In the operation, a conservation solution for transplantation was injected into the extracted right lung and cancer was removed after a cooling treatment was applied to last for eight hours. The lung was put back into the body after no cancer was confirmed in the lung. The patient recovered his vital capacity up to about 70% and can play golf and do other exercise, according to the hospital…….
The hospital has so far performed more than 70 operations for lung transplantation, accounting for the largest number among medical institutions in Japan.

via:lungcancer

asbestos lung mesothelioma

Lung cancer information about Asbestos.

Have you ever wondered why some chain smokers are lucky enough to get away without certain side effects, like lung cancer? While there are other poor souls just might get lung cancer without ever having smoked a single cigarette in their whole lives?
The truth is, smoking will merely increase your chances of getting lung cancer. But that doesn’t mean that smoking cigarettes is a 100 percent guaranteed way of contracting cancer. So what are the factors that trigger lung cancer, in addition to smoking? Or is there no correlation between the two?

 
Lung cancer is a disease that kills more than a million people annually. It is also the most common form of cancer, that is, more people will die from lung cancer than from any other type of cancer. Statistics tell us that 90 percent of lung cancer cases occur in smokers, that is to say, only 1 in 10 non-smokers are affected by lung cancer. But the real question to ask is: how many smokers are ultimately diagnosed with lung cancer?…..

Smokers might be struck down by a host of other diseases such as heart attacks, strokes, asthma or emphysema. But a huge chunk of them, about 10 to 15 percent, fall prey to lung cancer. Therefore, a pertinent question is: how can a smoker escape lung cancer?
 
A team at IARC (International Agency for Research on Cancer), in Lyon, has some answers. They have discovered that some smokers are inherently safe from lung cancer. Those smokers who have certain types of proteins occurring at a higher level in their systems and those who have richer amounts of vitamin B6 just might be able to avoid lung cancer. Vitamin B6 is found in bananas, vegetables, meat and nuts.

That team studied 900 lung cancer cases and discovered that a significant number of these cases had remarkably low amounts of vitamin B6 in their system. Methionine, which is an amino acid, was also found at low levels.

So does this mean that smokers who eat bananas, for example, can escape lung cancer? “…it’s still a little premature to say simply that if you change your diet and eat more foods with these vitamins then you’ll change your future lung cancer risk,” replies Paul Brennan. You could always quit smoking, though.

Other cancers receive less attention. These cancers may not have a warm and fuzzy side, but we agree that people diagnosed with them deserve our support and kindness.

But one cancer is noteworthy for the lack of empathy and compassion it elicits.

“Lung cancer is the ugly stepsister of cancer,” was how one person described it to me.

When she was diagnosed, most people assumed that she smoked. She didn’t. (Some 10 to 15 percent of people diagnosed with lung cancer are nonsmokers. For reasons not fully understood, lung cancer is more common in nonsmoking women than in nonsmoking men).

Even her friends who knew she didn’t smoke interrogated her to find the cause. There was an underlying sense that if she wasn’t at fault, someone or something else was.

Blame seems to be the unspoken word when lung cancer is discussed.

People with other cancers aren’t blamed. We don’t accuse them or even wonder if they did something to cause their cancers. The cancer just is.

Anyone who has had cancer can tell you how difficult it was to get the diagnosis and then to share that news with family and friends. Imagine how much more difficult it would be if you sensed people thinking — or even saying, “Well, that’s what you get for smoking.”……..

And, assuming that an individual did smoke, what difference does that make once they have lung cancer? Should we be less compassionate or less supportive? Absolutely not.

I’m hardly an apologist for smokers or for the tobacco industry. I hate it when smokers foul my air and increase my insurance rates.

But if you have lung cancer, you don’t need blame. You need kindness and support, given without judgment.

Differentiating whether a pulmonary neoplasm is primary or metastatic can be challenging for surgical pathologists, and is an important distinction for clinicians in determining the proper treatment protocols. Current biomarkers do not always aid lung tumor classification. The study’s authors identified a set of microRNAs that is expressed differentially between these two groups using microRNA microarray data generated from 76 formalin-fixed, paraffin-embedded (FFPE) samples of either primary lung cancer or metastatic tumors to the lung.

According to the study, “The tissue-associated expression of microRNA likely explains the remarkable finding that many tumors can be classified based solely on their microRNA expression signature. Here we show that microRNAs can serve as biomarkers for lung tumor classification.”

“These data offer further evidence of the flexibility and potential wide range of clinical applicability of our microRNA technology. The growing body of literature, as well as our commercial line of miRview™ tests, continue to demonstrate that microRNAs are highly reliable and powerful biomarkers for a wide range of indications,” noted Kenneth A. Berlin, President and CEO of Rosetta Genomics. …

About microRNAs

MicroRNAs (miRNAs) are recently discovered, small RNAs that act as master regulators of protein synthesis, and have been shown to be highly effective biomarkers. The unique advantage of microRNAs as biomarkers lies in their high tissue specificity, and their exceptional stability in the most routine preservation methods for biopsies, including Formalin Fixed Paraffin Embedded (FFPE) block tissue and fine needle aspirate (FNA) cell blocks. It has been suggested that their small size (19 to 21 nucleotides) enables them to remain intact in FFPE blocks, as opposed to messenger RNA (mRNA), which tends to degrade rapidly. In addition, early preclinical data has shown that by controlling the levels of specific microRNAs, cancer cell growth may be reduced. To learn more about microRNAs, please visit http://www.rosettagenomics.com .

About miRview™ Products

miRview™ products are a series of microRNA-based diagnostic tests developed by Rosetta Genomics. miRview™ mets accurately identifies the primary tumor site in metastatic cancer and Cancer of Unknown Primary (CUP) patients. miRview™ squamous accurately identifies the squamous subtype of NSCLC, which carries an increased risk of severe or fatal internal bleeding and poor response to treatment for certain targeted therapies. miRview™ meso diagnoses mesothelioma, a cancer connected to asbestos exposure, from other carcinomas in the lung and pleura. This test can be used to rule out mesothelioma in patients diagnosed with a tumor in the lung or pleura, who may have been exposed to asbestos in the past. miRview™ tests are designed to provide objective diagnostic data; it is the treating physician’s responsibility to diagnose and administer the appropriate treatment. The company’s tests are now being offered through distributors around the globe. For more information, please visit http://www.mirviewdx.com .

via:medicalnewstoday.com

24. April 2010 08:49

Biopsy-based study tilts field toward personalized treatment, more efficient clinical trials

The first lung cancer clinical trial to guide targeted therapies to patients based on molecular signatures in tumor biopsies is a step toward personalized care and more effective, efficient clinical trials for new drugs, study leaders reported today during the American Association for Cancer Research 101st Annual Meeting 2010.

Researchers at The University of Texas M. D. Anderson Cancer Center presented the results of the study that used an innovative statistical model to match four drugs to specific molecular signatures, or biomarkers, in the tumors of 255 stage IV non-small cell lung cancer patients who had received between one and nine previous treatments.

“New drugs that target molecular pathways help a small percentage of lung cancer patients, but right now there’s no way to determine who those patients are before treatment,” said Edward Kim, M.D., associate professor in M. D. Anderson’s Department of Thoracic/Head and Neck Medical Oncology and principal investigator on the Biomarker-Integrated Approaches of Targeted Therapy for Lung Cancer Elimination (BATTLE) clinical trials.

“BATTLE evaluated tumor biomarkers in hopes that we can treat lung cancer, which kills more people than any other type of cancer, like we treat breast or colon cancer, using validated biomarkers to guide treatment and improve survival,” Kim said. The National Cancer Institute estimates that 219,440 new cases of lung cancer were diagnosed in 2009 and 159,390 people died from the disease.

Kim said BATTLE also points the way to more precise clinical trials that will require smaller numbers of patients to test a targeted therapy rather than large trials open to all-comers. “Lung cancer research has been plagued by large, Phase III clinical trials that showed minor effects or even failed to enroll enough patients to finish,” Kim said.

“Two lung cancer tumors might appear identical under a microscope and have the same staging, but they behave differently,” said Waun Ki Hong, M.D., head of M.D. Anderson’s Division of Cancer Medicine and principal investigator on the BATTLE grant from the U.S. Department of Defense. “The name of the game now is to treat based on the molecular defects in the tumor.”

The Phase II clinical trial found evidence that each of the four drugs targets specific molecular signatures better than the other three. The drugs used in the trial were erlotinib (Tarceva-), sorafenib (Nexavar-), vandetanib (Zactima-) and erlotinib with bexarotene (Targretin-). Each drug is designed to target specific molecular pathways; currently, none has a validated biomarker to guide its use….

BATTLE’s end point was disease control at eight weeks, which recent research has found is a good indicator of overall survival. The study found, for example, that 61 percent of patients with a KRAS mutation in their tumors who took sorafenib had disease control at eight weeks, compared with 32 percent for the other three drugs. Erlotinib did best against EGFR mutations, vandetanib for high VEGFR-2 expression and the erlotinib-bexarotene fared best with Cyclin D1 defects or amplified numbers of the EGFR gene. These exploratory analyses raise interesting areas of future research.

Overall, 46 percent of patients on the trial had disease control at 8 weeks, compared with a historical experience of around 30 percent for late-stage lung cancer patients. Median overall survival was nine months, and 38 percent of patients survived to one year. Toxicities from the four drugs were minimal, with only 6.5 percent experiencing a significant side effect.

Kim cautioned that Phase II trial findings of biomarker effectiveness need to be validated in Phase III trials, which are typically sponsored by pharmaceutical companies or performed in cooperative groups.

A model for efficient clinical trials

By successfully collecting new tumor biopsies on each patient and employing a Bayesian adaptive randomization statistical model, BATTLE provides an example for improving clinical trials.

“BATTLE is an important step toward personalized medicine and marks a paradigm shift for clinical trials by demonstrating the feasibility of a biopsy-based, hypothesis-driven biomarker trial,” said Roy Herbst, M.D., Ph.D., professor in the Department of Thoracic/Head and Neck Medical Oncology and co-principal investigator on the BATTLE clinical trials.

Patients agreed to have a new biopsy for the trial, Kim said, which was crucial to the study design because it provided fresh information on the tumor’s molecular status that may have been altered by treatment since the patient’s previous biopsy.

“BATTLE employed an adaptive randomization approach that allowed the statistical model to learn as the clinical trial progressed,” said J. Jack Lee, Ph.D., professor in M. D. Anderson’s Department of Biostatistics.

The first 97 patients were equally randomized to BATTLE’s four arms. As the study progressed, information from patients’ biopsies and outcomes was employed by the model to guide assignment of drugs to new patients, who became more likely to receive a drug that had worked for earlier patients with the same tumor biomarkers.

The model leads to greater use of successful drugs and minimization or dropping of those less successful. While vandetanib helped those with VEGFR overexpression, it was dropped for patients with the KRAS mutation, Lee said.

By identifying biomarkers, and thus a potential patient population for a drug at Phase II, a follow-up Phase III will require smaller sample sizes and proceed more quickly than an all-comers trial with thousands of patients, Lee said.

Kim said future BATTLE trials will test combinations of therapies as well as single agents and will concentrate on the entire range of staging for lung cancer patients, including frontline therapy. Ultimately, the researchers plan to try the BATTLE approach in personalizing prevention clinical trials.

via:news-medical.ne

The mid-stage study, conducted at the University of Texas M.D. Anderson Cancer Center in Houston and funded by the U.S. Army, enrolled 255 patients with advanced lung cancer who had previously been treated with chemotherapy.

“We are still in the dark ages with how we treat lung cancer patients,” said Dr. Edwin Kim, associate professor at the center’s thoracic/head and neck oncology department and the study’s lead investigator. Currently, they are separated only into “histologic” categories such as small cell or non-small cell lung cancer, with subtypes like squamous or non-squamous.

“As far as molecular testing nothing is standardly done in lung cancer at this time,” Kim said.

For other types of cancer — such as breast and colon — such testing has become common in recent years amid the development of biologic drugs designed to work only against tumors with specific genetic or molecular characteristics.

Patients in the MD Anderson trial had their lung tumors biopsied and tested for several “biomarkers” including epidermal growth factor receptor, or EGFR; vascular endothelial growth factor, or VEGF; a gene known as KRAS; and another that encodes for a protein called Cyclin D1.

Erlotinib, sold by Roche Holding AG and OSI Pharmaceuticals Inc under the brand name Tarceva, is designed to block EGFR, a protein found in high amounts on many types of cancer cells….

Tarceva is cleared for treating lung cancer that has gotten worse following at least one chemo regimen and the companies’ are seeking approval for its use in patients whose disease has remained stable after chemotherapy.

The M.D. Anderson trial also looked at treatment with AstraZeneca PLC’s Zactima, or vandetanib, which has targets including VEGF, a protein tumors need to grow vessels to supply blood. AstraZeneca last year pulled its regulatory applications for Zactima in lung cancer after an updated analysis found no overall survival advantage when the drug was added to chemotherapy.

Other drugs in the study were Nexavar, or sorafenib, sold by Onyx Pharmaceuticals Inc and Bayer AG, for treatment of kidney and liver cancers, and bexarotene, sold under the brand name Targretin as a treatment for a type of lymphoma.

The trial’s end point was disease control at eight weeks, which is seen as an indicator of overall survival. “In our study, if you made it to eight weeks, survival was 11.5 months. if not, it was 7.5 months,” Kim said, noting that as patients were enrolled they were directed to regimens which proved successful for earlier patients with similar tumor types.

The study found that 61 percent of patients with a KRAS mutation in their tumors who took Nexavar had no tumor growth at eight weeks, compared with 32 percent for the other three drugs.

Tarceva did best against EGFR mutations, Zactima for high VEGF expression and the Tarceva-Targretin fared best with Cyclin D1 defects or amplified numbers of the EGFR gene, the researchers said.

Overall, 46 percent of patients on the trial had disease control at 8 weeks, compared with a historical experience of around 30 percent for late-stage lung cancer patients.

Researchers said toxicities from the four drugs were minimal, with 6.5 percent of patients having a significant side effect.

Kim said future trials are needed to test combinations of therapies as well as single agents, including trials in earlier-stage lung cancer patients.

Roche is conducting a late-stage trial looking at the effectiveness of Tarceva as a first-line treatment for lung cancer patients with EGFR mutations.

Results were to be presented in Washington on Sunday at a meeting of the American Association for Cancer Research.

(Reporting by Deena Beasley; editing by Carol Bishopric)

However, treatment with various substances to block these two enzymes has often been non-specific, and their efficacy has varied widely. This has made it difficult for researchers to assess the true potential of these enzymes as targets for medicines.

“We therefore developed genetic strategies in mice, known as transgenic mice, to switch off the genes coding for FT and GGT, enabling us to investigate whether a complete blockade of FT or GGT can inhibit the development of lung cancer, and whether this has side-effects in the lungs,” explains researcher Anna-Karin Sjögren, who led the study together with Meng Liu, both from the Department of Clinical and Molecular Medicine.

In their study, the researchers used transgenic mice which produce a mutated Ras protein that causes lung cancer. First, production of FT or GGT in these mice’s lungs was stopped by switching off the relevant genes…

“When we turned off the FT gene, the mice developed fewer lung tumours and lived longer,” says Meng Liu. “At cellular level, the blockade of FT meant that the tumour cells were no longer able to divide. When we blocked the production of GGT, we saw the same effects: inhibition of cell growth, fewer lung tumours and improved survival.”

In experiments where both genes were switched off at the same time, the number of lung tumours dropped sharply and the mice lived much longer. This means that the absence of these two enzymes does not have any obvious side-effects in the lungs, and that lung tumour cells seem to be more sensitive to the treatment than normal lung cells.

“Our findings show that FT and GGT are promising targets for the treatment of lung cancer,” the researchers explain. “The next step in our research is to find out whether blocking these enzymes can have side-effects in other tissues.”

For more information, please contact:
Researcher Anna-Karin Sjögren, Department of Clinical and Molecular Medicine, Sahlgrenska Academy, tel. +46 (0)31 342 4723, e -mail: anna-karin.sjogren@wlab.gu.se
Researcher Meng Liu, Department of Clinical and Molecular Medicine, Sahlgrenska Academy, tel. +46 (0)31 3422164, e-mail: meng.liu@wlab.gu.se

via.uni-protokolle.de

Exposure within houses is predominantly due to release of radon-containing subsurface air from the soil into the building. Radon can penetrate into houses through leaks in the base plate or in the walls in contact with the soil.

It is thought that 300 cases of lung cancer per year could be prevented in Germany if the maximum radon concentration in residences was reduced to 100 Bq/m³. It is also necessary to identify buildings with high radon levels and to take structural measures if necessary.

Occupational physicians have long known that radon can cause lung cancer, particularly in uranium miners. For individuals without occupational exposure, radon is regarded as the second most important cause of lung cancer after smoking.

via:physorg.com