Tuesday, December 28, 2010
about 13% breast pain in one breast as Symptoms of early breast cancer | Curative
about 13% breast pain in one breast as Symptoms of early breast cancer | Curative
Wednesday, December 15, 2010
Acquired defects in the FGFR1 gene could play a role in lung cancer
An overproduced receptor protein that shows up in a subset of lung cancers may offer a target of opportunity for new drugs and a glimmer of hope for some patients, researchers report.
Excess amounts of a protein known as FGFR1, or fibroid growth factor receptor 1, often show up in smokers who develop a hard-to-treat form of lung cancer, suggesting that tobacco smoke exposure damages the gene encoding this protein and steers cells toward cancer in some people. Researchers report the findings in the Dec. 15 Science Translational Medicine.
Acquired defects in the FGFR1 gene could play a role in lung cancer
Scientists have been investigating the four known FGFR genes for years, and defects in these genes have been linked to cancer of the lung, bladder, uterus, breast and blood, says Lynn Heasley, a physician and researcher at the University of Colorado Denver Anschutz Medical Campus in Aurora who wasn’t part of this study. “This is the first paper where you actually see amplification of the gene in primary [lung] tumors. In that way, it’s an important advance.”
Acquired defects in the FGFR1 gene could play a role in lung cancer
In gene amplification, multiple copies of a defective gene appear and the gene’s protein is overproduced, altering its effect on the cell’s processes. Several research groups have plans to test drugs that inhibit FGFR proteins in cancer patients whose tumors have the gene amplification.
In the new study, the researchers concentrated on squamous cell carcinoma of the lung, a deadly malignancy responsible for about one-fourth of lung cancers. It mainly hits smokers. Analysis of squamous cell tumors from 155 lung cancer patients showed that 15 had a defective FGFR1 gene. Of those 15 patients, 11 were current or former smokers, and data were unavailable for the other four.
The researchers then used a different technique to analyze samples of 153 other squamous cell lung tumors and found that the FGFR1 gene was amped up in 22 percent of them. But the defect turned up in only 1 percent of 581 nonsquamous cell lung tumors included in a publicly available database.
The scientists also tested an FGFR-inhibiting compound called PD173074 against 83 lung cancer cell lines. The compound blocked growth and caused cancer cell death in four of the cell lines, and three of those had an altered FGFR1 gene. When the scientists tested the compound on mice with squamous cell lung cancer, the animals whose tumors had a defective FGFR1 gene benefited from the treatment, showing marked tumor shrinkage.
The compound used in this study is unstable and probably won’t be suitable for people, says study coauthor Roman Thomas, physician and researcher at the Max Planck Institute for Neurological Research and the University of Cologne in Germany. But drug manufacturers, including Novartis and AstraZeneca, have developed other FGFR inhibitors aimed at treating patients.
Early-stage clinical trials of those FGFR inhibitors are recruiting breast cancer patients. Thomas and his colleagues are planning to test an FGFR inhibitor in lung cancer patients who screen positive for the altered FGFR1 gene.
“We’re still in the early days here,” Heasley says, but FGFR inhibitors might hold potential as drugs that can be aimed at tumors that arise in smokers.
Lung cancer takes the largest toll of all malignancies, killing more people than breast, prostate and colon cancer combined. While often treatable when it appears in nonsmokers, fewer options are available for squamous cell lung cancer and other forms that are more common among smokers.
ARTICLE FROM: http://www.sciencenews.org/view/generic/id/67639/title/Gene_linked_to_some_smokers%E2%80%99_lung_cancer
Excess amounts of a protein known as FGFR1, or fibroid growth factor receptor 1, often show up in smokers who develop a hard-to-treat form of lung cancer, suggesting that tobacco smoke exposure damages the gene encoding this protein and steers cells toward cancer in some people. Researchers report the findings in the Dec. 15 Science Translational Medicine.
Acquired defects in the FGFR1 gene could play a role in lung cancer
Scientists have been investigating the four known FGFR genes for years, and defects in these genes have been linked to cancer of the lung, bladder, uterus, breast and blood, says Lynn Heasley, a physician and researcher at the University of Colorado Denver Anschutz Medical Campus in Aurora who wasn’t part of this study. “This is the first paper where you actually see amplification of the gene in primary [lung] tumors. In that way, it’s an important advance.”
Acquired defects in the FGFR1 gene could play a role in lung cancer
In gene amplification, multiple copies of a defective gene appear and the gene’s protein is overproduced, altering its effect on the cell’s processes. Several research groups have plans to test drugs that inhibit FGFR proteins in cancer patients whose tumors have the gene amplification.
In the new study, the researchers concentrated on squamous cell carcinoma of the lung, a deadly malignancy responsible for about one-fourth of lung cancers. It mainly hits smokers. Analysis of squamous cell tumors from 155 lung cancer patients showed that 15 had a defective FGFR1 gene. Of those 15 patients, 11 were current or former smokers, and data were unavailable for the other four.
The researchers then used a different technique to analyze samples of 153 other squamous cell lung tumors and found that the FGFR1 gene was amped up in 22 percent of them. But the defect turned up in only 1 percent of 581 nonsquamous cell lung tumors included in a publicly available database.
The scientists also tested an FGFR-inhibiting compound called PD173074 against 83 lung cancer cell lines. The compound blocked growth and caused cancer cell death in four of the cell lines, and three of those had an altered FGFR1 gene. When the scientists tested the compound on mice with squamous cell lung cancer, the animals whose tumors had a defective FGFR1 gene benefited from the treatment, showing marked tumor shrinkage.
The compound used in this study is unstable and probably won’t be suitable for people, says study coauthor Roman Thomas, physician and researcher at the Max Planck Institute for Neurological Research and the University of Cologne in Germany. But drug manufacturers, including Novartis and AstraZeneca, have developed other FGFR inhibitors aimed at treating patients.
Early-stage clinical trials of those FGFR inhibitors are recruiting breast cancer patients. Thomas and his colleagues are planning to test an FGFR inhibitor in lung cancer patients who screen positive for the altered FGFR1 gene.
“We’re still in the early days here,” Heasley says, but FGFR inhibitors might hold potential as drugs that can be aimed at tumors that arise in smokers.
Lung cancer takes the largest toll of all malignancies, killing more people than breast, prostate and colon cancer combined. While often treatable when it appears in nonsmokers, fewer options are available for squamous cell lung cancer and other forms that are more common among smokers.
ARTICLE FROM: http://www.sciencenews.org/view/generic/id/67639/title/Gene_linked_to_some_smokers%E2%80%99_lung_cancer
Saturday, December 4, 2010
first pregnancy appears to the accumulation of risk, obesity and certain types of breast cancer
In the age of first pregnancy appears to the accumulation of risk, obesity and certain types of breast cancer. A groundbreaking study by University of Wisconsin Medical School and public health leaders said they have children or no life along with obesity, causing the risk of breast cancer. In the conception and the link between age and breast cancer may be strong women who never had children or who waited until 30 or later have a child.
The study consists of about 1912 to 1986 women born in 50000, of which 29,000 were diagnosed with breast cancer. Those aged 30 or over, while the pregnancy first child or a child has never been reported in the elevation of 2.5% of lobular breast cancer. Breast cancer, is clearly the most common form of breast cancer, but the lobular and mixed ductal, lobular breast cancer cases in the 20th century, the rapid increase in 90 years and accounts for 20 percent of all breast cancer events.
"Our study found that children who never or was at or after 30 children had a three times greater development of lobular breast cancer risk in obese women. Has been strong evidence that obesity, sedentary lifestyle and alcohol use can in breast cancer risk factors. These are all risk factors, women can change, "highlighted the cancer center from the Polly Newcomb.
Since lobular breast cancer lobular breast where it started, it may be difficult to find a breast X-rays. Ductal carcinoma, on the other hand, began to pipe lining in a milk and more easy to detect. Authors suggest that postmenopausal hormone replacement and the risk of lobular breast cancer linked.
The study, published in the journal Cancer.
The study consists of about 1912 to 1986 women born in 50000, of which 29,000 were diagnosed with breast cancer. Those aged 30 or over, while the pregnancy first child or a child has never been reported in the elevation of 2.5% of lobular breast cancer. Breast cancer, is clearly the most common form of breast cancer, but the lobular and mixed ductal, lobular breast cancer cases in the 20th century, the rapid increase in 90 years and accounts for 20 percent of all breast cancer events.
"Our study found that children who never or was at or after 30 children had a three times greater development of lobular breast cancer risk in obese women. Has been strong evidence that obesity, sedentary lifestyle and alcohol use can in breast cancer risk factors. These are all risk factors, women can change, "highlighted the cancer center from the Polly Newcomb.
Since lobular breast cancer lobular breast where it started, it may be difficult to find a breast X-rays. Ductal carcinoma, on the other hand, began to pipe lining in a milk and more easy to detect. Authors suggest that postmenopausal hormone replacement and the risk of lobular breast cancer linked.
The study, published in the journal Cancer.
Wednesday, December 1, 2010
Women’s lung cancer rate catching up with men’s
Recently a research shows that women patients with lung cancer dramatic increase in UK, as they fail to heed no-smoking message. Women have been urged to take anti-smoking messages more seriously.
Alexander Ives and Dr Julia Verne, of the NHS’s South West Public Health Observatory, found that: “Lung cancer incidence for females increased significantly from 1985-87 (32.3 per 100,000) to 2004-06 (35.4 per 100,000)”, a 10% rise. While the recent rate for men in England as 60 per 100,000. They said they identify women in England diagnosed with the disease between 1985 and 2006 from data of the UK Association of Cancer Registries.
Traditionally, Lung cancer of male are much more than women, but numbers of women being diagnosed are growing and it become the UK’s biggest cancer killer. The trend now has alarmed us, we should be urging female smokers to quit and calling on the NHS to do more to warn women of the dangerous habit. Women need to take on board that lung cancer is not a disease of men, it’s a disease of smokers, and either not take up smoking in the first place or quit cigarettes as a matter of urgency.
Lung cancer claims more Britons’ lives than any other form of the disease. It is reported that every day about 108 people are diagnosed with it, and of those 95 die. In the 1950s men diagnosed with lung cancer outnumbered women by six to one.
The Office of National Statistics released data last week, it showed that cancers are now the commonest cause of death in women, accounting for 159 deaths per 100,000 annually. It means Scotland has the UK’s highest rates of lung cancer, while cancer generally claims 181 lives per 100,000 women north of the border.
Except smoking, non-smoking cancers is increased too. It’s well known that long-term exposure to tobacco smoke is also the major causes of lung cancer. Air pollution is an other cause.
Alexander Ives and Dr Julia Verne, of the NHS’s South West Public Health Observatory, found that: “Lung cancer incidence for females increased significantly from 1985-87 (32.3 per 100,000) to 2004-06 (35.4 per 100,000)”, a 10% rise. While the recent rate for men in England as 60 per 100,000. They said they identify women in England diagnosed with the disease between 1985 and 2006 from data of the UK Association of Cancer Registries.
Traditionally, Lung cancer of male are much more than women, but numbers of women being diagnosed are growing and it become the UK’s biggest cancer killer. The trend now has alarmed us, we should be urging female smokers to quit and calling on the NHS to do more to warn women of the dangerous habit. Women need to take on board that lung cancer is not a disease of men, it’s a disease of smokers, and either not take up smoking in the first place or quit cigarettes as a matter of urgency.
Lung cancer claims more Britons’ lives than any other form of the disease. It is reported that every day about 108 people are diagnosed with it, and of those 95 die. In the 1950s men diagnosed with lung cancer outnumbered women by six to one.
The Office of National Statistics released data last week, it showed that cancers are now the commonest cause of death in women, accounting for 159 deaths per 100,000 annually. It means Scotland has the UK’s highest rates of lung cancer, while cancer generally claims 181 lives per 100,000 women north of the border.
Except smoking, non-smoking cancers is increased too. It’s well known that long-term exposure to tobacco smoke is also the major causes of lung cancer. Air pollution is an other cause.
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