Well what has happened to our weather. We have had so much rain today after a lovely sunny start the black clouds rolled over and dropped all the rain the held. It was running down the windows like a river. Crazy.
We still went to the car to take the dog out to the park, well I keep my sweets in the glove box and I love popping one in my mouth.
We did manage to get around the Park but the wind wasn’t very nice and even im my winter coat it was freezing,
It was a quieter day today now the EAF conference is over and people are returning to their homelands
Seems there was a lot of mutual business done and ideas shared so these will unravel in the future.
Yvonne shared this with us —
This is the Dr. J. Stumphius Recognition Award of the European Asbestos Forum, presented by Hans van der Wart of Shield Group International to Prof. Nico van Zandwijk (ADRI), who could be a Nobel Prize candidate for discovering a potential cure to mesothelioma. Showing many people lifting a burden together, the award perfectly represents the EAF motto: Sharing makes us stronger.
On finding more info I was surprised that Australia has a purpose built Asbestos Diseases Research Institute in Sydney.
Professor van Zandwijk’s major research interest is in thoracic oncology. He founded the department of Thoracic Oncology at the Netherlands Cancer Institute and was head of department from 1985 to 2008. His department was the first to study mediastinal staging, locoregional chemotherapy and photodynamic therapy in malignant mesothelioma. In 2007, Professor van Zandwijk was asked to become the inaugural director of the purpose built Asbestos Diseases Research Institute in Sydney. Over the years he has been involved in many clinical trials, translational research and mentoring more than 20 students who have become research leaders in the own right.
So many wonderful people out there working away at finding the answers.
We received an email from the Saatchi Bill Headquarters
Following the General Election and the state opening of Parliament the Medical Innovation Bill is to be reintroduced into Parliament.
A ballot was held on the evening of the state opening to determine the order of introduction of private members’ bills in the following days and weeks.
The Medical Innovation Bill is 28th in the queue and is due to be introduced into the House of Lords on June 8th 2015.
There is no guarantee that the Bill will get very far. There is a lot of competition for Parliamentary time and the majority of Private Member’s Bills do not progress to become Acts of Parliament.
Many thanks for all your support and interest in the Bill to date. We’ll keep you updated on the Bill’s progress.
House of Lords Private Members Ballot
This will start the pessimists nattering again and rising on twitter but I would rather be a pessimist and say Well done and lets get in for the fight.
I had another email to cancel the Date at the House of Commons June 23 with the British Lung Foundation but they have moved it to July 16th, I have to move my drug day to the Wednesday, so a busy week but it will be worth it .
The BLF will still be launching the most comprehensive overview of lung disease in the UK currently available, and the research being published will mark the 30th anniversary of the BLF. This will include lung disease rates and data specific to your area.
The launch will now take place at 4-6pm, Tuesday 14 July, in Terrace Dining Room A, House of Commons.
We would be delighted if you could still attend.
The event will be hosted by Dr Sarah Wollaston MP, and attended by parliamentarians, clinicians, researchers and officials. This new research will be a milestone in our understanding of the nation’s lung health.
Formal invitations will be sent out shortly.
30years is a huge achievement and they grow all the time
Campaigning for the future
This year is the 30th anniversary of the BLF. We will renew our determination to make a difference to people living with a lung condition and campaign for positive change in the nation’s lung health. Our focus will remain on COPD, lung cancer, mesothelioma and IPF. We will campaign to increase people’s awareness that feeling out of breath is something they need to take seriously and get checked out.
Stopping people getting lung disease remains a priority. We will push to ensure that laws on standardised tobacco packaging and the ban on smoking in cars carrying children are introduced, and that more is done to tackle smoking rates throughout the UK.
We will also continue to press for sustainable funding dedicated to mesothelioma research. It is unacceptable that the UK has the highest rate of mesothelioma in the world and there is so little research, even though there is no cure.
More support for IPF
Our IPF project will build on a successful first year. We will increase the number of BLF support groups, improve the reach of our health information, and campaign to raise awareness.
Helping children affected by lung conditions
Children’s lung health will be a new priority for the British Lung Foundation. We’ll start by consulting parents and health care professionals, and then plan how to raise awareness, provide information, and support families.
Continuing our research for better lung health
Over the past three decades, we’ve spent more than £24 million on scientific research into a wide range of lung conditions. In the next 12 months, we’ll start to put our new research strategy into action and aim to invest more in research in the future.
We’ll also conclude a major study to evaluate the nation’s lung health. This will draw together, for the first time, comprehensive information about respiratory disease across the UK. We will share findings and use them to campaign for improvements.
Bringing everyone together
We’re welcoming new trustees to our board to better represent people living with a lung condition and the wider health care community. Their experiences and point of view will have a big impact on our work and help us to carry out our ambitious plans in the years ahead.
We will strive to improve our support for everyone affected by a lung condition and to raise funds to support this important work.
But we need you to get involved. We could not do all that we do without you.
Find out more about what we achieved together in 2013-14 by checking out our
The best bit is saved until last
They are publishing my trial tomorrow
In a report of a proof-of-principle study of patients with colon and other cancers for whom standard therapies failed, researchers at the Johns Hopkins Kimmel Cancer Center say that mistakes in so-called mismatch repair genes, first identified by Johns Hopkins and other scientists two decades ago, may accurately predict who will respond to certain immunotherapy drugs known as PD-1 inhibitors. Such drugs aim to disarm systems developed by cancer cells to evade detection and destruction by immune system cells.
Results of the trial with pembrolizumab, marketed as Keytruda, will be presented at the American Society of Clinical Oncology 2015 Annual Meeting and published online May 30 in the New England Journal of Medicine.
“This study gives us a solid clue about how immunotherapy may work in cancer and how to guide immunotherapy treatment decisions based on the genetic signatures of a cancer rather than class of cells or organ of origin,” says Luis Diaz Jr., M.D., an oncologist at the Johns Hopkins Kimmel Cancer Center, a member of the Ludwig Center at Johns Hopkins and the director of the Swim Across America Laboratory at Johns Hopkins.
“Defects in mismatch repair genes are found in a small percentage of many cancer types, and this type of biomarker for immunotherapy response could apply to tumors containing errors in other DNA repair genes, as well,” says Dung Le, M.D., an oncologist at the Johns Hopkins Kimmel Cancer Center. “Using a predictive biomarker can help us direct the use of immunotherapy drugs to patients who are more likely to respond, avoiding giving people expensive and time-consuming treatments that are not likely to work or delaying the use of other treatments.”
For the Johns Hopkins-led study, scientists enrolled and treated 48 patients with cancer, primarily at The Johns Hopkins Hospital, and divided them into three groups. Other patients enrolled were from Providence Cancer Center in Oregon, the University of Pittsburgh Cancer Institute, Stanford University and The Ohio State University Comprehensive Cancer Center.
In one group of 13 patients with advanced colon and rectal cancers and mismatch repair gene defects, eight had partial responses to pembrolizumab, meaning their cancers shrunk by at least 30 percent in diameter. Four patients had prolonged disease stability, and one patient experienced disease progression. In another group of patients with colon and rectal cancer who had no defects in mismatch repair genes, all 25 failed to respond. In a third group of 10 patients with a variety of other cancers that tested positive for mismatch repair gene defects (four with pancreatic/bile duct cancers, two with uterine cancers, two with small bowel cancers, one with stomach cancer and one with prostate cancer), one patient with uterine cancer had a complete response, meaning there was no radiographic evidence of their cancer, five had partial responses, one had stable disease and three patients’ cancers progressed.
All patients had received and were no longer responding to previous therapies.
“It’s rare for patients with colon cancer who have failed all standard therapies to respond and most of them only have a few months to live,” says Kenneth W. Kinzler, Ph.D., co-director of the Ludwig Center at Johns Hopkins. “While it’s promising to see that patients with mistakes in mismatch repair genes responded more often to immunotherapy than those who did not have these mistakes, we need to test this idea in more patients and potentially earlier on in the sequence of therapies for these advanced cancers.”
Median overall and disease progression-free survival in the colon cancer group with mismatch repair-defect group have not been reached yet, since several patients in this group have continued to respond to the immunotherapy drug for more than 12 months. Median follow-up for this group is 36 weeks (ranging from five to 55 weeks). In the group of patients with colon cancer who lack the mismatch repair errors, median overall survival was 7.6 months, and median disease progression was 2.3 months. These patients were followed for up to 42 weeks. In the third group of patients with mistakes in mismatch repair genes, median overall survival has not been reached, and their median disease progression-free survival was 5.4 months after being followed for up to 42 weeks.
For the study, overall response rates and some disease progression-free survival rates were classified and assessed as “immune-related,” because patients often experience some tumor growth before shrinkage begins in those who respond. Typically, such initial tumor growth, also known as pseudo-progression, would prompt researchers to remove patients from a clinical trial, but scientists have recognized the temporary growth trend in immunotherapy trials and created new definitions of response to account for it, say the Johns Hopkins scientists.
The research team also accounted for differences in how long each patient had metastatic disease and his or her length of response to previous therapies.
Tests for mistakes in mismatch repair genes are commercially available and used routinely for newly diagnosed colon and endometrial cancer patients, according to Le. Pembrolizumab, sold by Merck, is approved by the Food and Drug Administration for certain patients with melanoma. The drug blocks a protein on immune cells called PD-1 and takes the brakes off of these immune cells so they can attack cancer cells.
Its cost can reach more than $100,000 per year per patient, a cost that gives urgency to sorting out which patients stand to benefit and which do not.
Mistakes in mismatch repair genes, which occur in sporadic and hereditary forms of colorectal, endometrial, stomach, biliary tract, pancreas, ovarian and small intestine cancer, disable cells’ ability to repair errors in the DNA replication process, which triggers unchecked cellular growth, a hallmark of cancer. The mutations were first identified in 1993 by co-authors of the current study, including Bert Vogelstein, M.D., of the Ludwig Center at Johns Hopkins and an investigator for the Howard Hughes Medical Institute; Nickolas Papadopoulos, Ph.D., and Kenneth Kinzler, Ph.D., also of Johns Hopkins’ Ludwig Center; and Albert de la Chapelle at Ohio State University.
Two decades later, an idea for the current study took root when Diaz and his Ludwig Center colleagues met with other Johns Hopkins scientists who led one of the first large clinical trials of a type of immunotherapy similar to the one used in the current study. In it, a single patient with colon cancer in the trial responded to the drug when other patients with colon cancer did not. The search began, Diaz says, for why that one patient responded.
Diaz and his colleagues previously proposed that immunotherapy may work best in patients with more mutations in their cancer cells, because multiple mutations trigger production of more abnormal proteins in cancer cells and, in turn, may cause the immune system to mount a bigger response against cancer cells with more “foreign” proteins. Knowing that a small percentage of patients with colon cancer have errors in mismatch repair genes, which produce thousands more mutations in tumors than patients without the defects, they guessed that the lone colon cancer responder in the earlier study had such error-prone mismatch repair genes, a guess that was subsequently verified when the team sequenced the genome of the patient’s tumor.