 2006
Canadian Press
THURSDAY, Oct. 12 (HealthDay News) - A protein that may help in the development of new anti-tumor drugs has been identified by Mayo Clinic researchers.

The protein - cyclin-dependent kinase 2 (CDK2) - acts as a "quality control inspector" during cell division, and also directs cell death for cells that are damaged during division.

Normal cells pause during the division process if they detect an inaccurate genetic code embedded in their DNA. If possible, repairs are made to those mistakes.

When those genetic code errors are irreparable, CDK2 modifies another cellular protein called FOX01 to send a signal that causes the damaged cell to die, the study found.

"Quality control within dividing cells is essential because mistakes during duplication of the genetic code can lead to cancer. CDK2 is a key protein component in the cellular mechanism that leads to repair of damaged DNA," Donald Tindall, co-leader of the Mayo Clinic Cancer Center prostate cancer research program, said in a prepared statement.

This finding offers scientists a potential "bulls eye" for targeting anti-tumor drugs.

The study was published in the current issue of Science.

MGI are being chased by ERX for mileston payment according to company, MGI pharma report results on wednesday.. expect great news!!!

potatohead - 13 Oct 2006 11:51 - 205 of 205
Pharmaceutical Feature: Cdk5 inhibitors as novel candidate ...Hawkings, EF Medical, EiRx Therapeutics Ltd, Elan IT, Eli Lilly ... Cdk5 differs from other members of the Cdk family being modulated by its activator, p35. ...

http://www.google.co.uk/search?hl=en&ned=uk&ie=UTF-8&q=CDK2+eirx&sa=N&tab=nw