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Endostatin gene therapy inhibits tumour growth
Newsdesk
Invasive melanoma on the rise in Californian Hispanics Rates of invasive melanoma have risen substantially in Hispanic people living in California, report US researchers (Cancer published online Jan 23, 2006; DOI: 10.1002/cncr.21654). Also, by contrast with non-Hispanic white people, Hispanic people tend to have thicker tumours with a worse prognosis. “We don’t know why Hispanics are getting melanoma”, says lead researcher Myles Cockburn, University of Southern California, Los Angeles, CA, USA, “but the fact that the number of cases is increasing at such a significant rate is worrisome”. Using data from the California Cancer Registry, the researchers found that, between 1988 and 2001, the rate of invasive melanoma in Hispanic men increased by 1·8% per year, with a 7·3% increase per year between 1996 and 2001. “There are several factors that could account for this increase, including inc-
reased sun exposure, which is a known factor”, says Ashfaq Marghoob, Memorial Sloan Kettering Cancer Center, New York, NY, USA. “In addition, not all Hispanics have the same skin tones.” Since many Hispanic people marry and have children with white people, melanoma genes could be introduced into the Hispanic gene pool, he adds. The study also found that about 54% of invasive melanomas in non-Hispanic white people measured less than 0·75 mm thick at diagnosis, compared with 44% of invasive melanomas in Hispanic men. 24% of tumours in nonHispanic white men and 35% of tumours in Hispanic men were greater than 1·5 mm thick at diagnosis. Overall, the increase in thick tumours in Hispanic people was far greater than the increase in thin or moderate tumours. Other studies have shown that some Hispanic people have less awareness of
their risk of melanoma than do white people. Moreover, most efforts for melanoma prevention are aimed at white people. Both these factors could contribute to later diagnosis of tumours in Hispanic people, when tumours have become thicker.
Leslie O’Hanlon
The sunshine state: invasive melanoma is increasing in Californian Hispanics
Endostatin gene therapy inhibits tumour growth The significantly decreased tumour size associated with injection of an adenovirus vector containing the human endostatin gene into a nasopharyngeal cancer model (published online in Int J Cancer Nov 14, 2005; DOI: 10.1002/ijc.21585) led to a phase I trial of the treatment, according to researchers. Endostatin expression also reduced the amount of angiogenesis. “Antiangiogenic therapy may be an important future addition to the multidisciplinary therapeutic approaches for nasopharyngeal cancer”, says researcher Wenlin Huang (Cancer Centre, Sun Yat-sen University, Guangzhou, Guangdong, China). William Wei (University of Hong Kong, Hong Kong, China) says: “This interesting study opens a path for further research, although there is still a long way before this [treatment] can be tested on patients”. http://oncology.thelancet.com Vol 7 March 2006
Previous work has shown that tumour growth depends on the process of angiogenesis: when a tumour grows it blocks its own blood supply, and new vessels are needed or cells die. Endostatin inhibits proliferation and movement of endothelial cells, which make new blood vessels, and initiates apoptosis, so expression of this protein might be a potential cancer treatment. Huang and colleagues studied mice with nasopharyngeal cancer. Tumours were injected with an adenovirus vector containing either the endostatin gene or a control gene; a third group of mice received a placebo injection. After 5 weeks, tumours injected with the adenovirus vector containing the endostatin gene were almost half the size of those given either of the control injections. Furthermore, endostatin-treated tumours had fewer blood vessels than did
those injected with either control, and any vessels that were present were malformed. Use of intratumour delivery by the researchers enabled the gene effect to last longer than in previous studies, 2 weeks compared with 1 day with intravenous administration. “The report demonstrated a method of delivery of endostatin gene for tumour control, and the authors should receive credit for this”, Wei says. Huang adds that “repeated gene delivery on a 2–3 week schedule could be necessary for effective treatment”. Huang says a phase I trial of the adenovirus-endostatin vector has been completed in patients with advanced solid tumours, including cervical and colon (www.clinicaltrials.gov/ct/show/ NCT00262327), and early findings show the vector is tolerated well.
Sarah Passey 199
Invasive melanoma on the rise in Californian Hispanics Rates of invasive melanoma have risen substantially in Hispanic people living in California, report US researchers (Cancer published online Jan 23, 2006; DOI: 10.1002/cncr.21654). Also, by contrast with non-Hispanic white people, Hispanic people tend to have thicker tumours with a worse prognosis. “We don’t know why Hispanics are getting melanoma”, says lead researcher Myles Cockburn, University of Southern California, Los Angeles, CA, USA, “but the fact that the number of cases is increasing at such a significant rate is worrisome”. Using data from the California Cancer Registry, the researchers found that, between 1988 and 2001, the rate of invasive melanoma in Hispanic men increased by 1·8% per year, with a 7·3% increase per year between 1996 and 2001. “There are several factors that could account for this increase, including inc-
reased sun exposure, which is a known factor”, says Ashfaq Marghoob, Memorial Sloan Kettering Cancer Center, New York, NY, USA. “In addition, not all Hispanics have the same skin tones.” Since many Hispanic people marry and have children with white people, melanoma genes could be introduced into the Hispanic gene pool, he adds. The study also found that about 54% of invasive melanomas in non-Hispanic white people measured less than 0·75 mm thick at diagnosis, compared with 44% of invasive melanomas in Hispanic men. 24% of tumours in nonHispanic white men and 35% of tumours in Hispanic men were greater than 1·5 mm thick at diagnosis. Overall, the increase in thick tumours in Hispanic people was far greater than the increase in thin or moderate tumours. Other studies have shown that some Hispanic people have less awareness of
their risk of melanoma than do white people. Moreover, most efforts for melanoma prevention are aimed at white people. Both these factors could contribute to later diagnosis of tumours in Hispanic people, when tumours have become thicker.
Leslie O’Hanlon
The sunshine state: invasive melanoma is increasing in Californian Hispanics
Endostatin gene therapy inhibits tumour growth The significantly decreased tumour size associated with injection of an adenovirus vector containing the human endostatin gene into a nasopharyngeal cancer model (published online in Int J Cancer Nov 14, 2005; DOI: 10.1002/ijc.21585) led to a phase I trial of the treatment, according to researchers. Endostatin expression also reduced the amount of angiogenesis. “Antiangiogenic therapy may be an important future addition to the multidisciplinary therapeutic approaches for nasopharyngeal cancer”, says researcher Wenlin Huang (Cancer Centre, Sun Yat-sen University, Guangzhou, Guangdong, China). William Wei (University of Hong Kong, Hong Kong, China) says: “This interesting study opens a path for further research, although there is still a long way before this [treatment] can be tested on patients”. http://oncology.thelancet.com Vol 7 March 2006
Previous work has shown that tumour growth depends on the process of angiogenesis: when a tumour grows it blocks its own blood supply, and new vessels are needed or cells die. Endostatin inhibits proliferation and movement of endothelial cells, which make new blood vessels, and initiates apoptosis, so expression of this protein might be a potential cancer treatment. Huang and colleagues studied mice with nasopharyngeal cancer. Tumours were injected with an adenovirus vector containing either the endostatin gene or a control gene; a third group of mice received a placebo injection. After 5 weeks, tumours injected with the adenovirus vector containing the endostatin gene were almost half the size of those given either of the control injections. Furthermore, endostatin-treated tumours had fewer blood vessels than did
those injected with either control, and any vessels that were present were malformed. Use of intratumour delivery by the researchers enabled the gene effect to last longer than in previous studies, 2 weeks compared with 1 day with intravenous administration. “The report demonstrated a method of delivery of endostatin gene for tumour control, and the authors should receive credit for this”, Wei says. Huang adds that “repeated gene delivery on a 2–3 week schedule could be necessary for effective treatment”. Huang says a phase I trial of the adenovirus-endostatin vector has been completed in patients with advanced solid tumours, including cervical and colon (www.clinicaltrials.gov/ct/show/ NCT00262327), and early findings show the vector is tolerated well.
Sarah Passey 199