Spring2012 Newsletter by HC120704135230

VIEWS: 4 PAGES: 20

									Action Alert
Spring 2012


Washington Update
Congressional Briefing

The CPF sponsored a congressional briefing with the American Thoracic Society and other patient groups on
February 29, 2012 at the Cannon Building on the U.S. House of Representatives side of the U.S. Capitol. CPF
volunteers attended the event called “Research in Lung Health: The Pathway to Cures for Pulmonary Fibrosis
& Pulmonary Hypertension”. The briefing was organized in cooperation with U.S. House of Representatives
members Reps. Kevin Brady (R-TX), Erik Paulsen (R-MN) & Lois Capps (D-CA).

Pulmonary Fibrosis and Pulmonary Hypertension, a commonly diagnosed secondary condition along with PF,
were the topics of the briefing and were presented by leaders in the field to help educate members of
Congress and their staffs on the important research going on in these areas and the impact the diseases have
on American lives.

The event featured National Heart, Lung, Blood Institute (NHLBI) Acting Director, Susan Shurin, M.D., who
spoke on the NHLBI’s research in lung health and disease and noted progress and challenges in PF and PH,
Victor Thannickal, M.D., the Ben Vaughn Branscomb Chair of Medicine in Respiratory Disease, at the
University of Alabama, spoke on the search for new therapies for PF while Serpil Erzurum, M.D., Chair of the
Department of Pathobiology at the Cleveland Clinic, discussed the advances in treatments in PH, a disease
that had no treatments just 10 years ago. The two diseases were compared, demonstrating how research can
lead to treatments.

Several PF patients and family members attended the event and were on hand to speak with members of
Congress and their staffs regarding their personal perspective on PF.



Dear CPF Friends:

The CPF is delighted to share the excellent research news you will read in this issue. We are all aware that researchers
have been profoundly challenged by PF, and answers cannot come fast enough. Fortunately, in recent days, we have
seen renewed excitement about research findings, based on what is a burgeoning dialogue between researchers and a
visible increase in the numbers of innovative approaches to solving the PF puzzle. We take seriously our job to both
provide funding for the research and also to help promote collaboration between fibrosis experts across the country.
Though that raises the challenge of looking further for ways to generate needed funding, it speaks volumes about the
momentum around the disease.

The legislative effort (Pulmonary Fibrosis Research Enhancement Act) continues to be a key task for the staff and our
members. As most of our readers will know, the PFREA was reintroduced in the 112th Congress and we have 66 co-
sponsors in the House as this newsletter was being finalized. Our members have been wonderful about helping us gather
new sponsors by contacting their legislators, but we still have holdouts and we know hearing from their constituents is
what turns them into supporters. So please be one of our activists – the effort will only succeed if everyone takes up the
battle. Go to our website and sign up as an advocate – we’ll get your letters to your congressman – it’s easy.

Please be an active participant in this important work. Become a Daughter of PF (to learn more, see page 13 of this
newsletter), or an advocate, or help us raise the funds we need to continue to work for a better future for PF patients. Our
success in the fight against PF is only possible because of your partnership with us. I hope we can count on everyone to
take up the cause so that we might be victorious.

Mishka Michon, CEO
Coalition for Pulmonary Fibrosis




CPF’S 10 YEARS OF ACCOMPLISHMENTS
2001- Creation of 1st Pulmonary Fibrosis patient-centered organization in the U.S.
2002- CPF establishes program for creation of support groups around the country
2002- First Living with IPF patient seminar held
2003- First national PF week
2005- Concurrent Congressional legislation recognizing need for PF efforts introduced by REP. Charlie
Norwood (Rep. Norwood died due to illness following lung transplant for PF)
2005- Breathing is Glorious (B.I.G.) Ball Fundraising Events
2006- CPF joins ATS’ Public Advisory Roundtable
2006- First joint ATS/CPF research partnership grant established
2007- Concurrent Resolution recognizing need for PF attention passed
2008- First-ever request for congressional allocation to PF introduced (PFREA) by Reps. Baird and Castle
(CPF partnered with the congressmen on the legislation)
2008- CPF joins first Human/Canine research coalition
2009- CPF launches redesigned website website and internet advocacy program
2009- CPF launches first Public Service Announcement
2010- CPF announces stellar Honorary Board of Directors
2011- CPF partners with Reps. Baldwin and Paulsen and Sens. Crapo and Coons To introduce PFREA in
112th Congress
2011- CPF establishes new national program Daughters of PF


Senator Kirk’s Recovery
The CPF extends our good wishes to Senator Mark Kirk (R-IL) in his recovery following a stroke earlier this
year. Sen. Kirk is a leader on the Pulmonary Fibrosis Research Enhancement Act and has been instrumental
in getting other Senators to sign onto the legislation. Sen. Kirk lost his father to PF and has served as honorary
chair of the CPF’s B.I.G. Ball fundraising event in Chicago. If you’d like to send your good wishes to the
Senator, you may do so by sending a card or letter by fax or mail using the information below. Keep in mind
that letters will be slow due to U.S. Postal service security measures regarding mail to members of Congress.
Letters sent to IL may take less time than to D.C. and fax will be the fastest delivery.

Chicago
230 South Dearborn, Suite 3900
Chicago, IL 60604
Phone: 312-886-3506
Fax: 312-886-2117
Washington, DC
524 Hart Senate Office Building
Washington DC, 20510
Phone: 202-224-2854
Fax: 202-228-4611


Pulmonary Fibrosis Research Enhancement Act (PFREA, H.R. 2505, S. 1350)
Continues to Make Progress – Is YOUR member of Congress supporting it with
his/her co-sponsorship?

The Pulmonary Fibrosis Research Enhancement Act (PFREA) is gaining momentum and your
help is needed to continue the progress and get the bill out of committee and put to a vote.

Call, email or mail your Member of the House of Representatives AND the U.S. Senate NOW and ask them to
sign onto H.R. 2505 (House) S. 1350 (Senate).

See the full list of current co-sponsors (a list that’s growing fast) to see if your Members are on board. Also,
and very importantly, please ASK your friends and family to do the same. The louder our voices (and more of
them), the more likely Congress is to pass the bill that will create the first National Patient Registry in PF to
help pave the way for treatments and a cure – NOW – not “some day”.

Let YOUR member of Congress and YOUR Senators know why YOU care about the PFREA and about your
personal connection to the disease.
Your member wants to hear that you – a constituent – care about
this bill.

What the CPF needs for you to do
Call or email your Senators and Member of the House of Representatives today to urge them to co-sponsor S.
1350 and H.R. 2505 – legislation that supports PF research and creates the first National PF Patient Registry.
You can simply send an email.

Email or call or post a request to your Facebook page twitter and ask all of your family and friends to please
take action. They will first need to register as an advocate – send them this link, too:
www.coalitionforpf.org/cpf_join.php?autologin=true

Currently, there are 66 Co-Sponsors in the House of Representatives

REPRESENTATIVES                         DeGette, Diana [CO-1]                    Hinchey, Maurice D. [NY-22]
Altmire, Jason [PA-4]                   Dicks, Norman D. [WA-6]                  Jackson, Jesse L., Jr. [IL-2]
Baldwin, Tammy [WI-2]                   Edwards, Donna F. [M.D.-4]               Jones, Walter B., Jr. [NC-3]
Boren, Dan [OK-2]                       Ellison, Keith [MN-5]                    Kaptur, Marcy [OH-9]
Brady, Kevin [TX-8]                     Emerson, Jo Ann [MO-8]                   Kind, Ron [WI-3]
Burgess, Michael C. [TX-26]             Faleomavaega, Eni F.H. [AS]              Kline, John [MN-2]
Butterfield, G. K. [NC-1]               Frank, Barney [MA-4]                     Kucinich, Dennis J. [OH-10]
Cohen, Steve [TN-9]                     Gallegly, Elton [CA-24]                  Lance, Leonard [NJ-7]
Connolly, Gerald E. “Gerry” [VA-11]     Gerlach, Jim [PA-6]                      Latham, Tom [IA-4]
Courtney, Joe [CT-2]                    Gonzalez, Charles A. [TX-20]             Loebsack, David [IA-2]
Crenshaw, Ander [FL-4]                  Grijalva, Raul M. [AZ-7]                 Lofgren, Zoe [CA-16]
Davis, Danny K. [IL-7]                  Gutierrez, Luis V. [IL-4]                Markey, Edward J. [MA-7]
McCollum, Betty [MN-4]                 Price, David E. [NC-4]                  Thompson, Glenn [PA-5]
McGovern, James P. [MA-3]              Rangel, Charles B. [NY-15]              Tierney, John F. [MA-6]
Michaud, Michael H. [ME-2]             Reyes, Silvestre [TX-16]                Towns, Edolphus [NY-10]
Miller, Brad [NC-13]                   Rogers, Mike D. [AL-3]                  Tsongas, Niki [MA-5]
Moran, James P. [VA-8]                 Roybal-Allard, Lucille [CA-34]          Walz, Timothy J. [MN-1]
Norton, Eleanor Holmes [DC]            Ryan, Tim [OH-17]                       Welch, Peter [VT]
Pascrell, Bill, Jr. [NJ-8]             Sanchez, Loretta [CA-47]                Woolsey, Lynn C. [CA-6]
Payne, Donald M. [NJ-10]               Schakowsky, Janice D. [IL-9]            Young, C.W. Bill [FL-10]
Perlmutter, Ed [CO-7]                  Schock, Aaron [IL-18]                   Young, Todd C. [IN-9]
Pingree, Chellie [ME-1]                Speier, Jackie [CA-12]
Platts, Todd Russell [PA-19]           Stark, Fortney Pete [CA-13]
Currently there are 13 co-sponsors in the Senate
SENATORS
Chris Coons (DE) - Sponor
Begich, Mark [AK]
Brown, Scott P. [MA]
Casey, Robert P., Jr. [PA]
Collins, Susan M. [ME]
Crapo, Mike [ID]
Franken, Al [MN]
Inouye, Daniel K. [HI]
Kirk, Mark Steven [IL]
Klobuchar, Amy [MN]
Leahy, Patrick J. [VT]
Merkley, Jeff [OR]
Murray, Patty [WA]



Coalition for Pulmonary Fibrosis proclaims September National Pulmonary
Fibrosis Awareness Month
Patient organization to rally patients, families, advocates to raise awareness and funding for
deadly lung disease

The Coalition for Pulmonary Fibrosis (CPF) has announced that the month of September 2012 will be
proclaimed “Pulmonary Fibrosis Awareness Month”. In previous years, the CPF has celebrated “National
Pulmonary Fibrosis Awareness Week” for one week each September, but expanding the time frame to a month
will help achieve greater national awareness and fundraising in the race to find treatments and a cure.

“It is our goal to expand our reach to communities and cities nationwide by having a grassroots awareness and
fundraising effort that will happen the entire month of September,” said CPF Chief Executive Officer Mishka
Michon. “It is critical that attention is driven to this devastating disease if we are to find answers for our
patients.”

National PF Awareness Month will include fundraising and awareness building efforts around the country
organized by patients, families and partners, as well as a week on Capitol Hill during which advocates will meet
with Members of Congress and their staffs. Those meetings focus on the dire need for increased
Congressional attention to the disease via their support of the Pulmonary Fibrosis Research Enhancement Act
(H.R. 2505, S. 1350) a bill that currently has 66 co-sponsors in the U.S. House of Representatives and 13 in
the U.S. Senate.

September 23-29 will be PF Week at the American Thoracic Society (ATS), a partner of the CPF. The CPF will
participate with the ATS to hold a webinar on PF for patients, families and caregivers as well as professionals
and will provide content for a webpage on the ATS website on the subject.
To join the CPF’s efforts for National PF Awareness Month, email the organization at info@coalitionforpf.org or
visit www.coalitionforpf.org to learn more.



“Awake ECMO” May Be Better For Lung Transplant Patients Than Mechanical
Ventilation
MedPage Today (1/23, Ullman) reports, “Extracorporeal membrane oxygenation (ECMO) as a bridge to lung
transplantation increased survival compared with mechanical ventilation in awake, spontaneously breathing
patients, according to a retrospective study” published in the American Journal of Respiratory and Critical Care
Medicine. Researchers found that “survival at six months was 80% in those receiving ‘awake ECMO’
compared with 50% in those who received mechanical ventilation (P=0.02)” and that patients “in the awake
ECMO group also had a shorter course of mechanical ventilation after transplant surgery (P=0.04).” However,
researchers “cautioned that more research was necessary to improve the technique’s safety and efficacy, and
to tailor the various modalities of extracorporeal life support in different patient populations



Patient Groups Collaborate to Co-Sponsor First Fibrosis across Organs
Symposium
Meeting may spur faster progress in lung, liver, kidney, heart and skin fibrosis; collaboration
could drive future treatments and cures

Patient groups applaud first-of-its-kind medical symposium that brought together experts in fibrotic diseases
from around the globe to explore the similarities that exist in fibrosis of different organ systems. The Coalition
for Pulmonary Fibrosis (CPF), The Pulmonary Fibrosis Foundation (PFF) and the Hermansky-Pudlak
Syndrome Network (HPS Network) co-sponsored the event that was convened by the American Thoracic
Society (ATS) March 8-11, 2012.

Fibrosis can affect the lung, liver, kidney, heart, skin and other areas of the body and claims millions of lives
globally. Most fibrotic diseases are progressive, irreversible and ultimately deadly. These high level
discussions, experts believe, will advance the understanding of related fibrotic mechanisms and lead to
treatment of fibrotic diseases. The meeting brought together top scientists, researchers and physicians from
academia, clinical practice and industry to identify the shared molecular and physiologic responses operative
during tissue injury and repair. More than 60 participants from around the world attended the meeting.

“It was inspiring to be part of this initial collaborative effort between these different specialties, especially as the
work to understand lung fibrosis has, as of yet, not produced any approved treatments in the U.S. The hope is
that answers may spring from a finding in one or many other organs,” said CPF
Chief Executive Officer Mishka Michon.

“We were pleased to see this meeting happen and to support the effort directly,” said Dan Rose, M.D.,
President and CEO of the PFF. “The level of participation by the doctors in each organ area was extraordinary
and they were excited to collaborate with experts in organ areas outside their specialties.”

The meeting’s objectives were to set the scientific priorities for future investigations in single organ and cross-
organ fibrotic disease, assess the currently available experimental models and their relevance to human health
and disease and to identify potential promising therapies for pathologic tissue fibrosis, including idiopathic
pulmonary fibrosis (IPF), also referred to as simply pulmonary fibrosis (PF) or lung fibrosis and fibrosis that
occurs in the heart, liver, kidney and skin.

“If fibrosis could be cured by determination, this meeting would be the end of (fibrotic) disease,” said Donna
Appell, CEO and Founder of the Hermansky-Pudlak Syndrome Network. “It is my hope that this meeting
inspires many productive areas in fibrosis research.”

The meeting was organized by a group of physicians, academic experts and patient advocates, including the
meeting’s founders, John Tosi, DDS and his wife, Teresa Barnes who chairs the ATS Public Advisory
Roundtable (PAR) and is vice president of the CPF. Other committee organizers were Kevin Brown, M.D., a
pulmonologist at National Jewish Health; Dennis E. Doherty, M.D., pulmonologist at University of Kentucky and
the Lexington, Kentucky Veteran’s Administration (VA) Medical Centers; and Dolly Kervitsky, RCP, CCRC, an
experienced respiratory therapist who is vice president of the PFF.



Researchers Find Critical Regulator To Tightly Control Deadly Pulmonary
Fibrosis
An international team of researchers led by Georgia State University scientists have found a key component in
the pathological process of pulmonary fibrosis, a fatal disease for which there is currently no cure.

The scientists found that a key human gene, CLYD, serves as a crucial negative regulator in the development
of the disease, halting its progression that leads to death. The research was published today in the journal
Nature Communications.

“In some patients, CLYD does not function as it should or its protein level is lower than in normal individuals,”
said Jian-Dong Li, director of the GSU Center for Inflammation, Immunity and Infection (CIII) and Georgia
Research Alliance (GRA) Eminent Scholar in Inflammation and Immunity.

“If this does happen, the human tissue repairing response can go out of control, leading to the development of
fibrosis,” added Li, senior author of the study and professor of biology at GSU.

According to the American Lung Association, about 140,000 Americans have been diagnosed with the
disease. Patients’ breathing symptoms worsen over time, and many patients live only three to five years after
diagnosis.
There are currently no effective medicines available to health care professionals to cure pulmonary fibrosis.
Professionals can treat the symptoms to reduce inflammation using steroids and immunosuppressants, but
there are serious side effects over time, including immune system suppression, which makes patients even
more susceptible to infections.

“The disease often develops after infection or injury. In the case of infections brought on by
Streptococcus pneumoniae, a form of pneumonia, the body’s immune system responds and tries to
repair the damage, but in the case of fibrosis, this repairing process is overactive and causes scarring
of the lungs,” said Jae Hyang Lim, a GRA Distinguished Investigator and assistant professor at the
CIII and Department of Biology.
The findings Li and his colleagues have presented have opened an exciting door to development of new
therapeutics to fight the disease by aiming their sights on the CLYD gene.

“These results tell us that we now have a key regulator to target,” said Binghe Wang, Director of the GSU
Center for Diagnostics and Therapeutics and GRA Eminent Scholar in Drug Discovery and a co-author of the
study.

“If we can target CLYD with a focus on regulating its protein level or activity, we may be able to better control
fibrosis,” said Wang, also chair of the Department of Chemistry at GSU. “There is a huge clinical potential in
saving the lives of these patients.”

The results are published in “CLYD Negatively Regulates Transforming Growth Factor-ß Signaling via
Deubiquitinating Akt,” Nature Communications, DOI: 10.1038/ncomms1776. The journal is online at
www.nature.com/ncomms/index.html.

Li said the support provided by the GRA is invaluable to the groundbreaking research performed by scientists
on the project. Li was named as a GRA Eminent Scholar in 2010, and Lim came to Georgia State’s CIII as a
GRA Distinguished Investigator in 2011. Prior to Li and Lim, Wang was named as a GRA Eminent Scholar in
2003.

“These studies are collaborative, multi-disciplinary efforts,” Li said. “The support from the GRA has allowed us
to build state of the art facilities at Georgia State which have been essential to making this essential life-
changing research possible.

For more information about the Center for Inflammation, Immunity and Infection at Georgia State University,
please visit http://inflammation.gsu.edu. To learn more about GRA, visit www.gra.org.

Please note: this is very early stage research in mouse models and we will advise you of any further developments on this
potential treatment pathway.




Blood Proteins Predict Survival in Idiopathic Pulmonary Fibrosis

A panel of blood proteins can predict which patients with the progressive lung disease idiopathic pulmonary
fibrosis (IPF) are likely to live at least five years or to die within two years, say researchers at the University of
Pittsburgh School of Medicine and Centocor R&D. The findings, published online in the American Journal of
Respiratory and Critical Care Medicine, could help doctors determine those patients in imminent need of a lung
transplant and those who can wait a while longer.

Fifty percent of IPF patients die within three years of diagnosis, but others will do well for long periods of time,
explained investigator Naftali Kaminski, M.D., professor of medicine, pathology, human genetics and
computational biology, Pitt School of Medicine, and director, The Dorothy P. & Richard P. Simmons Center for
Interstitial Lung Disease at UPMC. In the disease, breathing becomes increasingly impaired as the lungs
progressively scar.

“It’s hard to tell based on symptoms alone which patients are in the greatest danger,” Dr. Kaminski said. “This
biomarker panel has predictive power that can guide our treatment plan. It may also help us design more
effective research trials because we’ll be able to better match experimental therapies with the most appropriate
patients.”

The research team collected blood samples from 241 IPF patients. They measured the levels of 92 candidate
proteins in 140 patients and found that higher concentrations of five particular proteins that are produced by
the breakdown of lung tissue predicted poor survival, transplant-free survival and progression-free survival
regardless of age, sex and baseline pulmonary function. They then confirmed the results in a second group of
101 patients.

Based on both groups, the investigators developed the personal clinical and molecular mortality prediction
index (PCMI) that incorporates the gender, lung functions and levels of one of the proteins, called MMP7, in
the blood. Patients with a low PCMI were more likely to live more than 5 years while the median survival for
patients with high PCMI scores was 1.5 years.

“This indicates that these blood biomarker levels are not just a reflection of current severity of the lung disease,
but they are predictive of impending death,” said lead author Thomas Richards, Ph.D., assistant professor of
medicine and head of the Simmons Center biostatistics team.

“They have the potential to greatly improve our treatment strategies for IPF, in part by showing us which
patients have the most urgent need for lung transplant, which is currently the only cure for the disease,” added
senior author Kevin Gibson, M.D., medical director of the Simmons Center.

“These findings provide proof of the concept of personalized medicine.” noted Mark T. Gladwin, M.D., chief,
Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine. “We
can use a combination of biological and clinical markers to determine the very best care for each patient.

Drs. Kaminski, Gibson and colleagues have research projects underway to better understand how the
biomarkers change over time.

The team includes Kathleen O. Lindell, Ph.D., R.N., and others at the Simmons Center and Pitt School of
Medicine, as well as researchers from Centocor R&D in Radnor, PA.

Source: Health & Medicine




Keck School Researchers Find New Drug Target for Pulmonary Fibrosis

A team led by University of Southern California (USC) researchers has identified a target in lung cells that may
lead to new treatments for idiopathic pulmonary fibrosis, a progressive disease that ultimately robs a patient of
the ability to breathe.

Pulmonary fibrosis, characterized by scarring of the lung, affects about 128,000 people in the United States,
with about 48,000 new cases diagnosed annually, according to the Coalition for Pulmonary Fibrosis. Lung
damage caused by the disease can’t be repaired, and treatment has focused on improving quality of life.

The researchers discovered that inhibiting certain proteins blocks the interaction between two cellular
pathways thought to contribute to pulmonary fibrosis. The discovery represents a new approach to suppress
the disease. Their study appears in the March 2, 2012 edition of The Journal of Biological Chemistry, the
flagship journal of the American Society for Biochemistry and Molecular Biology.

“There is very little research available about the mechanisms that underlie direct interactions between these
cell signaling pathways, although previous studies have suggested that there is crosstalk between the two,”
said Zea Borok, senior author of the study and professor of medicine and biochemistry and molecular biology
at the Keck School of Medicine of USC.

“Anti-inflammatory treatments that traditionally have been used for pulmonary fibrosis are uniformly ineffective,”
added Borok, who is co-director of the Will Rogers Institute Pulmonary Research Center at USC. “Our
research suggests a new approach to treat a disease that is currently incurable.”

A cell signaling pathway consists of a series of signals that regulate cell behavior; studying these pathways
and how information is transmitted along them may help shed light on disease origins and therapies. Using rat
lung cells, Borok and her colleagues showed that the Wnt/–catenin and transforming growth factor — signaling
pathways directly interact with one another. The interaction appears to increase expression of the — smooth
muscle actin protein, a hallmark of a biological process associated with fibrosis formation. The researchers
confirmed that the interaction also occurs in human lung cells, and found that the interactions are dependent
on the CREB-binding protein (CBP).

The researchers suggest using ICG-001, an experimental CBP inhibitor developed by co-author Michael Kahn,
a USC Provost Professor in medicine and pharmacy, to stymie the pathway interaction. They posit that ICG-
001, which has been shown to be safe for clinical use in colorectal cancer patients, could be used as treatment
for pulmonary fibrosis. The next step is to study its efficacy in fibrosis patients.

“Pulmonary fibrosis is the most common of the interstitial lung diseases, with a fatality rate in line with cancer,”
Borok said. “These findings have the potential to provide an alternative treatment for patients afflicted by this
debilitating disease.”

Researchers from the City of Hope Beckman Research Institute collaborated on the project. First author
Beiyun Zhou, Ph.D., assistant professor of medicine at the Keck School, performed most of the work for the
study during her post-doctoral training in Borok’s laboratory. Other USC co-authors include Edward Crandall,
professor of medicine and chairman of the Department of Medicine at the Keck School; Parviz Minoo,
professor of pediatrics at the Keck School; and Cu Nguyen, lab manager at the Keck School. The study was
supported with funds from the Hastings Foundation, Whittier Foundation and National Institutes of Health.

Source: USC Office of Public Relations and Marketing, Monday, March 05, 2012




New Insights Come From Tracing Cells that Scar Lungs
Tracking individual cells within the lung as they move around and multiply has given Duke
University researchers new insights into the causes of idiopathic pulmonary fibrosis (IPF), a
disease which can only be treated now by lung transplantation.

IPF fills the delicate gas exchange region of the lung with scar tissue, progressively restricting breathing. The
Duke University Medical Center researchers have discovered that some commonly held ideas about the
origins of the scar-forming (fibrotic) cells are oversimplified, if not wrong.

“We are the first to show that pericytes, a population of cells previously described to play a role in the
development of fibrosis in other organs, are present in fibrotic lung tissue,” said Christina Barkauskas, M.D., a
pulmonary fellow in the Duke Division of Pulmonary, Allergy, and Critical Care Medicine.

The team found that pericytes move from blood vessels into fibrotic regions, and were in the damaged lungs of
both humans and mice. In mice, they also showed that the epithelial cells, which make up the lacy sacs called
alveoli, could divide and repair the damage in the gas-exchange location, but these cells were not the source
of scarring.

“We don’t know yet whether the pericytes make the scar matrix itself or just release signals that stimulate the
scarring process, but either way, they are a potential target for new therapies,” said Brigid Hogan, PhD, senior
author and chair of the Duke Department of Cell Biology.

The researchers used genetic lineage tracing to study the origin of cells that gathered in fibrotic areas. They
gave several different cell types an indelible fluorescent tag and then followed the cells over time.

The cells kept the tag even if they multiplied, migrated within the lung, or differentiated into another cell type.

Paul Noble, M.D., co-author and chief of the Pulmonary Division at Duke, said that identifying the source of the
lethal expansion of the scarring (fibroblast) cells is a critical missing link in understanding disease progression.

Previous studies had suggested that the epithelial cells in the alveoli are a source of fibroblast accumulation
after lung injury, he said.

“This study used the newest tracing approaches to conclusively demonstrate, however, that the alveolar
epithelium isn’t a significant source for fibroblast accumulation following lung injury in mice,” Noble said. “The
studies suggest that there may be several sources for the scar-forming cell accumulation in fibrosis, including
pericytes, which hadn’t been implicated in lung fibrosis until now.”

Noble said that the study data provide new insights into the sources of scar-forming cells and would help to
target the correct cell population that causes disease progression.

Now the researchers are focusing on what these cells may make that could promote a healing process. “One
idea is that perhaps in IPF these epithelial cells have lost the ability to repair damage to the lung, so that
scarring continues inexorably and cannot be restrained — perhaps we could find a way to assist the repair
process,” Hogan said. “Promoting the healing process might be another therapeutic approach.”

Other authors include Jason R. Rock and Yan Xue of the Duke Department of Cell Biology; Michael J. Cronce
and Jiurong Liang of the Duke Division of Pulmonary, Allergy and Critical Care Medicine; and Jeffrey R. Harris
of the Duke Division of Cellular Therapy. Jason Rock is now with the University of California, San Francisco.

Source: Duke Medicine News and Communications, December 1, 2011




Statins May Increase Risk of Interstitial Lung Abnormalities in Smokers
The findings were published online ahead of print publication in the American Thoracic Society’s
American Journal of Respiratory and Critical Care Medicine. January 6, 2012

Use of statins may influence susceptibility to or the progression of interstitial lung disease (ILD) in smokers,
according to a new study.

While some studies have suggested that statins might be beneficial in the treatment of fibrotic lung disease,
others have suggested that they may contribute to the progression of pulmonary fibrosis by enhancing
secretion of inflammasome-regulated cytokines, and numerous case reports have suggested that statins may
contribute to the development of various types of ILD.

“Based on earlier case reports of statin-associated ILD and data suggesting that smoking is associated with
the interstitial lung abnormalities (ILA) which underlie ILD, we hypothesized that statins would increase the risk
for ILA in a population of smokers,” said George R. Washko M.D., MMsC, and Gary M. Hunninghake M.D.,
MPH, of the Division of Pulmonary and Critical Care at Brigham and Women’s Hospital in Boston.
“Accordingly, we evaluated the association between statin use and ILA in a large cohort of current and former
smokers from the COPDGene study. In addition to the association between statin use and ILA we found in
humans, we also demonstrated that statin administration aggravated lung injury and fibrosis in bleomycin-
treated mice.” Bleomycin has been shown to induce lung inflammation and fibrosis.

Assessment included pulmonary function testing and CT scanning for radiologic features of ILA. Among 1,184
subjects with no evidence of ILA, 315 (27%) used statins, compared with 66 of 172 (38%) subjects with ILA.
After adjustment for a number of covariates, including a history of high cholesterol or coronary artery disease,
statin users had a 60 percent increase in the odds of having ILA , compared to subjects not taking statins. No
other positive associations between ILA and cardiovascular medications or disorders were detected. The
association between statin use and ILA was greatest with statins with higher hydrophilicity (readily absorbed or
dissolved in water), such as pravastatin, and in higher age groups.

The effects of statins on lung injury and fibrogenesis were also examined in a study in mice, which were
pretreated with pravastatin prior to intratracheal bleomycin administration. Statin use was found to exacerbate
bleomycin-induced lung fibrosis. In a further in vitro study, statin pretreatment was shown to enhance Nlrp3-
inflammasome activation through mitochondrial reactive oxygen species generation in macrophages. “These
results implicate activation of the NLRP3 inflammasome in fibrotic lung disease,” said Jin-Fu Xu M.D., and
Augustine M. K. Choi, M.D., of the Department of Pulmonary Medicine, Shanghai Pulmonary Hospital, Tongji
University School of Medicine, in Shanghai, China and the Division of Pulmonary and Critical Care at Brigham
and Women’s Hospital in Boston, respectively.

There were some limitations to both studies. Findings in the mouse model were not replicated in human
samples. All study subjects were current or former smokers, perhaps limiting the applicability of the results to
others. Cigarette smoking by itself may lead to pulmonary inflammation. Finally, the duration and dosage of
statin therapy was not available for the majority of patients.

“While statin use was associated with ILA in our study, caution should be used when extrapolating these
findings to the care of patients,” concluded Dr. Hunninghake. “The significant benefits of statin therapy in
patients with cardiovascular disease probably outweigh the risk of developing ILA, and statin use may benefit
some patients with respiratory disease. Clinicians should be aware, though, that radiological evidence of ILD
can develop in some patients treated with statins.”
Potential Therapy for Scleroderma Lung Disease Uncovered
Investigators, partially supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases,
have found that a deficiency in the protein caveolin-1 (cav-1) is linked to the development of interstitial lung
disease, the scarring of lung tissue that causes disability and death in people with Scleroderma. The scientists,
from the Medical University of South Carolina (MUSC) in Charleston, also showed that a special peptide called
caveolin scaffolding domain (CSD) inhibits progression of the disease in mice. The study was reported in
Fibrogenesis & Tissue Repair.

Scleroderma is an autoimmune disorder in which the immune system mistakenly attacks the body’s own
tissue. The systemic form of the disease, known as systemic sclerosis, is characterized by hardening and
scarring that can seriously affect both skin and internal organs. Scarring, also known as fibrosis, is caused by
overproduction of the protein collagen, not only by fibroblasts—a common cell found in connective tissue—but
also by fibrocytes, cells that come from monocytes and originate in the blood. Fibrocytes express a protein
called CXCR4, which helps fibrocytes migrate from the blood to lung tissue, where they contribute to lung
fibrosis.

In their study, Elena Tourkina, Ph.D., and her MUSC colleagues examined seven systemic sclerosis patients
with interstitial lung disease. These patients all had fibrocytes in their lungs, along with overexpressed CXCR4.
Lungs from healthy controls, however, showed no fibrocytes or overexpressed CXCR4.

From previous work, Dr. Tourkina’s group also knew that levels of cav-1 protein were significantly reduced in
the fibrotic lung tissue of people with systemic sclerosis, and in a mouse model of fibrotic lung disease. Her
team treated monocytes from lung-involved systemic sclerosis patients with the CSD peptide. Their results
showed reduced CXCR4 expression, and—using a laboratory procedure that mimics the movement of
monocytes into damaged lung tissue—reduced monocyte migration. The researchers also administered CSD
peptide to mice treated with bleomycin, which creates a model of systemic sclerosis in which the animals
develop lung fibrosis. This treatment, they found, slowed monocyte and fibrocyte migration to the lungs and
also slowed disease progression in the mice.

“Our results highlight the ability of CSD peptide to reduce fibrocyte migration to the lungs, thereby reducing
lung fibrosis,” says Dr. Tourkina. “CSD peptide may, in fact, be valuable as a therapy for interstitial lung
disease in systemic sclerosis patients.”

An estimated 49,000 adults in the U.S. have scleroderma, and lung involvement is emerging as the leading
cause of morbidity and mortality. Treatments for fibrotic lung disease have been only moderately successful,
and lung transplantation is often needed.

Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases (2012), “Mechanism, Potential Therapy for
Scleroderma Lung Disease Uncovered”


[The CPF is sharing this information because of the close association between Scleroderma and IPF]




Thank you to everyone who has stepped up to help raise funds to fight PF.
Every supporter, whatever your gift level, is making a difference. The recent
initiative to bring researchers together across organs is an example of the CPF’s
consistent work to generate change. Effective innovative research collaborations
rely completely on your generous support. Thank you for being part of our family.



CPF’s Daughters of PF Celebrates National Award Finalist Status, First
Anniversary

Program Invites New Members

Just a year ago, the Coalition for Pulmonary Fibrosis (CPF) launched a new effort inspired by the tens of
thousands of daughters (and others) who have seen a parent suffer from PF. This month, the Daughters of PF
program celebrates its first anniversary while also celebrating being named a finalist in the PR News Volunteer
Program Award.

From the hearts of daughters nationwide came the Daughters of PF program. The women’s stories are
compelling and inspiring and one-by-one, they are working to raise the recognition of PF nationwide. (Anyone
can join and there are sons who work diligently on this effort.)

Daughters are creating projects in their local areas to increase awareness and understanding of PF while
raising needed funds for research and patient support services. The daughters’ efforts are reflective of their
interests and talents and are allowing them to make a difference right where they are.

More than 200 women have joined Daughters of PF and the CPF invites new members to come on board. If
you or someone you know is a daughter of a patient past or present or a woman who has lost anyone they love
to PF,
please share the name of this program with them and ask them to join now.

To join, just send an email to daughters@coalitionforpf.org or call us at (888) 222-8541, ext. 702. You may
also join our Daughters group on Facebook and LinkedIn.

The Daughters of PF program has a growing number of daughters who are planning and holding events in
their local areas. Some are larger events, but many are small and the CPF can help anyone become
successful with an awareness and/or fundraising event. If you’ve even got an idea, let us know.

We can help you bring it to fruition and make you successful. Contact Su Hwang at (888) 222-8541, ext. 704 or
email her at shwang@coalitionforpf.org.



“I also lost someone who meant the world to me... my mother. She died in 2006. I have been looking and
searching of ways to help educate others and to also help find a cure for this horrible disease. I don’t know
much about fund-raising but I am willing to learn. Please include me in any way I can help.” — Lola

“I would like to join your program. My father is currently suffering from the disease and I would like to do
anything I can to help him and all other patients
suffering as well.” — Tracy




Woman Conquers Her Fear, Swims Nine Miles in Open Water to Raise
Awareness and Funds For Disease That Killed Her Father

Catherine Goodrum has been afraid of being in open water most of her life. In an effort to overcome her fear,
Goodrum joined a Total Immersion™ Women’s Swim Camp in St. John, U.S. Virgin lslands and turned the
experience into a tribute to her father who died from Pulmonary Fibrosis (PF) in 2009. Goodrum swam a total
of nine miles during the camp and used her personal victory to raise funds for the Coalition for Pulmonary
Fibrosis (CPF) and its Daughters of PF program.

“I watched my father suffer from this incurable lung disease and I could see the panic on his face as he
struggled to breathe. I realized the anxiety I felt when swimming was much the same kind of fear and panic. He
fought bravely and I knew I had to fight my fear as a tribute to him,” Goodrum said.

After a tragic sailing accident in her teens, Goodrum abandoned open water and didn’t return to swimming until
she was almost age 50.

Goodrum, who lives in Potomac Falls, VA, helps direct the Coalition for Pulmonary Fibrosis’ new Daughters of
PF program and encourages other women to do awareness and fundraising efforts of their own. Daughters of
PF is a program with more than 200 members, all women who have lost a parent or other loved one to PF and
want to raise awareness and funding for the CPF to find treatments and a cure.

“Catherine and the women of our Daughters of PF inspire us. They have experienced such profound loss with
the death of a parent or other loved one and have used their grief to fuel their efforts to raise awareness and
find a cure. Catherine’s effort is truly one of courage and determination,” said Mishka Michon, CEO of the CPF.

In the swim camp in St. John last week, Goodrum told her fellow camp swimmers about her fear of water, her
father’s death from PF and her fundraising effort along with the women and friends that supported her. Women
at the camp donned swim caps with the Daughters of PF logo and several have donated to her effort. The
women also gave her a first-ever award for the camper deemed to be most inspirational and deserving called
the Matilda Award.

Goodrum started a blog “The Adventures of Cat and Matilda” to document her year-long journey as the award
winner and to raise awareness of PF and support CPF efforts. To date, Goodrum has raised over $10,000 for
the CPF.



Walk for Their Next Breath 2011 — Nationwide Community Walk Events
Walking is easy for most people, but nearly impossible for the 128,000 Americans who suffer from Pulmonary
Fibrosis (PF). In celebration of our 10th Anniversary year in 2011, hundreds of people across the country
participated in our nationwide community walk campaign Walk for Their Next Breath. We thank everyone for
participating and here are some of their stories:
The First Annual Linda Biggs 5K Walk/Run, A Quest for Cure

Kathy Biggs, a licensed physical therapist, saw her mother-in-law suffer from PF, a disease that scars the
lungs and suffocates its victims. There was nothing even she, a medical professional, could do to help her.
Linda Biggs died March 21, 2009 at the age of 61.

“We felt really helpless,” said Kathy Biggs. “My husband and I wanted so much to help his mother breathe but
at the end, not even the supplemental oxygen could help her.”

An avid runner, Biggs and family held the first annual Linda Biggs 5K Walk/Run to raise awareness of the
disease and to pay tribute to Linda. She recently joined a new group called Daughters of PF, which is part of
the efforts of the CPF and inspires daughters and other family members to turn their grief and pain into action
by holding awareness and fundraising efforts in their local areas.

Nearly one hundred participants attended the inaugural walk at Lake Murray Dam in Lexington on Saturday,
October 15, 2011 and the Biggs family raised nearly $10,000.

“We are honored that the Biggs family is so involved in the cause and is helping the Coalition for Pulmonary
Fibrosis help families like theirs. Their efforts will not only build awareness and find treatments, but will pay
tribute to a wonderful woman who was lost to the disease,” said Mishka Michon, CEO of the CPF.

The Biggs family, placed billboard ads across the state of S.C. this summer to raise awareness of PF and did
so on their own dime. “We really want to get the word out far and wide about this devastating disease and help
others get diagnosed early,” said Biggs.

“Hope gives you courage when you tell yourself you’d rather give in. Everyone should always be given hope
and Linda’s family wants to be a part of generating hope to the many patients and families suffering from this
very unforgiving disease,” said Biggs.

Thank you to Biggs event sponsors: All-American Hose/Snap-Tite Hose; Galloway Family; Lucky’s Burger
Shack; Southern First; Biggs Family; David’s Fine Jewelry and DexterBonnieMegz.


Violet Rippy 5K Walk/Run
The Inaugural Violet Rippy 5K Walk/Run held on August 13, 2011 at Heinz Field in Pittsburgh, PA was the
second fundraiser for Tami Rippy a member of CPF’s Daughters of PF, who lost her mother Violet in March
2009. Previously, her coworkers at NEP Supershooters held a charity golf tournament (featured in the Summer
2011 Action Alert). Her dedicated volunteers included former SPORTSBEAT Co-Hosts Guy Junker and Stan
Savran. “We are honored to co-host this event for such a worthy cause that will not only build awareness and
funding for PF but will pay tribute to an incredible woman who was lost to the disease,” said Junker. Savran
said, “It’s a terrific opportunity to team up and focus on finding treatments and a cure for this deadly lung
disease.” The walk, raffle and silent auction drew over 200 participants and raised over $30,000. Next year’s
walk will be held August 11, 2012. Thank you to the event’s sponsors: Axial Advisory Group, LLC; NEP;
Montauk Energy; and SOS Global Express.
Walk in Honor of Gary Snyder
On September 17, 2011 in nearby Mechanicsburg, PA, another Daughters of PF member Heather Snyder held
a Walk in Honor of Gary Snyder, her father who was lost to PF in June 1981. At age 37, Heather herself was
diagnosed with PF making it a familial case (approx.10-15% PF cases are genetic) and although her father
was not able to get a lung transplant, Heather received her double lung transplant in February 2011. Heather
and her family are also dedicated, active members of the advocacy team that meets with legislators on Capitol
Hill to secure funding for PF research.

Orange County Walk in Tribute to Carlos Juarez
The Orange County Walk in Tribute to Carlos Juarez was held on August 17, 2011 in Laguna Niguel Regional
Park, and was hosted by Sandra Juarez-Runyon and family. Sandra’s father Carlos has been living for five
years with the disease and was able to attend. “My father’s journey with this disease takes such courage,
strength and incredible optimism. I want to try and help him and the thousands of other people who suffer from
the same disease with every step we take” she said. The walk attracted over 50 participants and encouraged
two of its participants, Liz and Wilma, to host their own walks in November (their stories continue below).
Thank you to event sponsors: Nicole Kennedy and family; Frank Gamboa; Dick Moore Family; Sylvia Velasco ;
and the Zarbakhsh Family.

Santa Monica Walk
Liz McDonald, inspired by the OC Walk earlier in the year, hosted the Santa Monica Walk on November 5,
2011 in memory of her father. Next year’s walk will be held in Oregon with the help of her sister Melinda.

ORANGE COUNTY Walk
Wilma Vijandre, who also participated in the OC Walk, went on to host her own Ontario Walk for PF on
November 12, 2012. Wilma has been living for seven years with PF and credits her family, friends and past
coworkers with keeping her spirits high while facing her challenges. The Inland Empire Support Group,
including its key leaders the Pacheco family, came to support Wilma. The Pachecos held their own successful
fundraiser at Corky’s Kitchen & Bakery/Guasti Cafe in September.



Inaugural Boston 5K
On October 8, 2011, the Inaugural Boston 5K was hosted by Mark Haberland, Dhruti Kalathia, and Monica
Snitily, who each have lost a family member to PF. The hosts and 20 other participants who came to honor
their loved ones, shared a picturesque fall walk along the Charles River. Together, they raised over $5,000.
This years walk will be held August 19, 2012.



Fourth Annual Walk for Your Next Breath
The Fourth Annual Walk for Your Next Breath, the namesake of our national campaign, was held in Franklin,
TN on October 15, 2011 and was hosted by Vanderbilt University Medical Center’s Middle Tennessee
Coalition for PF Support Group. This dedicated group of patients, families, and caregivers has come together
for the past four years raising PF awareness and nearly $100,000 to date (featured in the Fall 2010 Action
Alert). Thank you to volunteers who continue to provide catering, items for raffles, and entertainment as well as
event sponsors: Rose Barton; Brown Bag Marketing; Michael and Wendi Mason; James Moore, and Lynda
Oxley (Ms. Oxley lost her fight to PF just one week following the event).
CARLSBAD & SOMERSET WALKS
Two sisters, Vipashi and Jenny, hosted simultaneous walks on January 28, 2012 in memory of their
father Parimal Trivedi. In two separate parks, on two opposite coasts – California and New Jersey,
the two sisters (also members of CPF’s Daughters of PF) joined together with family and friends to
raise awareness and funds for PF.


CPF Board Members Host Chicago Dinner, Fall 2011

Vanessa Balbach Clarke and Jeff Harris of the Members of the CPF’s Board of Directors, hosted an intimate
dinner benefitting the CPF in the Chicago suburb of Lake Bluff. Mrs. Clarke lost her mother, Elaine Balbach, to
PF, and Mr. Harris his wife Mary, and both have remained committed advocates and supporters of the CPF’s
effort to find answers to the disease. The dinner was also in honor of Bill Aydt and Tad Carr, whose lives were
cut short by PF.

Guests were moved by a touching speech given by Mrs. Clarke’s son Arlo, who shared about the impact of his
grandmother’s battle with PF on him and the entire family. Mrs. Barbara Carr, who lost her husband, Tad, to
PF, spoke of the importance of the work of organizations like the CPF and the value of ongoing efforts to
inform the nation about the threat and the need for answers. Mishka Michon, CPF CEO, shared information
about what the CPF seeks to accomplish and how community involvement is vital to advancing the work.
Karen Curtiss, who assisted in the event design, spoke about her father Bill Aydt. Dr. Robert Love, a longtime
friend of the CPF and a distinguished physician in the area of PF at Loyola University Medical Center,
addressed the challenge of finding answers to this difficult disease.


Upcoming Events

Please go to the CPF website in the next weeks for further listings of dates and times of new
events.

MAY 12 - 5th Annual NYC Run-Walk-Hike for PF – New York, NY
MAY 12 - PF Walk – Pasadena, CA
MAY 17 - Casino Fundraiser – Hermosa Beach, CA
JUNE - Vic Vittorino Walk for Your Next Breath – Delanco NJ
JUNE 2 - “Living with Pulmonary Fibrosis” – a free conference hosted by the Mayo Clinic,
Jacksonville FL
JUNE 10       02 - Riding for PF – Raymond, ME
AUGUST 11 - Second Annual 5k Run/Walk for PF - Pittsburgh, PA
AUGUST 19 - Second Annual Boston Walk – Boston, MA
AUGUST - Portland Oregon Walk (Date TBD)
SEPTEMBER - Riverside California Walk (Date TBD)
FALL - Boston Walk, Brookline, MA (Date TBD)
To learn more about support groups in your area or to start one, visit www.coalitionforpf.org or
call us at (888) 222-8541 and we’ll send you a support group starter kit and help you promote your
new group.


Watch for news about a CPF cruise with special pricing for CPF members.
Patients are especially welcome. A notice will be posted on our website as soon
as we have details about this trip.
Please check our website www.coalitionforpf.org under the NEWS & EVENTS –
CPF EVENTS section for more event details



CPF Board of Directors
Marvin I. Schwarz, M.D. – Chairman
University of Colorado Health Sciences Center

Gregory Tino, M.D. – Vice Chairman
University of Pennsylvania Medical Center

Celeste Belyea, RN, RRT – Secretary
Ormond Beach, FL

Vanessa Balbach Clarke
Family member of PF patients, Chicago, IL

Terence F. Hales
Director of Real Estate, Americas Portfolio, Pfizer, New York, NY

Jeff Harris
Mary D. Harris Memorial Foundation, Chicago, IL

Paul W. Noble, M.D.
Duke University Medical Center

Deirdre R. Roney
Family member of PF patients, Malibu, CA

Stanley Weinstock
PF Patient, President, Biener Auto Group,
Great Neck, NY




CPF Scientific Advisory Board
James E. Loyd, M.D. – Chairman
Vanderbilt University Medical Center

Harold R. Collard, M.D.
University of California, San Francisco

Serpil C. Erzurum, M.D.
Cleveland Clinic Foundation

Adaani Frost, M.D.
Baylor College of Medicine
Marilyn Glassberg, M.D.
University of Miami/Jackson Memorial
Medical Center

Jeffrey Golden, M.D.
University of California, San Francisco

Kevin O. Leslie, M.D.
Mayo Clinic, Scottsdale, AZ

Fernando J. Martinez, M.D.
University of Michigan Medical Center

Steven Nathan, M.D.
Inova Fairfax Hospital, Falls Church, VA

Paul W. Noble, M.D.
Duke University Medical Center

Maria Padilla, M.D.
Mount Sinai Medical Center, New York, NY

Ganesh Raghu, M.D.
University of Washington Medical Center,
Seattle, WA

Glenn Rosen, M.D.
Stanford University Medical Center

Cecelia M. Smith, D.O.
Reading Hospital & Medical Center,
West Reading, PA

David Zisman, M.D.
Sansum Clinic, Santa Barbara, CA


Whether you are a PF patient, a family member of a patient, or are close to someone with PF, the
CPF is always just a phone call away. Our staff has counseled thousands of patients, and we are
always here to provide you with the resources and support you need. Please call
(888) 222-8541 to learn more.


CPF Staff
Mishka Michon
Chief Executive Officer
mmichon@coalitionforpf.org
(888) 222-8541, x.701


Teresa Barnes
Vice President, Patient Outreach &
Program Support
tbarnes@coalitionforpf.org
(888) 222-8541, x.702


Kristina Unutoa
Director, Finance and Accounting
kunutoa@coalitionforpf.org
(888) 222-8541, x.703


Su Hwang
Associate Director, Development
& Director of Special Events
shwang@coalitionforpf.org
(888) 222-8541, x.704




Supporting the CPF
The Coalition for Pulmonary Fibrosis (CPF) relies on the contributions of individuals, corporations and
associations who share our commitment to improving awareness and education of PF, and improving the
quality of life for patients fighting PF nationwide. Every service we offer is at no cost to the PF community.
Through your generous support, the CPF will continue to provide information, resources and support to more
than 128,000 PF patients, caregivers and families, and to the health care professionals who treat them.



Should you wish to make a tax-deductible contribution to the CPF, we encourage you to send your check or
money order to:
   Coalitionfor Pulmonary Fibrosis
   10866 W. Washington Blvd., #343
   Culver City, CA 90232

Contributions are also accepted online by using any major credit card safely and securely through our Web
site. Please access our contributions page at www.coalitionforpf.org/AboutUs/contribute/contributenow.asp, or
click “Contribute Now” from our home page. To contribute by phone using any major credit card, please call the
CPF at (888) 222-8541.

If you have any questions about your contribution to the CPF, or if you would like to make a restricted donation
to advance specific CPF programs or research efforts, please contact us at (888) 222-8541, or by email at
info@coalitionforpf.org.

								
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