According to results presented at the American Association for Cancer Research – National Cancer Institute – European Organization for Research and Treatment of Cancer Molecular Targets and Cancer Therapeutic Conference, the agent Telcyta™ (TLK286) plus Paraplatin® (carboplatin) produces significant responses in women with ovarian cancer that has stopped responding to platinum agents.
Ovarian cancer is a common malignancy occurring in women in the United States, with about 25,000 new cases diagnosed each year. More deaths are caused by ovarian cancer than any other cancer of the female reproductive system in the United States. The ovary makes female hormones and stores all the eggs that are released once a month during ovulation. There are two ovaries, one on each side of the uterus. Unfortunately, ovarian cancer does not produce clearly recognizable symptoms, if any, in early stages. Therefore, most cases of ovarian cancer are diagnosed at later stages, after the cancer has spread from its site of origin. Standard chemotherapy for the treatment of advanced ovarian cancers typically include a platinum compound, either Paraplatin® (carboplatin) or Platinol® (cisplatin). Once the cancer stops responding to or recurs following platinum-based therapy, it is referred to as platinum resistant or platinum refractory ovarian cancer. Treatment options are limited for patients with this stage of disease, with poor long-term survival.
Telcyta™ is an agent that is still in clinical trials, but is proving to be effective in various cancers. Telcyta™ is a molecule that is activated by an enzyme (protein and/or carbohydrate) called glutathione S-transferase P1-1 (GSTP1-1). GSTP1-1 is overexpressed in many cancer cells, but not in normal cells. In addition, overexpression of GSTP1-1 is associated with cells being resistant to anti-cancer effects of chemotherapy agents. When activated by GSTP1-1, Telcyta™ initiates processes in the cell that ultimately lead to cellular death. A benefit of this treatment approach is that Telcyta™ tends to target and kill only cancerous cells, resulting in minimal side effects.
Researchers recently conducted a clinical trial evaluating the addition of Telcyta™ to carboplatin in patients whose cancer stopped responding to previous platinum agents. Although patient enrollment for this trial is continuing, data analysis for 8 patients already treated with Telcyta™ on this trial has been reported. Treatment is given once a month. These patients had an average number of 3.5 previous therapies for ovarian cancer, including platinum-based chemotherapy. Following treatment with Telcyta™ and carboplatin, 7 of the 8 patients achieved a clinical benefit, with 1 patient achieving a complete disappearance of detectable cancer, 4 achieving a partial disappearance of cancer and 2 achieving disease stabilization. The longest duration of response has been 10 months. The combination of Telcyta™ and carboplatin was well tolerated, with hematologic (blood) side effects being consistent with that occurring with carboplatin alone.
The researchers concluded that Telcyta™ in addition to carboplatin produces significant anti-cancer responses in patients with ovarian cancer that has stopped responding to prior platinum agents. Telcyta™ has just been granted fast-track designation for third-line therapy in platinum refractory or resistant ovarian cancer and has submitted registration for the initiation of a clinical trial that is the last phase prior to FDA review. Patients with platinum refractory ovarian cancer may wish to speak with their physician about the risks and benefits of participation in a clinical trial further evaluating Telcyta™ or other novel therapeutic approaches. Two sources of information regarding ongoing clinical trials include the National Cancer Institute (
Reference: Telik. Telik’s Telcyta™ demonstrated 63% objective response rate in combination with carboplatin in platinum refractory or resistant ovarian cancer in a phase 1-2A trial. Available at: http://www.telik.com/NewFiles/pr_2003_1119d.html. Accessed November 2003.