Life's Roller Coaster

If I'm missing, or not taking messages sorry – I'm more angry about letting my friends down than YOU will ever be at being let down! Unfortunately that is sometimes a side effect of Cancer! Mea Culpa: may I blame being short fused & grumpy on it too! My first symptoms presented in Nov-1998 – Follow The Trail on >DIARY of CANCER< Immediately Below!

Early-Stage Breast Condition – May Not Require Cancer Treatment!

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Early-Stage Breast Condition
May Not Require Cancer Treatment

By GINA KOLATAAUG. 20, 2015

Therese Taylor of Mississauga, Ontario, had a mastectomy four years ago
after a diagnosis of ductal carcinoma in situ.
She now believes it was unnecessary.
Credit Michelle Siu for The New York Times

As many as 60,000 American women each year are told they have a very early stage of breast cancer — Stage 0, as it is commonly known — a possible precursor to what could be a deadly tumor. And almost every one of the women has either a lumpectomy or a mastectomy, and often a double mastectomy, removing a healthy breast as well.

Yet it now appears that treatment may make no difference in their outcomes. Patients with this condition had close to the same likelihood of dying of breast cancer as women in the general population, and the few who died did so despite treatment, not for lack of it, researchers reported Thursday in JAMA Oncology.

Picture Your Life: Faces of Breast Cancer
A radiologist uses a magnifying glass to check mammograms for breast cancer.
Well: Scientists Seek to Rein In Diagnoses of Cancer JULY 29, 2013
Essay: Cancer by Any Other Name Would Not Be as Terrifying NOV. 21, 2011
A year after Monica Long’s partial mastectomy, a pathologist determined that she never had cancer.
Prone to Error: Earliest Steps to Find Cancer JULY 19, 2010

Their conclusions were based on the most extensive collection of data ever analyzed on the condition, known as ductal carcinoma in situ, or D.C.I.S.: 100,000 women followed for 20 years. The findings are likely to fan debate about whether tens of thousands of patients are undergoing unnecessary and sometimes disfiguring treatments for premalignant conditions that are unlikely to develop into life-threatening cancers.

We asked our readers to share insights from their experiences with breast cancer. Here are some of their stories.

Diagnoses of D.C.I.S., involving abnormal cells confined to the milk ducts of the breast, have soared in recent decades. They now account for as much as a quarter of cancer diagnoses made with mammography, as radiologists find smaller and smaller lesions. But the new data on outcomes raises provocative questions: Is D.C.I.S. cancer, a precursor to the disease or just a risk factor for some women? Is there any reason for most patients with the diagnosis to receive brutal therapies? If treatment does not make a difference, should women even be told they have the condition?

Dr. Otis W. Brawley, chief medical officer at the American Cancer Society, said he was not ready to abandon treatment until a large clinical trial is done that randomly assigns women to receive mastectomies, lumpectomies or no treatment for D.C.I.S., and that shows treatment is unnecessary for most patients. But Dr. Brawley, who was not involved in the study, also said he had no doubt that treatment had been excessive.

“In medicine, we have a tendency to get too enthusiastic about a technique and overuse it,” Dr. Brawley said. “This has happened with the treatment of D.C.I.S.”

A majority of the 100,000 patients in the database the researchers used, from a national cancer registry, had lumpectomies, and nearly all the rest had mastectomies, the new study found. Their chance of dying of breast cancer in the two decades after treatment was 3.3 percent, no matter which procedure they had, about the same as an average woman’s chance of dying of breast cancer, said Dr. Laura J. Esserman, a breast cancer surgeon and researcher at the University of California, San Francisco, who wrote an editorial accompanying the study.

The data showed that some patients were at higher risk: those younger than 40, black women, and those whose abnormal cells had molecular markers found in advanced cancers with poorer prognoses.

D.C.I.S. has long been regarded as a precursor to potentially deadly invasive cancers, analogous to colon polyps that can turn into colon cancer, said Dr. Steven A. Narod, the lead author of the paper and a researcher at Women’s College Research Institute in Toronto. The treatment strategy has been to get rid of the tiny specks of abnormal breast cells, just as doctors get rid of colon polyps when they see them in a colonoscopy.

But if that understanding of the condition had played out as expected, women who had an entire breast removed, or even both breasts as a sort of double precaution, should have been protected from invasive breast cancer. Instead, the findings showed, they had the same risk as those who had a lumpectomy. Almost no women went untreated, so it is not clear if as a group, they did worse.

But some women who died of breast cancer ended up with the disease throughout their body without ever having it recur in their breast — many, in fact, had no breast because they had had a mastectomy. Those very rare fatal cases of D.C.I.S. followed by fatal breast cancer, Dr. Narod concluded, had most likely already spread at the time of detection. As for the rest, he said, they were never going to spread anyway.

Dr. Esserman said that if deadly breast cancers started out as D.C.I.S., the incidence of invasive breast cancers should have plummeted with rising detection rates. That has not happened, even though in the pre-mammography era, before about 1980, the number of women found to have D.C.I.S. was only in the hundreds. Nearly 240,000 women receive diagnoses of invasive breast cancer each year.

Those facts lead Dr. Narod to a blunt view. After a surgeon has removed the aberrant cells for the biopsy, he said, “I think the best way to treat D.C.I.S. is to do nothing.”

Others drew back from that advice.

Dr. Monica Morrow, chief breast cancer surgeon at Memorial Sloan Kettering Cancer Center, said it made more sense to view D.C.I.S. as a cancer precursor that should be treated the way it is now, with a lumpectomy or mastectomy. She questioned whether those women who were treated and ended up dying of breast cancer anyway had been misdiagnosed.

In some cases, pathologists look at only a small amount of tumor, Dr. Morrow said, and could have missed areas of invasive cancer. Even the best mastectomy leaves cells behind, she added, which could explain why a small number of women with D.C.I.S. who had mastectomies, even double mastectomies, died of breast cancer.

USPSTF data pointed to this lack of efficacy a YEAR AGO! And the published their findings and the media yawned, and the women’s groups…
Barry 7 minutes ago

A representative of the American Association of Cancer Surgeons responded, “But … But … But, how are we going to make our mortgage…
transposition 8 minutes ago

This finding is consistent with the growing body of evidence that our approach to breast cancer has been too aggressive, particularly when…

Dr. Brawley said the new study, by showing which D.C.I.S. patients were at highest risk, would help enormously in defining who might benefit from treatment. It could not show that the high-risk women — young, black or with tumors with ominous molecular markers — were helped by treatment because there were too few of them, and pretty much every one of them was treated. But Dr. Brawley said he would like to see clinical trials that addressed that question, as well as whether the rest of the women with D.C.I.S., 80 percent of them, would be fine without treatment or with anti-estrogen drugs like tamoxifen or raloxifene that can reduce overall breast cancer risk.

The notion that most women with D.C.I.S. might not need mastectomies or lumpectomies can be agonizing for those, like Therese Taylor of Mississauga, Ontario, who have already gone through such treatment. Four years ago, when she was 51, a doctor sent her for a mammogram, telling her he felt a lump in her right breast. That breast was fine, but it turned out she had D.C.I.S. in her left breast. A surgeon, she said, told her that “it was consistent with cancer” and that she should have a mastectomy.

“I went into a state of shock and fear,” Ms. Taylor said. She had the surgery.She regrets it. “It takes away your feeling of attractiveness,” she said. “Compared to women who really have cancer, it is nothing. But the mastectomy was for no reason, and that’s why it bothers me.”

But if D.C.I.S. is actually a risk factor for invasive cancer, rather than a precursor, it might be possible to help women reduce their risk, perhaps with hormonal or immunological therapies to change the breast environment, making it less hospitable to cancer cells, Dr. Esserman said.

“As we learn more, that gives us the courage to try something different,” she said.

The stakes in this debate are high. Karuna Jaggar, executive director of Breast Cancer Action, an education and activist organization, said women tended not to appreciate the harms of overtreatment and often overestimated their risk of dying of cancer, making them react with terror.

“Treatment comes with short- and long-term impacts,” Ms. Jaggar said, noting that women who get cancer treatment are less likely to be employed several years later and tend to earn less than before. There are emotional tolls and strains on relationships. And there can be complications from breast cancer surgery, including lymphedema, a permanent pooling of lymphatic fluid in the arm.

“These are not theoretical harms,” Ms. Jaggar said.

To view the original article CLICK HERE
.
Regards,
Greg_L-W.
.
 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
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Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
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You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
Accuracy & Copyright Statement: CLICK HERE
Summary, archive, facts & comments on UKIP: http://UKIP-vs-EUkip.com
DO MAKE USE of LINKS & >Right Side Bar< & The Top Bar >PAGES<
Also:
Details & Links: http://GregLanceWatkins.com
UKIP Its ASSOCIATES & DETAILS: CLICK HERE
Views I almost Totally Share: CLICK HERE
General Stuff archive: http://gl-w.blogspot.com
General Stuff ongoing: http://gl-w.com
Health Blog. Archive: http://GregLW.blogspot.com
Health Blog. Ongoing: http:GregLW.com

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BCG Treatment for Bladder Cancer

BCG Treatment for Bladder Cancer
.

 Please Be Sure To

& Link to my My Blogs
To Spread The Facts World Wide

To Give Hope & Information

 .
Regards,
Greg_L-W.
.
 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
.
You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
Accuracy & Copyright Statement: CLICK HERE
Summary, archive, facts & comments on UKIP: http://UKIP-vs-EUkip.com
DO MAKE USE of LINKS & >Right Side Bar< & The Top Bar >PAGES<
Also:
Details & Links: http://GregLanceWatkins.com
UKIP Its ASSOCIATES & DETAILS: CLICK HERE
Views I almost Totally Share: CLICK HERE
General Stuff archive: http://gl-w.blogspot.com
General Stuff ongoing: http://gl-w.com
Health Blog. Archive: http://GregLW.blogspot.com
Health Blog. Ongoing: http:GregLW.com

TWITTER: Greg_LW

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Chimeric Antigen Receptor T-Cell Therapy for Cancer

Chimeric Antigen Receptor T-Cell Therapy for Cancer
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Chimeric Antigen Receptor T-Cell Therapy

Tumor-targeting T-cell therapies are generating remarkable remissions in hard-to-beat cancers—and attracting millions of dollars of investment along the way.

By Vicki Brower | April 1, 2015

 
BUILDING A BETTER T-CELL: By modifying T cells to express chimeric antigen receptors (CARs) that recognize cancer-specific antigens, researchers can prime the cells to recognize and kill tumor cells that would otherwise escape immune detection. The process involves extracting a patient’s T cells, transfecting them with a gene for a CAR, then reinfusing the transfected cells into the patient.© LUCY READING-IKKANDALast December, scientists at Juno Therapeutics reported at the American Society of Hematology (ASH) meeting that, in an ongoing Phase 1 trial, its chimeric antigen receptor (CAR) T-cell therapy, JCAR015, put 24 of 27 adults with refractive acute lymphoblastic leukemia (ALL) into remission, with six patients remaining disease free for more than a year (ASH 2014, Abstract 382, 2014). This disease is extremely hard to treat and progresses rapidly when it becomes refractory; most patients die within a few months. “This response rate is unprecedented for patients who had stopped responding to all other treatments,” says Michel Sadelain, a founding director of Memorial Sloan Kettering’s Center for Cell Engineering and a cofounder of Juno.
Founded just a year earlier, the Seattle-based company now has four CD19-targeting CAR T-cell therapies in trials. The premise is simple: extract a patient’s T cells from blood and train them to recognize and kill cancer by modifying them with a viral vector to express an artificial, or chimeric, receptor specific for a particular cancer-associated antigen—in this case, CD19, an antigen expressed in  B-cell–related  blood cancers—then reinfuse the cells back into the patient. (See illustration at left.) The engineered cells recognize and kill cancerous cells, while reactivating other immune players that have been dampened by cancer’s inhibitory signals. “CAR therapy is at the same time cell therapy, gene therapy, and immunotherapy,” says Sadelain. “It represents a radical departure from all forms of medicine in existence until now.” Promising preclinical results have moved Juno’s CD19 therapies into trials for ALL, non-Hodgkin’s lymphoma, and chronic lymphocytic leukemia (CLL), and the company has three more CAR T-cell immunotherapies for a number of solid cancers close behind.

A few weeks after the ASH meeting, Juno went public for a whopping $264.6 million, the largest biotech initial public offering (IPO) of 2014. Within a month, the company’s valuation rose from $2 billion to $4.7 billion, the largest among biotechs in a decade. By the end of 2016, the company plans to have 10 drug trials for six diseases up and running using CAR T cells produced in a brand-new manufacturing facility.

And Juno is not alone. This relatively new sector is experiencing a frenzy of scientific activity, corporate partnering, and financing that took off in late 2013, continued throughout 2014, and moved straight into the new year with no sign of letting up. By now, most major pharmaceutical companies have jumped into the CAR T-cell arena. In the past two years alone, at least half a dozen companies have made deals worth hundreds of millions of dollars up front, with much more expected in the future as products move through the pipeline. (See chart below.) This influx of funding is now supporting dozens of clinical trials.

While most of these studies are currently aimed at late-stage disease for which other therapeutic options have failed, researchers in the field anticipate that these immunotherapies could replace standard cancer treatments in the future. “While we are evaluating these therapies in advanced cancer now, we absolutely believe that they have the potential to become frontline therapies,” Sadelain says.

Long time coming

CAR T-cell therapy has had a lengthy run-up to what may appear to be overnight success. The first CAR T cells were developed at the Weizmann Institute of Science in Israel in the late 1980s by chemist and immunologist Zelig Eshhar. In 1990, Eshhar took a year-long sabbatical to join Steven Rosenberg at the National Institutes of Health, where they prepared CARs that targeted human melanoma. “We designed CAR T cells to overcome a number of problems in getting T cells to attack cancer,” says Eshhar. These problems included a tumor’s ability to escape immune recognition by silencing the major histocompatibility complex molecules and the generally immunosuppressive tumor microenvironment.


NEW AND IMPROVED CARs: Zelig Eshhar and Steven Rosenberg constructed the first CAR T cells using a modular design, including a specific cancer-targeting antibody outside the cell, a transmembrane component, and an intracellular costimulatory signaling domain that amplifies the activation of the CAR T cells. Second- and third-generation CAR T-cell technologies have added additional costimulatory domains within the cells, as well as additional receptors to improve targeting of the T-cell attack and minimize side effects.
© LUCY READING-IKKANDA

Eshhar and Rosenberg constructed the CAR T cells with a modular design that included a specific cancer-targeting antibody, and later added a costimulatory signaling domain that amplifies the activation of the cells, giving them a stronger signal to multiply and kill cancer cells. Since that early work, researchers in both academia and industry have developed and tweaked each section of the modular design. (See illustration above.) “Ultimately, we needed 20 years to learn how to supercharge these cells to deliver anticancer activity,” says Arie Belldegrun, president and CEO of Kite Pharma in Santa Monica, California, which is assessing CAR T cells in six trials for B cell leukemia and lymphomas, and glioblastoma. Eshhar, a member of Kite Pharma’s scientific advisory board, continues to collaborate with Rosenberg, who serves as a special advisor to the company.

Juno is now working on two second-generation CAR technologies that incorporate mechanisms to further amplify T-cell activation or to dampen it, in the case of adverse reactions. (See “Safety concerns.”) These so-called “armored” chimeric antigen receptors are designed to combat the inhibitory tumor microenvironment by incorporating a signaling protein such as IL-12, which stimulates T-cell activation and recruitment. Juno believes “armored CAR” technology will be especially useful for solid tumors, whose microenvironment and potent immunosuppressive mechanisms can make raising antitumor responses more challenging.

Like Juno, Houston, Texas–based Bellicum Pharmaceuticals is working on refinements for next-generation CAR T-cell treatments. To better control antigen activation by its CAR T cells, for example, Bellicum is separating its dual costimulatory domain from the antigen-recognition domain, moving it onto a separate molecular switch that can be controlled by the small-molecule drug rimiducid. These T cells, known as GoCAR-Ts, can only be fully activated when they are exposed to both cancer cells and the drug.

In addition to altering the components of the CAR T cells themselves, researchers are also experimenting with different methods to introduce the receptors into the patients’ cells. At MD Anderson Cancer Center in Houston, Laurence Cooper and his colleagues are using a nonviral system called “Sleeping Beauty,” licensed from the University of Minnesota’s Perry Hackett, that relies on a transposon derived from fish to paste any desired gene into the genome. “This system employs electroporation [an electric current] to introduce elements of the Sleeping Beauty system into T cells,” says Cooper, who hopes the system will be less complex and cheaper to use than viral vectors.

While CAR T cells are being tested first as monotherapies, researchers are also giving thought to how best to use CAR T cells with other immunotherapies in the future. “We are excited about combining checkpoint inhibitors such as PD-1 [programmed death-1] inhibitors and anti-CTLA4 [anti-cytotoxic T-lymphocyte antigen 4] drugs with CAR T cells,” Eshhar says.

A frenzy of deal making

Over the past few years, the industry has been a hive of activity, with a half dozen companies forging deals valued at more than a half billion dollars in total. In addition to the perceived financial potential of these therapies, the feeding frenzy may in part be attributable to the fact that regulatory authorities are giving CAR T-cell treatments priority review for filling unmet medical needs. Many of these therapies are receiving orphan or breakthrough status from the US Food and Drug Administration (FDA), bringing expedited regulatory review, which translates into earlier realization of financial benefits from more rapid market entry. In November 2014, for example, the FDA granted orphan status to Juno’s JCAR015. Kite’s KTE-C19 for refractory aggressive non-Hodgkin’s lymphoma also recently received the designation from both the FDA and the European Medicines Agency. And the University of Pennsylvania /Novartis’s CTL019 for ALL received breakthrough status last July.

CAR T-CELL DEALS

Institution/Company Date Partner Terms
University of Pennsylvania August 2012 Novartis Undisclosed
Celgene March 2013 Bluebird Bio, Baylor College of Medicine Unspecified upfront payment plus up to $225 million per product in option fees and milestone payments
Cellectis June 2014 Pfizer $80 million upfront plus up to $185 million per product and royalties
Cellectis January 2015 Ohio State University Undisclosed
Kite Pharma January 2015 Amgen $60 million upfront and up to $525 million per product in milestone payments, plus royalties on sales and IP licensing
Md Anderson January 2015 Ziopharm, Intrexon $100 million in stock and $15–20 million/year for 3 years

A new report by EP Vantage, the editorial team at life science market intelligence firm Evaluate Ltd, notes that while investor enthusiasm for this sector is unlikely to diminish anytime soon, “there may be hidden dangers” for those in it to make a big return. “CAR T therapy looks like it’s becoming little short of a revolution in the treatment of some cancer types, but numerous risks are being lost in the hype,” writes report author Jacob Plieth, a biochemist by training. “It is important to appreciate the risks as well as the opportunities to have a clear understanding of the market potential of these therapies and their developers.”

Clinical results spark hope

In 2011, the Penn group described the results of an early trial of its CTL019 CAR T-cell treatment in three advanced chronic lymphocytic leukemia (CLL) patients (Sci Transl Med, 3:95ra73, 2011). The findings—including two patients who have now remained in remission 4.5 years after their treatment—served as an early demonstration that CAR T cells can successfully treat patients with late-stage disease. The team has now tested CAR T-cell therapies in about 125 people, with six different trials underway for pediatric and adult ALL, CLL, multiple myeloma, and non-Hodgkin’s lymphoma. Other CAR T-cell therapies are in trials for solid tumors, including ovarian, breast, and pancreatic cancers, and mesothelioma and glioblastoma.

CAR T-CELL BIOTECH IPOs

Company Date Value
Kite Pharma June 2014 $134.1 million
Bellicum December 2014 $160 million
Juno December 2014 $264.6 million
Cellectis March 2015 $228 million

“One of the exciting things about these cells is that they expand to high numbers and maintain long-term functional persistence,” says David Porter, a leukemia specialist and director of blood and marrow transplantation at Penn.

In a recent Penn study of 30 children and adults with relapsed or refractory ALL who received CTL019, 90 percent achieved total remission, and 78 percent were still living at the end of the study two years later (NEJM, 371:1507-17, 2014). Moreover, “very few patients—three—got a bone marrow transplant after CTL019, suggesting that this could be a replacement for bone marrow transplant and not just a bridge to transplant,” added senior author Stephan Grupp, director of translational research for the Center for Childhood Cancer Research at the Children’s Hospital of Philadelphia.

At ASH, Grupp discussed a follow-up study, including 39 pediatric patients, which showed a 92 percent complete remission rate following CTL019 treatment. Of those, 76 percent remain in complete remission after six months (ASH 2014, Abstract 380, 2014). “The first ALL patient treated is still in remission nearly three years later,” says Grupp. In September, Novartis pledged $20 million to build a Center for Advanced Cellular Therapeutics to manufacture CAR T cells on the Penn campus, to be completed next year. Penn is now conducting pilot trials aimed at solid tumors, including mesothelioma; ovarian, breast, and pancreatic cancers; and glioblastoma.

A team at the National Cancer Institute, including Rosenberg, has also reported successes with CAR T cell therapy, focusing on patients with refractory diffuse large B-cell lymphoma, an aggressive disease for which survival without treatment is measured in months. Following treatment with CD19-targeting T cells, 22 of 27 patients had either complete or partial remissions; 10 have remained cancer free for up to 37 months (ASH 2014, Abstract 550, 2014). These and other trials have demonstrated that CAR T-cell therapies can successfully treat leukemias and lymphomas in some patients for whom there are no other treatments.

There are currently many other CAR T-cell trials underway in leukemia and lymphoma, and more beginning in the near future. Scientists in this arena are energized by these and other results, and many see CAR T-cell therapies as the future of cancer treatment. “I believe these trials indicate that chemotherapy may be on its way out,” says MD Anderson’s Cooper.

Vicki Brower is a freelance science writer living in New York City.

SAFETY CONCERNS
Despite the growing number and length of remissions using CAR T-cell therapy to treat leukemias and lymphomas, key challenges remain—first and foremost, safety. There have been a half-dozen treatment-related deaths in the University of Pennsylvania and Juno trials in the past few years that involve a major side-effect of CAR T-cell therapy called cytokine-release syndrome (CRS). T-cell activation causes the release of inflammatory cytokines, producing symptoms including high fevers, aches, hypotension, and, more rarely, pulmonary edema and neurologic effects such as delirium.

Researchers tie the severity of what they call a “cytokine storm” to tumor burden—a patient’s total mass of cancer tissue or quantity of malignant cells. One hypothesis for this is that higher tumor burden seems to incite a stronger immune reaction. Moreover, the deaths have all occurred in adults, some of whom had serious underlying medical issues, and others who had undiagnosed infections. Interestingly, children seem relatively resistant to severe CRS and, when they get it, are more easily managed, says Michel Sadelain of Memorial Sloan Kettering and Juno. “Adults do not tolerate the treatment as well as children, in whom the cells differ in speed of action and persistence,” Sadelain says. Treatment with an anti-IL6 antibody, or in severe cases, corticosteroids, can mitigate a cytokine storm’s severity, as can dosing with lower numbers of CAR T cells.

“In our trial [on diffuse large B-cell lymphoma], we saw that toxicity was reduced in patients who received low-dose chemotherapy rather than high-dose [prior to CAR T-cell treatment], and lower numbers of engineered T cells [than given previously],” says James Kochenderfer of the National Cancer Institute (NCI).

Bellicum is partnering with the University of Leiden in the Netherlands and the NCI, among others, to develop “suicide switches,” or safety on-and-off switches that are incorporated into CAR T-cell candidates to control T-cell activation and proliferation. And Juno’s second-generation “armored” CAR technologies include mechanisms to dampen T-cell activation. “It will be important to find new ways to overcome toxicity of CAR T cells,” says the Weizmann Institute’s Zelig Eshhar.

To view the original of this article CLICK HERE
.
Regards,
Greg_L-W.
.
 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
.
You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
Accuracy & Copyright Statement: CLICK HERE
Summary, archive, facts & comments on UKIP: http://UKIP-vs-EUkip.com
DO MAKE USE of LINKS & >Right Side Bar< & The Top Bar >PAGES<
Also:
Details & Links: http://GregLanceWatkins.com
UKIP Its ASSOCIATES & DETAILS: CLICK HERE
Views I almost Totally Share: CLICK HERE
General Stuff archive: http://gl-w.blogspot.com
General Stuff ongoing: http://gl-w.com
Health Blog. Archive: http://GregLW.blogspot.com
Health Blog. Ongoing: http:GregLW.com

TWITTER: Greg_LW

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The Value Of Controlling Blood Pressure In Early Life

The Value Of Controlling Blood Pressure In Early Life
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Keeping Blood Pressure Low in Those Under 50

Higher blood pressure in young adulthood increases the risk for coronary heart disease, a new study found.

Researchers followed almost 3,500 men and women for 25 years with periodic physical examinations beginning in 1985, when all were healthy and 18 to 30 years old. They calculated their cumulative exposure to high blood pressure over the years.

The scientists, writing in The Journal of the American College of Cardiology, studied left ventricular dysfunction — damage to the part of the heart that pumps blood to the entire body except the lungs. Left ventricle impairment is a main cause of heart failure. They found the higher the blood pressure, the greater the damage to the left ventricle. In addition, even after adjusting for other risk factors, chronic high blood pressure in young adulthood increased coronary calcium in middle age to a degree similar to that of the initial stages of atherosclerosis.

“This paper highlights that in the first half of adult life, it’s very important to keep blood pressure as low as one can,” said the lead author, Dr. João A.C. Lima, a professor of medicine at Johns Hopkins, adding that “130/80 or 130/70 should be the goal for people under 50.”

Current guidelines advise treatment at 140/90 for people ages 30 to 59.

To view the original of this article CLICK HERE

Cumulative Blood Pressure in Early Adulthood and Cardiac Dysfunction in Middle AgeThe CARDIA Study

Commentary by Dr. Valentin Fuster

Satoru Kishi, MD; Gisela Teixido-Tura, MD, PhD; Hongyan Ning, MD; Bharath Ambale Venkatesh, PhD; Colin Wu, PhD§; Andre Almeida, MD; Eui-Young Choi, MD; Ola Gjesdal, MD; David R. Jacobs, Jr., PhD; Pamela J. Schreiner, PhD; Samuel S. Gidding, MD; Kiang Liu, PhD; João A.C. Lima, MD
J Am Coll Cardiol. 2015;65(25):2679-2687. doi:10.1016/j.jacc.2015.04.042
 

Abstract

Background  Cumulative blood pressure (BP) exposure may adversely influence myocardial function, predisposing individuals to heart failure later in life.

Objectives  This study sought to investigate how cumulative exposure to higher BP influences left ventricular (LV) function during young to middle adulthood.

Methods  The CARDIA (Coronary Artery Risk Development in Young Adults) study prospectively enrolled 5,115 healthy African Americans and whites in 1985 and 1986 (baseline). At the year 25 examination, LV function was measured by 2-dimensional echocardiography; cardiac deformation was assessed in detail by speckle-tracking echocardiography. We used cumulative exposure of BP through baseline and up to the year 25 examination (millimeters of mercury × year) to represent long-term exposure to BP levels. Linear regression and logistic regression were used to quantify the association of BP measured repeatedly through early adulthood (18 to 30 years of age) up to middle age (43 to 55 years).

Results  Among 2,479 participants, cumulative BP measures were not related to LV ejection fraction; however, high cumulative exposure to systolic blood pressure (SBP) and diastolic blood pressure (DBP) were associated with lower longitudinal strain rate (both p < 0.001). For diastolic function, higher cumulative exposures to SBP and DBP were associated with low early diastolic longitudinal peak strain rate. Of note, higher DBP (per SD increment) had a stronger association with diastolic dysfunction compared with SBP.

Conclusions  Higher cumulative exposure to BP over 25 years from young adulthood to middle age is associated with incipient LV systolic and diastolic dysfunction in middle age.

Central Illustration

Early Adulthood Blood Pressure and Middle-Age Left Ventricular Function

Blood pressure (BP) trends with increasing age. The trajectory slope shows mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) with increasing age for white and black men and women. All BP measurements over 25 years were within guideline acceptable range (A and B). Systolic and diastolic function with increasing cumulative SBP and DBP. (C) For left ventricular (LV) systolic function, there were no differences in left ventricular ejection fraction (LVEF) among cumulative SBP deciles; meanwhile, higher deciles of cumulative SBP produced a lower 4-chamber longitudinal peak systolic strain rate (Ell_SRs) compared with the lowest SBP (0% to 10%) decile. For LV diastolic function, early peak diastolic mitral velocity/peak early diastolic mitral annular velocity (E/e′) ratio increased in higher deciles of cumulative SBP compared with the lowest decile. Higher deciles of cumulative SBP were associated with lower 4-chamber longitudinal peak early diastolic strain rate (Ell_SRe) versus the lowest decile. (D) In considering cumulative DBP deciles, the same trends were seen for LVEF, as well as when comparing the higher deciles with the lowest group for Ell_SRs, E/e′ ratio, and Ell_SRe.

Perspectives

COMPETENCY IN MEDICAL KNOWLEDGE: BP in early adulthood is related to later systolic and diastolic ventricular dysfunction.

TRANSLATIONAL OUTLOOK: Further studies are needed to determine whether specific lifestyle interventions implemented to reduce DBP in early adulthood prevent HF from developing later in life.

 For more details from JACC CLICK HERE
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Greg_L-W.
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 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
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You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
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YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
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Putting Stents To The Test & Treating Heart Attacks

Putting Stents To The Test & Treating Heart Attacks
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A cardiologist showing the blocked arteries of a patient who had a right and left catheterization procedure at Our Lady of Lourdes Medical Center in Camden, N.J. Credit Mark Makela for The New York Times

Millions of Americans have had stents — small wire cages — inserted in their coronary arteries to prop them open. And many are convinced the devices are protecting them from heart attacks. After all, a partly blocked artery is now cleared, and the pain in a heart muscle starved of blood often vanishes once the artery is open again.

But while stents unquestionably save lives of patients in the throes of a heart attack or a threatened heart attack, there is no convincing evidence that stents reduce heart attack risk for people suffering from the chest pains known as stable angina. These are people who feel tightness or discomfort walking up a hill, for example, because a partly blocked coronary artery is depriving their heart of blood. But the pain or tightness goes away if they stop and rest or just stay still. And there is a reasonable argument that drugs — cholesterol-lowering statins in particular — might be just as good at reducing such pain.

“It is kind of amazing that we don’t have the evidence,” said Dr. David J. Maron, the director of preventive cardiology at Stanford.

Photo

 
Dr. David J. Maron, the director of preventive cardiology at Stanford, examining angiograms. Credit Peter Earl McCollough for The New York Times

Now, the National Heart, Lung and Blood Institute is trying to find out whether stents do in fact prevent heart attacks. The answer could change the standard of care for the more than half a million Americans annually who receive a new diagnosis of heart disease after they see a doctor for angina. Heart disease remains the biggest killer of Americans despite significant treatment advances in the past decade.

The typical treatment for angina is to thread a narrow catheter up from a blood vessel in the groin to the heart, squirt in a dye that allows a cardiologist to see blockages in arteries on X-rays, and then insert a stent in the blocked areas. Stents are safe but expensive. Medicare payments vary depending on what kind of stent is used and how many, but are generally above $10,000 and can be more than $17,000.

And stents are not always a permanent solution to chest pain, as Albert Nassar of Brooklyn discovered. When he had angina four years ago, the reason seemed clear and the solution straightforward. An angiogram — the test in which dye is injected into the coronary arteries — showed one was 90 percent blocked. When a doctor inserted a stent to open that artery, the pain vanished.

But three years later, Mr. Nassar, 59, again felt tightness in his chest as he rode a recumbent bike at the gym. He said he expected another stent, but his cardiologist surprised him. He told Mr. Nassar that the medical profession does not actually know if stents help people like him with moderate to severely blocked coronary arteries.

Then he asked Mr. Nassar if he would be part of the National Heart, Lung and Blood Institute clinical trial, known as Ischemia, and have his treatment decided randomly between two options. If he was assigned to one group, his doctors would look at his blocked artery with X-rays and open it mechanically with a stent or, if the X-rays showed he was among the minority whose blockage could not be opened with a stent, with bypass surgery. He would also be asked to take drugs and change his lifestyle to protect his heart. In the other, his treatment would consist solely of drugs and the lifestyle changes. There would be no peeking at his blockage.

Mr. Nassar leapt at the chance and when he was assigned to take the drugs — a statin, blood pressure drugs and an aspirin — he was delighted.

“I didn’t feel the urge to have another surgical procedure,” he said. “I’ve had enough of those.”

The idea that opening blocked arteries saves lives dates to the 1970s and ’80s. In those decades, neither stents nor statins were used. The only treatment for blocked arteries was bypass surgery, a major operation in which the ribs are split open and a patient is put on a heart-lung machine while the heart is stopped. A surgeon bypasses the blockage with a blood vessel taken from elsewhere in the body.

Studies at the time had found that surgery was better for patients with severe blockages of major coronary arteries than not having surgery.

Stents were introduced in the 1990s, and because they relieved pain and were far less invasive than bypass surgery, they became the treatment of choice. Doctors and patients started to believe they also saved lives in stable patients, though there was no solid evidence of that.

“The thought was, better to go in and open it up,” said Dr. Harmony R. Reynolds, a cardiologist at NYU Langone Medical Center and a principal investigator in the study that Mr. Nassar joined. “But now meds have gotten so good that it is not clear surgery adds anything for stable patients.”

Researchers tried to get an answer with a big federal study, called Courage, that was published in 2007. But many cardiologists said the study was flawed and they did not believe its conclusion that stents failed to prevent heart attacks and deaths.

In Courage, as in the new study, participants were given stents and intensive drug therapy —– a statin, blood pressure drugs and aspirin — or just the medicines. The criticism, though, was that doctors may have cherry-picked patients, excluding the sickest. Because angiograms revealed blockages in arteries before patients were invited to enroll in the trial, doctors who believed stents were lifesaving may never have asked patients with the most severe disease to join the study.

The result, skeptics said, was that most patients in the study were at such low risk that it did not matter which treatment they received. They were certain to do well, so the study proved nothing about whether stents worked.

Because of the doubts about that study and ingrained habits, medical practice was largely unchanged by its findings. A recent study, which analyzed recorded conversations between cardiologists and patients with stable angina, found that 75 percent of the cardiologists recommended stents and when they did, their patients almost always complied. And, the study found, on the rare occasions when the cardiologists presented both stents and medical treatment as options, none of the patients chose stenting.

The new study aims to avoid the methodological flaw in the 2007 Courage study. Patients who agree to participate are not given angiograms before being assigned a treatment. Instead, they are accepted into the trial on the basis of noninvasive tests that indicate blocked arteries and high risk of a heart attack. Their doctors know only that an artery is blocked — not which one or how much — so they are not able to pluck out patients they believe need stents and prevent them from entering the trial.

Photo

 
A coronary stent. They are safe, but expensive. Credit Peter Earl McCollough for The New York Times

Underlying the debate about the utility of stents is an uncertainty about how and why heart attacks occur.

For years, the common notion was they were caused by a plumbing problem. In this view, plaque — pimplelike lumps — partly blocked a coronary artery and grew until no blood could get through, and a stent was needed to open an artery before it closed completely.

But a leading hypothesis says there is no predicting where a heart attack will originate. It could start anywhere there is plaque, even if the plaque is not obstructing the flow of blood in an artery. Unpredictably, a piece of plaque can burst open. Blood starts to clot on the injured area. Soon, the blood clot clogs blocks the artery. The result is a heart attack.

It is known that certain plaques, with thin walls and bursting with fat-filled white blood cells, are prone to rupture. A study published in 2011 found that only a third of heart attacks originated in plaques that were blocking at least half of an artery, as seen on an angiogram. The rest began with the rupture of plaques that appeared to be causing no problems.

According to this view of how and why heart attacks happen, stenting would not be protective because people with atherosclerosis have arteries studded with plaque. The partly blocked area visible in an angiogram is no more likely to be the site of a heart attack than any other with plaque. But statins could work because they change the nature of plaques, making them less likely to rupture.

Although stents relieve chest pain, today’s medical therapy can, too, though it may take weeks or months.

But proving whether stents make a difference is turning out to be harder than expected. Many doctors and patients have such strong opinions about the value of stenting that recruitment for the new study has been difficult. Stents have become part of the fabric of heart disease care. Former President George W. Bush, for example, had a treadmill stress test in the summer of 2013 as part of a physical examination. When the test indicated he might have a blocked artery, he had an angiogram. It showed a partial blockage that a cardiologist opened with a stent.

The challenge now is to get Ischemia done and get some answers that might not be disputed. In the past two years, researchers randomized nearly 2,000 patients for the trial at the 300 participating medical centers. The plan is to 

Treating a Heart Attack

Doctors must first reopen the blocked artery and restore the flow of blood to the heart muscles.

Doctors insert a hollow catheter through the groin or an arm, threading it up a major artery and into the heart.

A deflated balloon is passed through the catheter to the site of the blockage.

The balloon is surrounded by a metal mesh stent. Inflating the balloon opens the artery and locks the stent in place.

Hospitals have been working to reduce the time needed to insert stents in patients having heart attacks.

“Cardiologists think this is a very important study intellectually,” said Dr. Maron, who is one of the study’s authors. “But when it comes to their own patients, some cardiologists balk, even though they know we don’t have the answer.”

The issue potentially affects many heart patients. “Half the people over 65 have blockages,” Dr. Gregg W. Stone, an interventional cardiologist at Columbia, said. “If you have some degree of atherosclerosis, you have blockages.”

And once a stress test or an angiogram reveals a blockage, it can be hard to ignore a partly blocked artery, hard to avoid thinking a stent has to help.

“People believe that if they have a blockage, they have to fix it mechanically,” said Dr. Judith S. Hochman, the study chairwoman for the Ischemia trial and a cardiologist at NYU Langone. “It seems logical, but in medicine, many things that seem logical are not true.”

Not only do cardiologists find it hard to fight their own feelings that stenting makes sense, they also find it hard to persuade patients to try medical therapy, said Dr. Brahmajee Nallamothu, an interventional cardiologist at the University of Michigan.

The concept that stenting helps, he said, “is a paradigm so deeply set on the part of the public and a lot of doctors that it is tough to overcome.”

Mr. Nassar was one of the rare patients who did not hesitate to enter the trial. Though stents had relieved his pain in the past, they were no panacea. Like most heart patients, he had never taken the most important drug for those with his condition: a statin.

So far, he says he is happy with his drug treatment. His angina is gone.

“I feel no pain,” he said.

To view the original of this article CLICK HERE

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Regards,
Greg_L-W.
.
 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
.
You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
Accuracy & Copyright Statement: CLICK HERE
Summary, archive, facts & comments on UKIP: http://UKIP-vs-EUkip.com
DO MAKE USE of LINKS & >Right Side Bar< & The Top Bar >PAGES<
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PANCREATIC CANCER It May Be Too Late If You Wait!

PANCREATIC CANCER It May Be Too Late If You Wait!
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The Silent Killer: 7 Early Warning Signs Of Pancreatic Cancer

shutterstock_209300635

Pancreatic cancer is known as the silent killer. It’s largely asymptomatic until it’s too late to successfully treat, which is why you should be particularly vigilant. Here’s seven early warning signs of pancreatic cancer.

 

1. Abdominal pain
Abdominal pain can mean many things. However, over 90% of pancreatic cancer patients experience some sort of abdominal discomfort. The pancreas is located in the middle of the upper abdomen, so if you get any persistent pain in that area, it might be a good idea to see your doctor.

2. Jaundice
Pancreatic cancer can form tumours, which block the bile ducts to the liver causing yellowing of the skin and discolouration of the eyes. If you notice any discolouration of your skin, it’s a good indication that your liver isn’t functioning properly, and it’s worth getting it checked out.

3. Diabetes
Most commonly, diabetes is a result of obesity and an unhealthy lifestyle. However, when it is paired with any of these seven symptoms, it could be an indication that something else is wrong. If you experience any diabetic symptoms suddenly, and lead a healthy life, ask your doctor to consider other causes.

4. Weight loss
Most forms of cancer cause significant weight loss, without any change to your diet. Cancers use up metabolic energy, and alter hormone production. If you notice any sudden weight loss, it’s worth having a check-up, as it could be anything from a thyroid problem, to Coeliacs disease, to cancer.

5. Bloating
Bloating can be a sign of other health issues, like a food intolerance, poor diet or dehydration. However, when paired with other common cancer symptoms, it might be time to seek advice.

6. Stool changes
If you notice any discolouration in your stool, it’s important to go and seek medical advice, as this can be sign of many cancers. A block in the bile duct can often produce light coloured, chalk like stools, which could suggest problems with the pancreas or liver.

7. Dermatitis
Blocked bile ducts can also cause issues with the skin, including patchiness, flakiness and itching. If you notice any rapid changes to your complexion, combined with any of the other symptoms, such as jaundice, the problem might be more than skin deep.

To view the original of this article CLICK HERE

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Regards,
Greg_L-W.
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 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
.
You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
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Cancer Doctors Offer Way to Compare Medicines, Including by Cost

Cancer Doctors Offer Way to Compare Medicines, Including by Cost
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Alarmed by the rapid escalation in the price of cancer drugs, the nation’s leading oncology society unveiled on Monday a new way for doctors and patients to evaluate different treatments — one that pointedly includes a medicine’s cost as well as its effectiveness and side effects.

The release by the American Society of Clinical Oncology of what it calls its “value framework,” is part of a change in thinking among doctors, who once largely chose drugs based on their medical attributes alone. The major cardiology societies, for instance, are also now starting to factor cost into their evaluation of drugs.

“The reality is that many patients don’t get this information from their doctors and many doctors don’t have the information they need to talk with their patients about costs,” Dr. Richard Schilsky, chief medical officer of the oncology society, said in a news conference on Monday.

He said the price of new cancer drugs now averaged about $10,000 a month, and some cost $30,000 a month, which can mean prohibitive co-payments even for some patients with good insurance. “Many cancer patients are facing severe financial strain, even bankruptcy in some cases,” he said.

The value framework envisions considering two costs: the out-of-pocket costs for the patient and the overall cost of a drug to the health system.

Evaluating the latter cost would put doctors in the role of being stewards of societal resources. That is somewhat of a controversial role for doctors, since it might conflict with their duty to the patient in front of them. But the oncology society said it did not see those roles as being in conflict.

Some of the sample valuations presented by the society were far from flattering for the drugs involved.

Roche’s Avastin, when added to chemotherapy, had a net health benefit of 16 out of 130 possible points when used as an initial treatment for advanced lung cancer. Its monthly cost was $11,907.87, compared to $182.09 for the chemotherapy alone.

Eli Lilly’s Alimta for that same use had a net heath benefit of zero with a cost exceeding $9,000 a month compared to about $800 a month for the drugs it was compared to in the clinical trial.

A spokeswoman for Lilly said the trial analyzed by the oncology society understated Alimta’s effectiveness because it covered a broad population, whereas Alimta is approved for only one type of lung cancer. A spokeswoman for Roche said Avastin was the first drug to help lung cancer patients live longer than a year, and that the choice of treatments for life-threatening diseases was complex and personal.

The framework, published online Monday by The Journal of Clinical Oncology is more a proposed methodology that will now be open for public comment. It will take time to input the data on the effectiveness, side effects and costs of each drug, and convert it to a system that can be used on computers and mobile phones.

There is no requirement that doctors use the framework and it remains to be seen if they will. But the authors of the document say it is a start.

“It allows the patient and the doctor to at least talk through the issues,” said Dr. Lee N. Newcomer, senior vice president for oncology at UnitedHealthcare, the big insurance company, and a member of the task force that developed the framework. “Before, the information wasn’t there.”

UnitedHealthcare is mounting a similar effort of its own, Dr. Newcomer said. Starting this month, it is requiring oncologists to get prior approval from the insurance company for every cancer drug they administer. The company will then track what happens to patients and eventually provide information to doctors about how well each drug works.

Concern about cancer drug prices has been rising for years and doctors have been becoming increasingly vocal. At its annual meeting late last month, the oncology society included a talk sharply criticizing the prices of cancer drugs as part of its plenary session.

Randy Burkholder, vice president for policy and research at the Pharmaceutical Research and Manufacturers of America, the drug industry trade group, said that drugs represented only 20 percent of cancer treatment costs. He also said that the big clinical trials that the oncology society used to make its value calculations might not be as relevant as treatment becomes increasingly personalized based on genetic analysis of a patient’s tumor.

Some experts say that ideally, the price of a drug should reflect its value, but that does not seem to be the case with cancer drugs. A recent study by researchers from the National Cancer Institute, published in JAMA Oncology, surveyed cancer drugs approved from 2009 through 2013. It found that prices did not correlate very well with how novel a drug was or whether it prolonged life versus just shrinking tumors.

The framework computes a score — called the net health benefit — based on clinical trial data.

Drugs for advanced cancer are given a score from 0 to 130. Up to 80 of the points are based on a drug’s effectiveness in prolonging lives, delaying the worsening of cancer or shrinking tumors. Then up to 20 points can be added or subtracted based on side effects. And up to 30 bonus points can be granted if the drug relieves cancer symptoms or allows a patient to go without treatment for a period of time.

The costs of the drug are listed separately, rather than incorporated into the final score for a drug. That is a step short of what is done in some evaluations, such as those by the National Institute for Health and Care Excellence in Britain, in which drugs are rated by the cost per extra year of life they provide, adjusted by side effects and symptoms.

Researchers at Memorial Sloan Kettering Cancer Center recently announced a tool that allows people to evaluate the cost-effectiveness of cancer drugs.

These other institutions “take the next step to say ‘What do we think about this amount of benefit at this cost?’” said Dr. Steven D. Pearson, president of the Institute for Clinical and Economic Review, a nonprofit organization that evaluates the clinical and cost effectiveness of treatments.

Dr. Lowell E. Schnipper, chairman of the task force that developed the oncology society’s framework, said that patients wanted to know how medically effective a drug is. Adding the cost into an overall rating would obscure that information, he said.

Each drug is evaluated based on how it did in clinical trials compared to a control group, and the control groups can be different. That makes it difficult to compare one drug to another.

“This is not a way of ranking drugs,” said Dr. Schnipper, who is clinical director of the cancer center at Beth Israel Deaconess Medical Center in Boston. “This is simply a way of understanding the outcome of a clinical trial.”

To view the original of this article CLICK HERE

.
Regards,
Greg_L-W.
.
 Please Be Sure To
& Link to my My Blogs
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!

.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
.
You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .

Posted by: Greg Lance-Watkins

tel: 01594 – 528 337
Accuracy & Copyright Statement: CLICK HERE
Summary, archive, facts & comments on UKIP: http://UKIP-vs-EUkip.com
DO MAKE USE of LINKS & >Right Side Bar< & The Top Bar >PAGES<
Also:
Details & Links: http://GregLanceWatkins.com
UKIP Its ASSOCIATES & DETAILS: CLICK HERE
Views I almost Totally Share: CLICK HERE
General Stuff archive: http://gl-w.blogspot.com
General Stuff ongoing: http://gl-w.com
Health Blog. Archive: http://GregLW.blogspot.com
Health Blog. Ongoing: http:GregLW.com

TWITTER: Greg_LW

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