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<title>Cancer medical service</title>
<link>http://www.bufotanine.com/englishcancer/</link>
<description>Ê×Ò³ÐÂÎÅ</description>
<item id="0">
<title><![CDATA[GM-CSF&nbsp;potentiates&nbsp;rituximab&nbsp;in&nbsp;follicular&nbsp;lymphoma]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=183</link>
<description><![CDATA[
NEW YORK (Reuters Health) - The addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) to therapy with rituximab results in high response rates in patients with relapsed follicular lymphoma, French researchers report. 

"Rituximab is a major drug in follicular lymphoma," senior investigator Dr. Jean-Francois Rossi told Reuters Health, "but with only a 6% complete response and 40% objective response at relapse."

"To improve quality and duration of response and to avoid chemotherapy," he added, "we combined GM-CSF as an immune modulator with rituximab in a prospective phase II study."

Dr. Rossi of CHU Montpelier and colleagues evaluated 33 patients treated with GM-CSF 5 mcg/kg/day from day 1 to day 8 and with rituximab 375 mg per square meter on day 5 of a 21-day cycle repeated four times. The findings appear in the June 1st issue of the Journal of Clinical Oncology.

In total, 23 patients (70%) showed an overall response, and there was a "high complete response rate -- 45% -- and prolonged duration of response," Dr. Rossi said.

The median progression-free survival was 16.4 months, but it was significantly higher in patients with a complete response (median, 33.2 months) compared with those who had a partial response (median, 7.6 months).

There were no serious adverse events and overall, say the investigators, "these results provide a solid basis for future examination of the immunotherapy combination regimen of GM-CSF plus rituximab in a multicenter study."

In fact, Dr. Rossi said, "this approach will be tested in a multicenter phase II study" with newly diagnosed patients.

]]></description>
<pubDate>2008-07-15 14:20:28</pubDate>
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<item id="1">
<title><![CDATA[Bevacizumab&nbsp;shows&nbsp;significant&nbsp;activity&nbsp;in&nbsp;liver&nbsp;cancer]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=182</link>
<description><![CDATA[
NEW YORK (Reuters Health) - Bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), may be an option in nonmetastatic unresectable hepatocellular carcinoma (HCC), according to the results of a phase 2 study reported in the July issue of the Journal of Clinical Oncology. 

The multicenter study, led by Dr. Abby B. Siegel of Columbia University College of Physicians and Surgeons in New York, involved 46 patients with HCC and compensated liver disease. Twelve patients received bevacizumab 5 mg/kg and 34 patients received 10 mg/kg every two weeks until disease progression or treatment-limiting toxicity occurred. 

Six patients (13%) had objective responses, and 65% of patients were progression-free at 6 months.

Overall survival was 53% at 1 year, 28% at 2 years and 23% at 3 years.

Grade 3-4 adverse events included hypertension in 15% and thrombosis in 6%. Grade 3 or higher hemorrhage occurred in 11%, including one fatal variceal bleed.

"After we amended the protocol to require endoscopy for at-risk patients, we had no further variceal bleeds," Dr. Siegel noted during an interview with Reuters Health. "We subsequently had two more serious bleeds (4%), which is within the same range as bleeding rates seen in trials of bevacizumab in lung cancer."

Her group is planning several trials using bevacizumab "with other targeted and chemotherapeutic agents in hepatocellular carcinoma both at Columbia and across the country," Dr. Siegel noted. 

"Several studies are evaluating whether moving bevacizumab 'up front' to the adjuvant setting may be helpful," she added. "This is a mechanistic question, because nobody knows whether bevacizumab will be able to help eradicate minimal residual disease, or whether it works best when there is existing measurable disease."

]]></description>
<pubDate>2008-07-15 14:19:00</pubDate>
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<item id="2">
<title><![CDATA[Lapatinib&nbsp;promising&nbsp;for&nbsp;advanced&nbsp;ErbB2-amplified&nbsp;breast&nbsp;cancer]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=181</link>
<description><![CDATA[
NEW YORK (Reuters Health) - In a phase II trial, the investigational agent lapatinib was well tolerated and showed clinical activity as first-line therapy against locally advanced or metastatic breast cancer in women with ErbB2-amplified disease, investigators report. 

They note in their paper in the June 20 issue of the Journal of Clinical Oncology that lapatinib is an oral, selective inhibitor of epidermal growth factor receptors ErbB1 and ErbB2, or Her-1 and HER-2/neu.

Dr. Henry L. Gomez of the Instituto Nacional de Enfermedades in Lima, Peru, led an international study of 138 patients with ErbB2-amplified locally advanced or metastatic breast cancer who were randomized to either lapatinib 1500 mg once daily or lapatinib 500 mg twice daily. 

Clinical response was assessed at 8 and 12 weeks and then every 12 weeks until there was disease progression or until the drug was discontinued for another reason.

Median treatment time was 17.6 weeks. The overall response rate (i.e., complete plus partial response rates) was 24%, and 31% of patients showed clinical benefit (complete response, partial response or stable disease for at least 24 weeks). 

The median time to response was 7.9 weeks. The progression-free survival rate was 63% at 4 months, and 43% at 6 months. 

The most common drug-related adverse events were diarrhea, rash, pruritus and nausea. These events were primarily grade 1 or 2. 

There were no significant differences in clinical activity or the adverse event profile between the dosing schedules.

The investigators conclude that the results support further evaluation of lapatinib in first-line treatment of early-stage ErbB2-overexpressing breast cancer.

]]></description>
<pubDate>2008-07-15 14:17:51</pubDate>
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<item id="3">
<title><![CDATA[Pegylated&nbsp;interferon&nbsp;improves&nbsp;melanoma&nbsp;recurrence-free&nbsp;survival]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=180</link>
<description><![CDATA[
NEW YORK (Reuters Health) - Adjuvant treatment of resected stage III melanoma with pegylated interferon alfa-2b is associated with a significant improvement in recurrence-free survival, according to the results of a randomized phase III trial. 

Dose and duration of treatment could be key factors in determining the benefit of adjuvant interferon alfa-2b for melanoma, Dr. Alexander M. M. Eggermont, from Erasmus University Medical Center in Rotterdam, the Netherlands, and co-investigators note. As such, pegylated interferon may offer advantages over standard interferon because it could provide longer exposure to the drug, while still maintaining tolerability.

As reported in The Lancet for July 12, the researchers assessed recurrence-free survival and other outcomes in 1256 patients who were randomized to receive pegylated interferon or observation for an intended duration of 5 years.

Interferon was begun at a dose of 6 micrograms/kg per week for 8 weeks and then reduced to 3 micrograms/kg per week for the remainder of the study. The median duration of interferon therapy was 12 months.

During a median follow-up period of 3.8 years, 328 recurrence events were logged in the interferon group compared with 368 in controls, yielding a hazard ratio of 0.82 (p = 0.01). The corresponding 4-year recurrence-free survival rates were 45.6% and 38.9%.

No significant difference in overall survival was seen between the groups, the report indicates.

Grade 3 and 4 events were noted in 40% and 5% of interferon-treated patients, respectively, and in 10% and 2% of observation patients. The most common grade 3 or 4 event in the interferon group was fatigue (16%), followed by hepatotoxicity (11%), and depression (6%). Thirty-one percent of interferon-treated patients stopped therapy due to toxic effects.

In a related editorial, Dr. Vernon K. Sondak, from the University of South Florida in Tampa, and Dr. Lawrence E. Flaherty, from Wayne State University School of Medicine in Detroit, comment that while the findings suggest that the pegylated interferon regimen studied will be an attractive alternative to high-dose interferon, the study's follow-up period was too short to allow for definitive conclusions. This is especially true for patients with N1 disease, they add.

]]></description>
<pubDate>2008-07-15 14:16:30</pubDate>
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<item id="4">
<title><![CDATA[Lapatinib&nbsp;appears&nbsp;safe&nbsp;in&nbsp;patients&nbsp;with&nbsp;breast&nbsp;cancer]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=179</link>
<description><![CDATA[
NEW YORK (Reuters Health) - Pooled data from 44 studies indicate that the tyrosine kinase EGFR and HER2 inhibitor lapatinib exhibits low cardiotoxicity in cancer patients. 

"This study," lead investigator Dr. Edith A. Perez told Reuters Health, "represents a thorough analysis of the prospectively collected data of more than 3,500 patients treated with lapatinib for HER2-positive breast cancer."

In the June issue of Mayo Clinic Proceedings, Dr. Perez of the Mayo Clinic in Jacksonville, Florida, and colleagues observe that HER2 pathway inhibitors can cause cardiac dysfunction. 

However, cardiac events (i.e., decreases in left ventricular ejection fraction) were reported in only 60 (1.6%) of 3689 patients. Two patients had two such events. Fifty-three of the events were asymptomatic and these patients received no cardiac-related therapy. 

In the 40 patients in whom cardiac outcome was determined, 35 (88%) had full or partial recovery, regardless of whether they continued or discontinued lapatinib. No cardiac deaths were attributed to lapatinib.

"The data," concluded Dr. Perez, "demonstrate a reassuringly low rate of clinically evident or asymptomatic cardiac effects. Further studies in comparative trials will allow us to place the data in the context of other anti-HER2 agents."

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<pubDate>2008-07-15 14:15:18</pubDate>
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<item id="5">
<title><![CDATA[Atorvastatin&nbsp;and&nbsp;celecoxib&nbsp;synergistic&nbsp;against&nbsp;colon&nbsp;cancer&nbsp;cells]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=178</link>
<description><![CDATA[
NEW YORK (Reuters Health) - Atorvastatin and celecoxib synergistically induce cell cycle arrest and apoptosis in colon cancer cells, according to a report in the May 1st International Journal of Cancer. 

"Taking statins and NSAIDS may produce synergistic beneficial effect in the reduction of risks for colon cancer and other cancer types," Dr. Chung S. Yang told Reuters Health. "However, this point needs to be studied more extensively in observational epidemiological studies and in future clinical trials." 

Dr. Yang from Rutgers, The State University of New Jersey, Piscataway, and colleagues used two human colon cancer cell lines to investigate the interaction between atorvastatin and celecoxib and to elucidate the mechanisms underlying the synergy. 

Atorvastatin and celecoxib interacted synergistically to inhibit growth of both cell lines, the researchers report, and both cell lines were more sensitive to the synergy than were normal human intestinal epithelial cells. 

The drug combination arrested colon cancer cells in G0/G1 phase and increased apoptosis of colon cancer cells, the report indicates. 

"The strong synergy between atorvastatin and celecoxib on cell cycle arrest and apoptosis is of great importance for potential increase of chemoprevention and treatment efficacy by this combination in humans for colorectal cancer," the researchers explain. "The increased efficacy could also reduce celecoxib dose to minimize possible detrimental side effects, while receiving beneficial effect of atorvastatin in cardiovascular health." 

Dr. Yang said his group is "interested in establishing collaborations with clinicians to conduct human cancer chemoprevention trials with atorvastatin and celecoxib in the future." 

Furthermore, Dr. Yang added, "Drs. Xi Zheng and Allan Conney in our department also observed the inhibitory effect of the combination of atorvastatin and celecoxib in the inhibition of prostate cancer progression in a xenograft model. We are planning a human trial on prostate cancer prevention in collaboration with Dr. Robert Dipaola." 

]]></description>
<pubDate>2008-07-01 14:29:59</pubDate>
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<item id="6">
<title><![CDATA[Painkillers&nbsp;don&#39;t&nbsp;protect&nbsp;against&nbsp;melanoma]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=177</link>
<description><![CDATA[
NEW YORK (Reuters Health) - Lab evidence suggests that the class of painkillers known as nonsteroidal anti-inflammatory drugs (NSAIDs) could play a role in preventing melanoma, but a large study has failed to find any evidence to support this possibility. 

Dr. Maryam M. Asgari at Kaiser Permanente Northern California in Oakland and colleagues analyzed data on approximately 64,000 white individuals aged 50-76 years with no history of melanoma when they enrolled between 2000 and 2002. 

The subjects reported their use of NSAIDs -- including aspirin, ibuprofen, naproxen, celecoxib, rofecoxib, piroxicam and indomethacin -- during the previous 10 years. Information was also collected on lifestyle, diet, cancer risk factors, and family history of skin cancer.

Almost two-thirds of the subjects had regularly taken an NSAID at least once a week for 1 year in the decade prior to study enrollment, the researchers report in the Journal of the National Cancer Institute. Overall, 349 new cases of malignant melanoma occurred by the end of 2005.

"After adjusting for melanoma risk factors and indications for NSAID use, no association between NSAID use and melanoma risk was found," Asgari's group reports.

They also discerned no link between the dose of any NSAID and the aggressiveness of melanomas.

"The search must continue for a good chemopreventive agent for melanoma," the researchers conclude

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<pubDate>2008-07-01 14:25:54</pubDate>
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<item id="7">
<title><![CDATA[Glaxo&#39;s&nbsp;Cervarix&nbsp;vaccine&nbsp;faces&nbsp;further&nbsp;delay]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=176</link>
<description><![CDATA[
LONDON (Reuters) - GlaxoSmithKline Plc does not expect to win U.S. approval for its key cervical cancer vaccine Cervarix until late 2009, marking a further delay for the product. 

The delay, announced on Monday, is good news for Merck & Co Inc, which sells the rival blockbuster vaccine Gardasil. Its stock jumped 3 percent while Glaxo shares were flat in a sharply higher market for European drugmakers.

Glaxo said it had responded to outstanding questions about Cervarix raised by the U.S. Food and Drug Administration but had decided to augment its application with results from a further Phase III study, called HPV-008.

Data from this trial are expected to be submitted to the U.S. regulator in the first half of 2009 and an FDA decision on the application is anticipated up to six months later.

"Study 008 is a key study that will be completing later this year, and we expect the final results will strengthen the U.S. label for Cervarix," Barbara Howe, Glaxo's head of North American vaccine development, said.

Interim data from the HPV-008 study were filed in the original application for the vaccine in March 2007. Glaxo added it did not expect the FDA to require new clinical studies for approval.

Cervarix is arguably the most important new product for Glaxo this decade but its path to market in the United States has been problematic, with the FDA delaying approval last December, pending more information.

Glaxo said in February it would reply to the U.S. watchdog before the end of the second quarter.

MERCK'S GAIN

Few analysts had expected Cervarix to win a U.S. green light this year but several had been banking on a 2009 approval.

Deutsche Bank analysts said it now seemed unlikely Cervarix would be available and reimbursed in time for the 2009 back-to-school season in the United States.

Tim Franklin of Dresdner Kleinwort, who had penciled in U.S. Cervarix sales of $150 million in 2009, said he would revise his sales forecasts.

"I don't think the FDA will rush to approve it -- I don't think we will see Cervarix on the market until 2010 now," he said.

Cervarix is approved in Europe but U.S. sales will be pivotal to its commercial success.

It competes against Merck's Gardasil, which is available on both sides of the Atlantic, and is already established as $1-billion-plus product, with global revenues of $390 million in the first quarter of this year.

Both vaccines are designed to be given to girls and young women to protect against cancer-causing strains of the sexually transmitted human papillomavirus (HPV).

But the two vaccines have different properties. In particular, Cervarix uses a novel adjuvant, or additive, which Glaxo says makes it longer lasting.

Analysts, however, say the FDA is extremely cautious about approving new adjuvants because of the theoretical risk of side effects, increasing the regulatory hurdle for Glaxo's vaccine.

Morgan Stanley analysts predicted in a note last month that Cervarix would not get approved in the United States until 2014.

]]></description>
<pubDate>2008-07-01 14:25:04</pubDate>
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<item id="8">
<title><![CDATA[Avastin&nbsp;prolongs&nbsp;survival&nbsp;in&nbsp;colorectal&nbsp;cancer]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=175</link>
<description><![CDATA[
ZURICH (Reuters) - A new phase III study of Roche's Avastin (bevacizumab) shows significantly improved survival in patients with metastatic colorectal cancer irrespective of K-Ras gene mutations, the Basel-based drug maker said on Monday. 

Roche said the findings were important because other biologic combinations are ineffective in patients with this gene mutation, which occurs in half of colorectal cancer patients.

Data from the randomized, controlled AVF2107 study involving more than 800 previously untreated metastatic colorectal cancer patients was presented on Monday at the World Congress on Gastrointestinal Cancer (WCGC) in Barcelona, Spain.

In the study, Avastin was combined with standard chemotherapy with irinotecan, fluorouracil and leucovorin (IFL).

Roche said results showed an 82% increase in progression-free survival in patients with normal K-Ras gene, compared to chemotherapy alone. Avastin also showed a 57% increase in overall survival versus chemotherapy alone in the same patient group.

In patients with K-Ras gene mutations, a 69% increase in progression-free survival was observed, compared with chemotherapy alone.

In January 2008, Avastin was given a broad label in the EU allowing it to be used in combination with fluoropyrimidine-based chemotherapy for first and later treatment lines in patients with metastatic colorectal cancer. 
 
 

]]></description>
<pubDate>2008-07-01 14:21:59</pubDate>
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<item id="9">
<title><![CDATA[Cisplatin&nbsp;not&nbsp;effective&nbsp;in&nbsp;anal&nbsp;cancer:&nbsp;study]]></title>
<link>http://www.bufotanine.com/englishcancer/show.php?tid=174</link>
<description><![CDATA[
CHICAGO (Reuters) - Treating anal cancer patients with the cancer-fighting drug cisplatin to try to shrink tumors before beginning standard therapy did not boost survival rates, and is not recommended, U.S. researchers said on Tuesday. 

Evidence from pilot studies led oncologists to believe giving patients cisplatin, a platinum-based drug commonly used to fight various cancers, would shrink the primary tumor and attack the disease that had spread to lymph nodes.

The idea was to give patients a head start before surgery, further chemotherapy and radiation treatment.

Anal cancer, which the American Cancer Society said will affect 5,000 Americans this year, is particularly deadly when the tumors exceed 2 inches (5 cm) in size. Mortality rates from the cancer have not improved since the early 1990s, the Cancer Society said.

"However, it is clear from this data that cisplatin is not the drug to use and its use should be discontinued in standard therapy," Dr. Jaffer Ajani of the University of Texas M.D. Anderson Cancer Center, who led the study, said in a statement.

In the study of 644 patients, 60 percent of those who received the current standard treatment -- the chemotherapy drugs fluorouracil plus mitomycin along with radiation -- were likely to survive five years disease-free. That compared to the disease-free survival rate of 54 percent among those treated with cisplatin followed by fluorouracil and radiation.

Overall survival rates were also slightly higher in the standard treatment group, of whom 28 patients died compared to 54 in the cisplatin group, Ajani's team reported in the Journal of the American Medical Association.

In addition, 19 percent of the cisplatin group had colostomies, in which patients' waste is diverted through the abdomen into a bag they must carry around, compared to 10 percent of standard treatment group.

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<pubDate>2008-04-23 21:58:07</pubDate>
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