Sunday, 21 September 2014

65,000th visit...

Today will see the 65,000th visitor!

Friday, 19 September 2014

Lloyds Bank: Where you're better off dead than alive!

I'm starting a new blog so that people can share their experiences and dealings with Lloyds Bank Bereavement Centre.  Click here...New blog

My Mother, Ellen Patricia Sencier, died on my birthday back in December last year. She named my brother Paul and I as joint executors. I have a younger brother Andre, and a sister, Jacqueline. On this new blog I will be detailing events from when I first tried to contact my Mother's branch in Clacton just after her death, up until this week, when for the first time in 9 months, I finally got a reply! This was only because I had complained to the Banking Ombudsman. But should I have had to go that far?   

Nearly 50 attempts to get someone/anyone to communicate with me, failed.
E-mails, faxes, phone calls and letters all went unanswered until this week. 

It's a compelling story, unbelievable in places and a series of events that divided our family forever.

Monday, 8 September 2014

Prostate cancer drug candidate shows great promise...

By Arthur Hirsch, The Baltimore Sun
6:16 p.m. EDT, September 6, 2014

A white powdered chemical compound emerged from two University of Maryland School of Medicine laboratories more than 10 years ago with a name destined for oblivion, but a future that now looks promising as a treatment for the most challenging cases of prostate cancer.
Today, VN/124-1 is a drug candidate with a name — galeterone — a pharmaceutical company founded on its potential and a record of strong preliminary results in clinical trials with human patients.
The Food and Drug Administration has put galeterone on a fast track for approval to treat prostate cancer, which kills about 30,000 men a year in the United States. Researchers in hospitals and clinics across the country and in Canada are finishing the trial's second round and preparing for the third, expected to begin early next year.
Dr. Kevin J. Cullen, director of the University of Maryland's Marlene and Stewart Greenebaum Cancer Center, acknowledged that results are preliminary, but he said it's an auspicious beginning.
"I can think of maybe one other drug in the 30 years I've been doing oncology that showed these kind of results," Cullen said. He called it an "incredibly promising start for this medicine."
Dr. Mario Eisenberger, heading the clinical trial at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, said the drug has had impressive results, but "I don't think anyone can say at this point in time whether galeterone is going to be better than the other" drugs already used to treat prostate cancer.
Before galeterone was a medicine, it was a compound born of a collaboration that began in 1996 between two University of Maryland researchers, Angela M. H. Brodie and Vincent C.O. Njar.
The approach was built on work for which Brodie has won some of the most prestigious awards in the field — research not in prostate but breast cancer. In the last 10 years, she won the Charles F. Kettering Prize and the Dorothy P. Landon-AACR Prize for Translational Cancer Research for her work in the 1970s and 1980s helping to develop compounds that block production of estrogen, the female hormone, that fuels the growth of most breast cancers.
More recently, she's turned her attention to prostate cancer, which feeds on the male hormone. She wondered if the approach that worked with estrogen would work with the androgens, or hormones, that fuel prostate cancer: testosterone and the more potent dihydrotestosterone.
Up to now, one main treatment for the most challenging prostate cancers has been shutting down androgen production from the testicles. The procedure, referred to as castration, is most commonly done today by medication not surgery. The testicles produce about 90 percent of the body's androgen. Most of the rest is produced by the adrenal glands, and a small measure from the prostate tumor itself.
Njar and Brodie were looking for a way to fight prostate cancer that continutes after castration.
Their approach is one in a succession of hormone-based treatments that have been used for years, but it's different in combining several effects at once. This one works in three ways to interfere with androgen's effect on prostate cells.
The medication decreases androgen production and interferes with the process by which the substance binds to the prostate cell molecule that responds to the hormone, known as the receptor. These effects have been produced before, but galeterone is the only medication that also appears to damage the receptor itself.
The triple threat showed impressive results in tests with mice about 10 years ago. Brodie and Njar and their research team published results in the Journal of Medicinal Chemistry in 2005, concluding that the compound "is a potent inhibitor of human prostate tumor growth and is remarkably more effective than castration."
After that publication, Tokai Pharmaceuticals, a company in Cambridge, Massachusetts, named and licensed the compound as "galeterone." Clinical trials with human patients started in November 2009.
To fund its anticipated growth, Tokai applied in August to sell $75 million of stock in an initial public offering. While its stock sale is pending, company officials are not available for comment.
According to information posted on Tokai's website, researchers have given the drug to 200 patients in the first two trial phases.
Of the 49 patients in the first trial, 24 showed 30-percent reduction in prostate specific antigen, or PSA, and 11 showed a 50-percent cut. Elevated levels of PSA can be, but are not necessarily, a marker for prostate cancer.
In the second phase, 51 patients — both with and without metastasis, or cancer spread beyond the prostate — followed for 12 weeks also showed significant PSA reductions. Of this group, 82 percent to 85 percent experienced reductions of about a third, three-quarters saw a reduction by at least half.
Cullen said he was struck by the results even in the first phase, conducted less for effects on the cancer than to see how well patients can tolerate the medication at low doses. With such low doses in the first phase of a clinical trial, results like that are "almost unprecedented," he said.
In the third phase of the trial, galeterone will be compared to existing treatments, Brodie and Njar said, and could take up to another year.
The FDA "fast track" can in some cases cut years off the time it takes to bring a drug to market, Eisenberger said.
Galeterone causes none of the adverse effects associated with chemotherapy, including nausea and hair loss. So far, Brodie said, the chief side effect could be deficiency of cortisol, but that has not been a problem so far. The hormone plays a role in regulating blood sugar, suppressing immune response and metabolizing fat, protein and carbohydrates.
Eisenberger said the effects can include fatigue and itching, but nothing requiring cortisol treatment.
Brodie and Njar are making no bold pronouncements at this point, just eagerly awaiting further results.
"We are cautiously optimistic," Njar said.
"It's a wonderful thing if we can save lives," Brodie said.

Saturday, 6 September 2014

Exciting new tool to test cancer drugs and personalize cancer treatment...

Stained pathology slides of a patient’s tumor (right) and of an organoid made from that tumor (left).
Credit: Image courtesy of Memorial Sloan Kettering Cancer Center
Research led by investigators at Memorial Sloan Kettering Cancer Center has shown for the first time that organoids derived from human prostate cancer tumors can be grown in the laboratory, giving researchers an exciting new tool to test cancer drugs and personalize cancer treatment.
The researchers, whose results were published today in Cell, successfully grew six prostate cancer organoids from biopsies of patients with metastatic prostate cancer and a seventh organoid from a patient's circulating tumor cells. Organoids are three-dimensional structures composed of cells that are grouped together and spatially organized like an organ. The histology, or tissue structure, of the prostate cancer organoids is highly similar to the metastasis sample from which they came. Sequencing of the metastasis samples and the matched organoids showed that each organoid is genetically identical to the patient's cancer from which it originated.
"Identifying the molecular biomarkers that indicate whether a drug will work or why a drug stops working is paramount for the precision treatment of cancer," said Yu Chen, MD, PhD, Assistant Attending Physician in the Genitourinary Oncology Service and Human Oncology and Pathogenesis Program at MSK. "But we are limited in our capacity to test drugs -- especially in the prostate cancer setting, where only a handful of prostate cancer cell lines are available to researchers."
With the addition of the seven prostate cancer organoids described in the Cell paper, Dr. Chen's team has effectively doubled the number of existing prostate cancer cell lines.
"We now have a new resource at our disposal that captures the molecular diversity of prostate cancer. This will be an invaluable tool we can use to test drug sensitivity," he added.
The use of organoids in studying cancer is relatively new, but the field is exploding quickly according to Dr. Chen. In 2009, Hans Clevers, MD, PhD, of the Hubrecht Institute in the Netherlands demonstrated that intestinal stem cells could form organoids. Dr. Clevers is the lead author on a companion piece also published in Cell today that describes how to create healthy prostate organoids. Dr. Chen's paper is the first to demonstrate that organoids can be grown from prostate cancer samples.
The prostate cancer organoids can be used to test multiple drugs simultaneously, and Dr. Chen's team is already retrospectively comparing the drugs given to each patient against the organoids for clues about why the patient did or didn't respond to therapy. In the future, it's possible that drugs could be tested on a patient's organoid before being given to the patient to truly personalize treatment.
After skin cancer, prostate cancer is the most common cancer in American men -- about 233,000 new cases will be diagnosed in 2014. It is also the second leading cause of cancer death in men; 1 in 36 men will die of the disease.
Despite its prevalence, prostate cancer has been difficult to replicate in the lab. Many mutations that play a role in its growth are not represented in the cell lines currently available. Cell lines can also differ from their original source, and because they are composed of single cells, they do not offer the robust information that an organoid -- which more closely resembles a living organ -- can provide.

Story Source:
The above story is based on materials provided by Memorial Sloan Kettering Cancer Center. The original article was written by Julie Grisham.  

Wednesday, 3 September 2014

Scottish Independence? If in doubt read on...

Would you vote for the package below? Because essentially, that's what you will be doing if you vote 'No'!

"Imagine Scotland was already independent and we were about to have a referendum on whether to join a union with the rest of the UK.
Could the Pro-union side convince us that getting together would be better when we were told what would happen to Scotland after such a union? 

Some bullet points from the campaign…

-Your main Parliament will move 600 miles away, and your MPs will be in a tiny minority & will therefore have limited ability to effect policy on your behalf

-Scotland will get a government it didn’t vote for.

-All of your oil and gas revenues will be handed over to the treasury in London.
-Even though not 1 inch of track will touch Scottish soil your taxpayers will contribute £4.2bn to the HS2 project.
-Your taxpayers will also subsidise the crossrail project to the tune of £4.2bn
-The biggest nuclear weapons facility in Western Europe will be built on the river Clyde, just 30 miles from your largest city.
-Even though you only have 8.2% of the UK’s population you will contribute 9.9% of the UK’s total tax take yet will only receive 9.3% of that tax take back to spend in Scotland (you will lose £4.4bn per year to the UK treasury)
-You will devolve all of the economic levers you have used to shape your economy directly to London and will now only have control of 7% of your economy
-Even though 79% of your MP's voted against it we will privitise your publicly owned mail service
-Even though 91% of your MPs voted against the bedroom tax in your parliament, we will impose it.
-Even though 82% of your MP's believed that a VAT increase would be detrimental to your economy, we will impose a VAT increase.
-You will join a country whose health and education services are rapidly being privatised.
-Now and again you’ll get dragged into an illegal foreign war.
-An austerity budget will be imposed from London cutting jobs and threatening vital public services even though 81% of your MP's voted against the cuts.
-The financial regulation system will be so weak and so lax that your whole economy will be brought to the brink of collapse.
-The most weak and vulnerable in society, instead of getting the protection and support they deserve will be interrogated and humiliated in an effort to get them off the meagre levels of support to which they are entitled.

Who in Scotland would vote for such a package?

Who would vote for that union?

So why would anyone vote to remain in such a union now?

This is about democratic ownership, social responsibility and the fact that Scotland on its own will be economically stronger from day one of independence....."

(I discovered this article when Forbes Manson shared it on Facebook)