Banish unneeded salt and sugar from your diet!

Reducing Sugar and Salt
Discover how you can reap the benefits of cutting back on sugar and salt without sacrificing taste, flavor, or enjoyment!

Dear Peggy,

Your body needs less than one gram of sodium a day. That's under half a teaspoon of table salt. But if you are like most Americans, you consume up to four times that amount. The result? Increased risk of high blood pressure, heart disease, and stroke.

As for added sugar, most of us consume more than twice the recommended daily amount, increasing the risk of obesity, diabetes, and even depression.

In Reducing Sugar and Salt, the doctors at Harvard Medical School give you the know-how to successfully monitor and effectively control the amount of sugar and salt you and your family take in each day.

The report exposes dozens of foods with "hidden" sodium and sugar. For example, a tuna salad sub sandwich can have up to 1,300 milligrams of sodium — more than the daily recommendation — while a bowl of raisin bran delivers 19 grams of added sugar (the equivalent of five teaspoons!)

Reducing Sugar and Salt will give you the facts about how a high-sodium diet can lower bone density, why "lactose-free" does not mean ''sugar-free,'' and whether you're wasting your money on sports drinks when H₂O will do. It also brings you up to date on sugar substitutes, and why you might want to cut back on diet soda.

The report offers strategies for cutting back on sugar and salt at home or dining out. You'll learn smart shopping and cooking tricks that make meals delicious while limiting sodium. You'll find out which fruits are lowest — and highest — in sugar, seven ways to spice up your meals without salt, and satisfying ways to retrain your taste buds to low-salt, low-sugar eating.

Reducing Sugar and Salt also gives you a host of flavorful recipes that minimize or eliminate sugar and salt, from delectable breakfast treats to wholesome lunches and dinners, not to mention perfect-ending desserts and even late-night snacks.

Be good to your body — and yourself. Order your copy of this timely Special Health Report today.

To your good health,

Anthony L. Komaroff, M.D.
Professor of Medicine, Harvard Medical School
Senior Physician, Brigham and Women's Hospital
Editor in Chief, Harvard Health Publications

Harvard Medical School offers special reports on over 50 health topics. Visit our Web site at http://www.health.harvard.edu to find reports of interest to you and your family.

Copyright © 2012 by Harvard University.

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Teva Oncology is excited to announce FDA approval of SYNRIBO^™ for Injection
for the treatment of adult patients with chronic or accelerated phase chronic
myeloid leukemia (CML) with resistance and/or intolerance to two or more
tyrosine kinase inhibitors (TKIs). This indication is based upon response rate. There are no trials verifying an improvement in disease-related symptoms or increased survival with SYNRIBO.

Indication

• SYNRIBO is indicated for the treatment of adult patients with chronic or accelerated phase chronic myeloid leukemia (CML) with resistance and/or intolerance to two or more tyrosine kinase inhibitors (TKIs). This indication is based upon response rate. There are no trials verifying an improvement in disease-related symptoms or increased survival with SYNRIBO.
• =========================================================== 
• for more info, go to the site!

Lifetime Carbohydrate Load

At the CRBCM we believe that stricter recommendations about carbohydrate reduction in diet should be instituted sooner in life. Certainly, by the time you are 20 to 25 years of age, there should be a sharp decrease in the daily sugar portion. Most adult growth has occurred by then and transition to open obesity initiates from there.
"I am gaining weight and find it difficult to lose it even with exercise". There is no weight loss without a sharp decrease in carbohydrates! We need to start believing that after a certain age: "You just have had all the carbohydrates in your life". We need to have carbohydrate charts able to tell us that we have consumed 60 percent of our lifetime carbohydrate requirement.   People will understand this! They will know where they stand. We also believe that exercise, despite its important accomplishments, to be mainly a weight maintenance strategy, unless you are a top runner/bodybuilder. Other benefits of exercise are more important: they include improvement in fighting cancer progression. So keep it up!
One needs to workout for hours to lose weight significantly. And in our busy life, one finds time and impetus hard to come by. Exercise must be individualized to be successful, but communities offer less and less individualized care. People with extensive arthritis most likely end up stopping exercising altogether. We have no program adjusted for them. Those on oxygen also stop exercising; again they need some individualized program. Our disabled need adjusted programs. Diet remains an integral part to exercise for health preservation!

To expand the idea, we believe physicians should provide patients with a lifetime health chart to tell them where they stand as compared to a 90-year old person. We can debate all night long, but 90 years is pretty good. I know that those close or past this age will feel excluded. I remember the oncologists in a conference room trying to define who is an "Elderly". Every few years, as we all become older, we keep pushing that elderly-age to stay out!

LIFETIME HEALTH CHART OR STATUS: THAT'S AN IDEA! LET'S PATENT THIS QUICK!

Is A Cure For Cancer Near?

December 10, 2012 | Filed under Health Care | Posted by Doug Johnson

Emily Whitehead photo via

The New York Times is reporting that a disabled form of H.I.V. is being used to reprogram patient’s immune systems to genetically to kill cancer cells.

PHILIPSBURG, Pa. — Emma Whitehead has been bounding around the house lately, practicing somersaults and rugby-style tumbles that make her parents wince.
It is hard to believe, but last spring Emma, then 6, was near death from leukemia. She had relapsed twice after chemotherapy, and doctors had run out of options.
Desperate to save her, her parents sought an experimental treatment at the Children’s Hospital of Philadelphia, one that had never before been tried in a child, or in anyone with the type of leukemia Emma had. The experiment, in April, used a disabled form of the virus that causes AIDS to reprogram Emma’s immune system genetically to kill cancer cells.
The treatment very nearly killed her. But she emerged from it cancer-free, and about seven months later is still in complete remission. She is the first child and one of the first humans ever in whom new techniques have achieved a long-sought goal — giving a patient’s own immune system the lasting ability to fight cancer.
…Three adults with chronic leukemia treated at the University of Pennsylvania have also had complete remissions, with no signs of disease; two of them have been well for more than two years, said Dr. David Porter. Four adults improved but did not have full remissions, and one was treated too recently to evaluate. A child improved and then relapsed. In two adults, the treatment did not work at all. The Pennsylvania researchers were presenting their results on Sunday and Monday in Atlanta at a meeting of the American Society of Hematology.
Despite the mixed results, cancer experts not involved with the research say it has tremendous promise, because even in this early phase of testing it has worked in seemingly hopeless cases. “I think this is a major breakthrough,” said Dr. Ivan Borrello, a cancer expert and associate professor of medicine at the Johns Hopkins University School of Medicine.

Targeted fighting of cancer at the cellular level makes a lot of sense. The problem has always been how to destroy those cancer cells without destroying everything else. This is a very promising development.

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1.  CRBCM will find out what happened at the ASH regarding this reserach.
2.  Despite the reported success which is impressive, could restoring one thing cure everyone (Driver Mutation)?  Cancer cells are different from the normal cells in so many ways that it is hard to believe that this technique is the cure-all. Indeed, 4 patients did not achieve complete remission. These failures send the researchers back to the drawing boards.
3.Computer models are the way to go. The proper answer is to make an inventory of critical changes compared to normal, and address these changes sequentially or concurrently to improve our success.
4. The last point leads to the importance of mapping technology improvement.
5. Nice to see DR IVAN BORRELLO mentioned; I referred a few patients to him while working at Midatlantic Kaiser Permanente.  I worked there for 14 years!

This is definitively informative for those looking who are looking for a comprehensive presentation of target of therapy. We will review the m-TOR today!

These diagrams have been assembled by Cell Signaling Technology (CST) scientists and outside experts to provide succinct and current overviews of selected signal transduction pathways. Knowledge about each signaling pathway has been synthesized and integrated into understandable paradigms of cellular communication. Please send suggestions for developing new pathways to info@cellsignal.com.
The proteins in each pathway are linked to a search on the PhosphoSitePlus^® website, which is an expert-curated knowledge base of protein phosphorylation plus other post-translational modifications in vertebrates. A matching collection of product search pathways is also online.

Requirements: Using these pathways requires JavaScript and the free Adobe Flash Player version 10 or higher. To view the pathway PDFs, you will need the free Adobe Acrobat Reader.

Chromatin / Epigenetic Regulation

• Protein Acetylation
• Histone Methylation
• Examples of Crosstalk Between Post-Translational Modifications
• Histone Modification Table

MAP Kinase Signaling

• Mitogen-Activated Protein Kinase Cascades
• MAPK/Erk in Growth and Differentiation
• G-Protein-Coupled Receptors Signaling to MAPK/Erk
• SAPK/JNK Signaling Cascades
• Signaling Pathways Activating p38 MAPK

Apoptosis

• Apoptosis Overview
• Inhibition of Apoptosis
• Death Receptor Signaling
• Mitochondrial Control of Apoptosis

Autophagy

• Autophagy Signaling

PI3 Kinase / Akt Signaling

• PI3K / Akt Signaling
• PI3K / Akt Binding Partners Table
• PI3K / Akt Substrates Table

Cellular Metabolism

• Insulin Receptor Signaling
• AMPK Signaling
• Warburg Effect

Translational Control

• Translational Control: Overview
• Translational Control: Regulation of eIF2
• Translational Control: Regulation of eIF4E and p70 S6 Kinase
• mTOR Signaling

Cell Cycle / DNA Damage

• Cell Cycle Control: G1/S Checkpoint
• Cell Cycle Control: G2/M DNA Damage Checkpoint

Immunology and Inflammation

• Jak/Stat Signaling: IL-6 Receptor Family
• Jak/STAT Utilization Table
• Jak and Cytokine Receptor Mutants in
  Cancer Table
• NF-κB Signaling
• TLR Pathway
• B Cell Receptor Signaling
• T Cell Receptor Signaling

Neuroscience

• Amyloid Plaque and Neurofibrillary Tangle Formation in Alzheimer's Disease
• Dopamine Signaling in Parkinson's Disease

Stem Cells, Development, and Differentiation

• Wnt/β-Catenin Signaling
• Notch Signaling
• Hedgehog Signaling In Vertebrates
• TGF-β Signaling
• Hippo Signaling
• ESC Pluripotency and Differentiation

Cytoskeletal Regulation and Adhesion

• Regulation of Actin Dynamics
• Regulation of Microtubule Dynamics
• Adherens Junction Dynamics

Other

• Angiogenesis
• ErbB/HER Signaling
• Ubiquitin/Proteasome
• Ubiquitin Ligase Table

Feedback
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This is definitively informative for those looking who are looking for a comprehensive presentation of target of therapy.   We will review the m-TOR today!

Apoptosis. 2006 Feb;11(2):143-9.

Cathepsin-regulated apoptosis.

Chwieralski CE, Welte T, Bühling F.

Source

Institute of Immunology, Otto-von-Guericke-University, Magdeburg, Germany.

Abstract

Apoptosis can be mediated by different mechanisms. There is growing evidence that different proteolytic enzymes are involved in the regulation of apoptosis. Cathepsins are proteases which, under physiologic conditions, are localized intralysosomally. In response to certain signals they are released from the lysosomes into the cytoplasm where they trigger apoptotic cell death via various pathways, including the activation of caspases or the release of proapoptotic factors from the mitochondria. Here, we review different mechanisms that induce the release of lysosomal enzymes, and the functional relevance of defined cathepsins in defined models of apoptosis.

PMID:

16502253

[PubMed - indexed for MEDLINE] 

===========================================================

Once again we remind our readers that the failure of chemotherapy to lead to a cure has led to the belief that trying to kill the cell indiscriminately has proven somewhat futile.

Giving only less than 20% cure rates.  We needed to be smart by exploiting natural path to death. Indeed the cell has a naturally programmed death called Apoptosis.  Our approach to cure is to find ways to induce cancer cells into Apoptosis.  It is apparent that Apoptosis whenever triggered appears to be better in achieving death of cancer cells.  There are also some non Apoptotic ways to cancer cell death that we discussed in our previous posts.

In Mitochondria, membranous events release Cytochrome C which in turn activates the Caspase family to lead to cell death.  (BAX is linked to Caspase activation)

In the Lysosmes, membranous events seems to free more Cathepsins to lead to Cell death.  We also have shown that Ion Pumps maintain intralysosomal Ph gradiant to allow function of various Hydrolases which function only at Acidic Ph.

Autophagia and Necrosis are some of the other path to cell death.  Our task is to know how to harness these powerful pathways to death.  Response rates are up to 75% in LUNG CANCER using current Oncogene drivers recommendation.

Not all members of the influential House Appropriations Committee were happy with who showed up to testify

FRIDAY NEWS LINKS: Amid Claims of Nonprofit Privacy, CPRIT Foundation & State Cancer Agency Come Under Scrutiny of State Legislators

Houmanitarian December 21, 2012

Video Link: Cancer Cronyism Allegations Examined at Texas Capitol Hearing
(KHOU & KVUE News)

Paul Webber, Associated Press
AUSTIN — A foundation that boosts executive salaries at Texas’ troubled $3 billion cancer-fighting effort defended to critical lawmakers Thursday a policy that keeps donors confidential while being lectured over appearances of pay-to-play politics.
Facing pointed and occasionally combative questions from state budget-writers, officials with the Cancer Prevention and Research Institute of Texas appeared before a public panel for the first time since prosecutors announced a criminal probe into the beleaguered agency and Gov. Rick Perry called for a moratorium on new awards.
Not all members of the influential House Appropriations Committee were happy with who showed up to testify. Absent were the three top agency executives who have resigned in the past eight months: Executive Director Bill Gimson, Chief Commercialization Officer Jerry Cobbs and Chief Scientific Officer Alfred Gilman.
All three are principal players surrounding $11 million in taxpayer funds that were awarded in 2010 to a private startup despite the project bypassing an independent review. Republican Jim Pitts, chairman of the House committee, left the door open to the agency’s former leadership being hauled in front of lawmakers as soon as January.
That left Barbara Canales, vice president of the nonprofit CPRIT Foundation and a member of the agency’s governing board, answering recurring and tough questions about the role of the nonprofit arm. One of the foundation’s chief purposes is to supplement the salaries of top institute executives, including Gimson, whose annual salary was $300,000.
The foundation has denied media requests to make its donor list public. “We have a balancing act to weigh here as board members, and to protect the privacy of our donors so they’re not unfairly solicited,” Canales said.
Rules prohibit donors from being awarded institute grants, Canales and CPRIT officials testified. But Democrat Rep. Sylvester Turner — who said, “We want an organization with integrity, not a slush fund” — and other lawmakers pressed for certainty that foundation donors were not connected to grant winners.
“What I can tell you is: To the best of my knowledge, it is not our policy to accept donors who are also grant” recipients, Canales said.
Republican Rep. Myra Crownover and other board member said the mere appearance was problematic. “The pay-to-play potential — maybe there should be more division,” Crownover said. The foundation has raised around $700,000 in each the last two years, according to Canales.
Thursday’s hearing came a day after Perry and other state leaders called for a moratorium on new grants until confidence is restored in a once-celebrated agency that has been thrown into upheaval in just three years. The institute controls the nation’s second-largest pot of cancer research dollars, behind the National Institutes of Health.
(Read more of this story at the Houston Chronicle)
RELATED COVERAGE:

MAPPING CANCER AND CLUSTERS OF DIFFERENTIATION

MAPPING CANCER AND CLUSTERS OF DIFFERENTIATION.

One important aspect of the fight for the cure is to obtain cancer distribution MAP in an individual.  Certainly, one would not attack an enemy without knowing its size, quantity/quality, distribution and location.  One of the challenges with cancer is that it comes from normal cells, therefore any attack we plan should include a component regarding how to avoid hurting the normal cell which relies on same survival strategies and components as the cancer cell!  Luckily, the cancer cell wants to avoid many of the natural death processes.  It wants to migrate and invade other organs, and where it has newly invaded, it wants to grow faster than the local cells and therefore creates a nutrition supply system that favors it!   With each of the new needs the cancer wants to acquire, it has to develop new sets of molecules and mechanisms not necessarily expressed by the normal cell.  These are globally called CLUSTERS OF DIFFERENTIATION OR CD. These include changes in membrane receptors, driver mutations, status of activation of now known targets in various pathways, and of course changes in transcription factors, DNA and even chromatin conformations.

These clusters of differentiation have been divided according to not only how we could use them, but how the cancer cell uses them.  We call them Predictive as they can help us predict the existence and behavior of cancer.  They are Prognostic when they determine cancer resilience  to a given treatment and define or influence the outcome of the patient.  They are Diagnostic when they point to the existence of cancer (these include the so called "Tumor Markers").

Mapping cancer today is limited.  Staging cancer today is a crude way of mapping the extent of cancer.  But in this day and age when we can visualize radiological changes in the metabolism, knowing the exact location and number of cancer cells everywhere in our body, it appears to be an achievable goal.  The cure will not be secured until we can count remaining enemies.  This knowledge will also help define cure.  There is a perception in the treating physician community that cure is not Zero cancer cells.  That we could be "cured" despite a residual amount of cancer.  How much and where is not clear!  Those who believe in a threshold number of cancer cells for active disease assert that, under the threshold, the immune system keeps things under control.
Molecular Therapy attacking Clusters of Differentiation have been attached to chemotherapy drugs and to radiation particles to kill exclusively cancers cells that have them.  Campath, Rituxan and others follow these mechanisms.  Suffice is to say we need more sophisticated ways to MAP CANCER IN OUR BODIES!  THIS WILL BE THE STRONGEST DIAGNOSTIC, PREDICTOR AND DETECTOR OF CANCERS!

 MERRY CHRISTMAS / JOYEUX NOEL TO ALL!

"I say to you today, my friends that in spite of the difficulties and frustrations of the moment, I still have a dream"

Christmas Reflections at CRBCM!

"I say to you today, my friends that in spite of the difficulties and frustrations of the moment, I still have a dream" and with this dream we will rise again to fight another day because we have understood that as long as we live another day, a door may be opened again, another chance may come along, we got to stay prepared and keep looking forward for an opportunity.  There are in life many pits, but all have a bottom here on earth, and even in the darkness of those pits, as long as we live, our imagination will help us rise again.  It is our call, the cause is too important to quit.
Those who came before us have left these words because they lived the horrors of life, went through them and came out the other side still whole.  They left these words so that we do not give up, but instead keep strategizing even when faced by a wall of negative forces.  We need to keep on advancing because only positive steps can generate new consequences.  Not doing a thing is to lose control of the outcome.  So at CRBCM we believe in new steps until life is irreversibly taken from us.  So in these Christmas days, let celebrate persistence and resolve.  What we fight against will not go away until we stand up to it!  Merry Christmas to all.

Cancer Prevention and Research Institute of Texas

Add caption

The New England Journal of Medicine

Original Article

Inhibition of the Hedgehog Pathway in Advanced Basal-Cell Carcinoma

Daniel D. Von Hoff, M.D., Patricia M. LoRusso, D.O., Charles M. Rudin, M.D., Ph.D., Josina C. Reddy, M.D., Ph.D., Robert L. Yauch, Ph.D., Raoul Tibes, M.D., Glen J. Weiss, M.D., Mitesh J. Borad, M.D., Christine L. Hann, M.D., Ph.D., Julie R. Brahmer, M.D., Howard M. Mackey, Ph.D., Bertram L. Lum, Pharm.D., Walter C. Darbonne, M.S., James C. Marsters, Jr., Ph.D., Frederic J. de Sauvage, Ph.D., and Jennifer A. Low, M.D., Ph.D.

N Engl J Med 2009; 361:1164-1172September 17, 2009DOI: 10.1056/NEJMoa0905360

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Background Mutations in hedgehog pathway genes, primarily genes encoding patched homologue 1 (PTCH1) and smoothened homologue (SMO), occur in basal-cell carcinoma. In a phase 1 clinical trial, we assessed the safety and pharmacokinetics of GDC-0449, a small-molecule inhibitor of SMO, and responses of metastatic or locally advanced basal-cell carcinoma to the drug.

Full Text of Background...

Methods

We selected 33 patients with metastatic or locally advanced basal-cell carcinoma to receive oral GDC-0449 at one of three doses; 17 patients received 150 mg per day, 15 patients received 270 mg per day, and 1 patient received 540 mg per day. We assessed tumor responses with the use of Response Evaluation Criteria in Solid Tumors (RECIST), physical examination, or both. Molecular aspects of the tumors were examined.

Full Text of Methods...

Results

The median duration of the study treatment was 9.8 months. Of the 33 patients, 18 had an objective response to GDC-0449, according to assessment on imaging (7 patients), physical examination (10 patients), or both (1 patient). Of the patients who had a response, 2 had a complete response and 16 had a partial response. The other 15 patients had either stable disease (11 patients) or progressive disease (4 patients). Eight grade 3 adverse events that were deemed to be possibly related to the study drug were reported in six patients, including four with fatigue, two with hyponatremia, one with muscle spasm, and one with atrial fibrillation. One grade 4 event, asymptomatic hyponatremia, was judged to be unrelated to GDC-0449. One patient withdrew from the study because of adverse events. We found evidence of hedgehog signaling in tumors that responded to the treatment.

Full Text of Results...

Conclusions

GDC-0449, an orally active small molecule that targets the hedgehog pathway, appears to have antitumor activity in locally advanced or metastatic basal-cell carcinoma. (ClinicalTrials.gov number, NCT00607724.)

Figure 1Mechanism of Action of GDC-0449 and Response to Treatment.

Figure 2GDC-0449 Activity in Patients with Locally Advanced Basal-Cell Carcinoma.

Article Activity

238 articles have cited this article
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This article point to the importance that targets of therapy should not only focus on steps within the main pathways but also on regulator of speed of reaction.  Basal  Cell cancer generally do not metastasize but once the speed of reaction is increased or promoted, the disease becomes more aggressive.  The Hedgehog genes promotes this disease and have been recently targeted effectively to show response to therapy.

Metabolic reaction can be promoted by a promoter gene in the main DNA, or by a variety of transcription genes which ultimately lead to a set of enzymes which ultimately accelerate the reaction.

It is also important to try to pay attention to Gradiants of Morphogens which apparently   govern cellular differentiation based of cell position in the body.  Controlling such determination may prove a way to impose changes within cancer cells!

It is of interest that in Breast cancer, basaloid type, the stage of disease had been reported to be "late" or advanced at diagnosis. This fact in combination with a triple negative status of this cancer lead to a poor prognosis.  Is Reducing the speed of reaction a critical component of future treatment in this disease? This type of Breast cancer is genetically similar to Ovarian cancer, therefore it fair to conclude that Target therapy successes in basal cell like breast cancer could be replicated in Ovarian cancer and vice-versa?

ADVANCES IN PROSTATE CANCER

In advanced prostate cancer TREAT FIRST LINE WITH PROVENGE TO EXTEND SURVIVAL

Prescribing Information

PROVENGE extends median survival beyond 2 years in patients with asymptomatic or minimally symptomatic metastatic castrate resistant prostate cancer PROVENGE reduced the risk of death by 22.5% vs the control group (P=0.032)¹

Overall Survival Benefits of PROVENGE1,2

Data originally published in The New England Journal of Medicine: Kantoff PW, Higano CS, Shore ND, et al; for the IMPACT Study Investigators. Sipuleucel-T immunotherapy for castration-resistant prostate cancer. N Engl J Med. 2010;363:411-422. Average time to subsequent therapy with docetaxel in the IMPACT trial was approximately 1 year.¹

PROVENGE provides a sustained survival benefit and a durable immune response PROVENGE provided a survival benefit every year studied³

Overall Survival Benefit for PROVENGE3

*(Percent PROVENGE-percent control)/percent control.

Percentage of Patients Alive: ITT Population (95% CI)3 1 year 2 years 3 years 4 years PROVENGE 81.1% (76.9, 85.3) n=274 52.1% (46.4, 57.7) n=129 31.7% (25.7, 37.8) n=49 20.5% (14.0, 26.9) n=14 Control 72.4% (65.6, 79.1) n=123 41.2% (33.5, 49.9) n=55 23.0% (15.5, 30.5) n=19 16.0% (8.5, 23.4) n=4

ITT=intent-to-treat.

PROVENGE provided a durable immune response²

•  A sustained immune response to PROVENGE was seen out to 26 weeks in the pivotal study (the last time point measured)

PROVENGE provides a safety profile you and your patients can manage

Only 1.5% of patients treated with PROVENGE in the pivotal trial discontinued treatment due to adverse events²

The most common adverse events reported in the PROVENGE group were chills, fatigue, fever, back pain, nausea, joint ache, and headache²

INDICATION PROVENGE® (sipuleucel-T) is approved by the FDA as an autologous cellular immunotherapy for the treatment of asymptomatic or minimally symptomatic metastatic castrate resistant (hormone refractory) prostate cancer.

IMPORTANT SAFETY INFORMATION PROVENGE is intended solely for autologous use and is not routinely tested for transmissible infectious diseases. In controlled clinical trials, serious adverse events reported in the PROVENGE group included acute infusion reactions (occurring within 1 day of infusion) and cerebrovascular events. Severe (Grade 3) acute infusion reactions were reported in 3.5% of patients in the PROVENGE group. Reactions included chills, fever, fatigue, asthenia, dyspnea, hypoxia, bronchospasm, dizziness, headache, hypertension, muscle ache, nausea, and vomiting. No Grade 4 or 5 acute infusion reactions were reported in patients in the PROVENGE group. The most common adverse events (incidence ≥ 15%) reported in the PROVENGE group were chills, fatigue, fever, back pain, nausea, joint ache, and headache. Please see the Full Prescribing Information.

Visit www.PROVENGE.com to learn more about treating advanced prostate cancer

REFERENCES

1. Kantoff PW, Higano CS, Shore ND, et al; for the IMPACT Study Investigators. Sipuleucel-T immunotherapy for castration-resistant prostate cancer. N Engl J Med. 2010;363:411-422. 2. PROVENGE [package insert]. Dendreon Corporation; June 2011. 3. Data on file. Dendreon Corporation.

©2012 Dendreon Corporation. All rights reserved. P-A-10.12-281.00