A Worldwide Support Network For Chronic Myelogenous Leukemia
Posted by rob on July 31, 2005 under Uncategorized | 
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Metal artist Robert Foster stands in front of his work titled ‘Moon Beneath the Sea’ at a exhibition featuring a range of designs using aluminium at the Melbourne Museum.
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A young girl rides a tricycle under a cascade of water from an open fire hydrant along 151st Street in upper Manhattan.
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Paraiso Beach – From hljscj
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Chinese Mongolian models parade the latest in traditional fashion, designed by a Mongolian designer, during the Naadam festival on the grassland of Gegental Steppe in China’s Inner Mongolia region.
Posted by rob on July 27, 2005 under Uncategorized | Be the First to Comment
Ambit Biosciences has announced the discovery of a new drug that may work on the T315I
mutation which causes Gleevec resistance in CML patients. This may become another
important new drug in the CML pipeline.
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A Kyrgyz nomad rides his horse in the Son-Kul Lake, the ancient Great Silk Road from Kashgar to Bishkek.
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Grazing on Son Kul Plateau : A horse grazes as a rainbow appears in the sky on the Son-Kul plateau, 3013 metres above sea level located on the ancient Great Silk Road from Kashgar to Bishkek.
Posted by rob on July 25, 2005 under Uncategorized | Be the First to Comment
Supporters of US Lance Armstrong wave US flags during the 21st stage of the 92nd Tour de France cycling race between Corbeil-Essonnes and the Champs-Elysees in Paris. US Lance Armstrong secured his seventh Tour de France yellow jersey following the 21st and final stage of this year’s race.
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Sunday, July 24, 2005
The Oregonian
Erin Zammett arrived at her Manhattan office and dialed her voice mail. The message from her doctor was vague but insistent. She returned the call immediately. “There’s something wrong with your blood,” he told her. “You need to get down here right away.
“Don’t wait.”
Tests revealed chronic myelogenous leukemia, or CML, a disease that causes bone marrow to produce too many white blood cells. She was 23, and the first part of her life — two decades of growing, studying, working, playing — snapped shut. The second part gaped before her, pitch-black and unmapped.
It’s how she dealt with the all-too-common diagnosis of cancer that set her apart, that brought her to Oregon and her story to tens of thousands. And it’s why her Portland doctor has called her “the face of a new generation of cancer.”
Her response to her diagnosis in many ways reflects the traits of her generation of young creatives. She placed special value on her independence, and her online research skills gave her tools for taking charge of her prognosis. She bubbled with energy and resourcefulness. And, given her youth, dying was not on her to-do list.
She brought her own personality to the struggle, too. She’s a perfectionist who insists on dotting every “i” and crossing every “t.” And she’s compulsively well-organized, which helps her fight her battle on multiple fronts.
When Erin learned of her CML, she was fresh out of college and working as an editorial assistant — translation: lowest rung on the journalism ladder — at Glamour magazine. The editor-in-chief asked her to document her illness in the magazine, certain that readers would be interested in getting to know a young cancer patient. A photographer documented every facet of her treatment, from bone-marrow biopsies to chemotherapy injections.
The bimonthly columns resonated with readers, and word spread to the cancer community. Speaking engagements filled her datebook. She and her sister Melissa set a fundraising record for the New York City chapter of the Leukemia & Lymphoma Society: $36,000 in six weeks. Erin went on to testify before Congress, to appear on “Nightline,” “Today” and “Good Morning America,” and to write a book called “My (So-Called) Normal Life.”
Part of a documentary
When Erin walked into the oncology waiting room at Oregon Health & Science University in late June, receptionists and nurses ribbed her about her entourage.
“Well, look at all those cameras!”
“Darn it, I didn’t wear any makeup today!”
Erin’s retinue included her mother, Cindy, two reporters, two photographers and 33-year-old filmmaker Kris Carr, who is shooting a documentary called “Crazy Sexy Cancer.” The film focuses on six young women — Kris Carr and Erin Zammett included — who are fighting the disease. Carr is planning to screen her film in January at the Sundance Film Festival and will likely include footage from Erin’s Portland trip.
After her 2001 diagnosis, Erin had three options: a bone-marrow transplant, which requires a genetic match, causes infertility, carries a 15 percent mortality rate and is the only known cure for CML; a course of the drugs Interferon and chemotherapeutic Ara-C, which works in only 30 percent of patients; and Gleevec, a new drug developed at OHSU.
When she heard about Gleevec, she launched a research project to learn more about it. She was intrigued by what she found. Gleevec is a small orange pill that targets only cancer cells, not healthy ones, and causes few side effects while putting many patients into remission. Erin chose it as her path of treatment. In addition, she participated in a clinical trial that combined Gleevec with injections of Ara-C. She began flying to Portland every three months, her entourage in tow.
While Erin’s well-documented visits to OHSU reflect what she calls her “cancerlebrity,” she views the hospital — and Portland — as a retreat. She now gets checkups every three months in New York and really only needs to come to Portland once a year. She chooses to visit more often because she likes her doctor and the city.
Her mother joins her and the two of them shop (her mother could drive to Woodburn Factory Stores blindfolded); eat (they love Veritable Quandary); and sightsee (they’re fond of the coast and Multnomah Falls).
But the cross-country flights are about more than good bargains and good food. Because of her fundraising work, Erin says, she thinks more about other cancer patients than herself. It’s on her Portland trips that she focuses on her own disease.
A nurse led Erin into an exam room and took her blood pressure, temperature and pulse. Then came the moment Erin dreads: the weigh-in. She grudgingly stepped onto the scale and looked away.
“Do you want to know?” the nurse asked with a smile.
“God, no,” Erin groaned. “I’m getting married in three weeks.”
After another nurse took Erin’s blood, Dr. Michael Mauro arrived to go over her charts. Before discussing Erin’s health, he asked about wedding preparations.
“Are you coming?” her mother, Cindy, asked.
“Yes, we’ll definitely be there,” Mauro replied.
“Oh good. Because you didn’t send in your R.S.V.P.,” Cindy said with a smile. “Busy curing cancer, I guess.”
Erin and Mauro, who headed her clinical trial, have become good friends. Mauro, 36, grew up on Long Island, just 10 minutes from the Zammetts, and trained with Erin’s New York oncologist.
According to Mauro, Erin is in “very, very deep remission,” having achieved what is called a major molecular response to her treatment. When Erin was diagnosed with CML, her white-blood-cell count was more than 100,000; today, it’s 5.8. In 2001, 98 percent of Erin’s cells showed leukemia; today, the disease is barely detectable.
Although Mauro predicts that Erin will be in a prolonged remission, he says that projecting her prognosis to her entire lifetime is hard because of her treatment’s novelty. Before Gleevec, most CML patients had five years to live; today, Mauro says, a patient such as Erin, who will take Gleevec indefinitely, could be in remission for 15 to 20 years. The drug isn’t a cure, however, and those who stop taking it are likely to relapse.
Mauro admires Erin’s dedication to raising cancer research money and awareness. The common perception of cancer, Mauro says, is that it affects older people; he thinks Erin’s youth and vitality bring attention to new treatments.
To that end, Erin works as a voluntary spokesperson for Novartis, the company that manufactures Gleevec. Many print advertisements for the drug, which have appeared in national magazines and newspapers, feature a photo of Erin in the Glamour offices and the words: “Deadly cancer at 23. Complete remission at 24.” “One-stop shopping”
Erin’s excitement was palpable as she strode into the bridal shop on Northwest Lovejoy Street. She was clearly looking ahead, past her cancer. “I get to try on my wedding dress!” she chirped.
Anne Mauro, her doctor’s wife and a couture gown designer, greeted Erin with a warm hug. They met in 2003, before Erin was even in the market for a wedding dress, a coincidence that later enabled Erin to engage in what she calls “one-stop shopping”: come to Portland for a cancer checkup, stay for a dress fitting at Anne Mauro Designer Bridal.
Erin emerged from the dressing room to a chorus of “oohs.” She gazed into a full-length mirror, examining the dress from every angle.
Her perfectionism surfaced as she focused on the rear view. “I’m a little worried about my back fat,” she said, pinching a minuscule amount of skin beneath her shoulder blade.
Her mother rolled her eyes. “Erin, you don’t have any back fat,” she said, her Long Island accent betraying a hint of annoyance.
“Mom, even the thinnest person in the world can have back fat,” Erin retorted.
Anne quietly assured her that the dress fit her perfectly and that it was designed to be snug in the back so that the halter would fit properly. Cindy chimed in with a motherly translation: “It has to be snug in the back, or your boobs are going to fall out.”
The room erupted in laughter, one more testament to the way Gleevec helps cancer patients live almost perfectly normal lives.
Her mother’s comment appeased Erin, who twirled in front of the mirror. “I love it! I totally love it! It’s perfect!” she said, grinning.
“You look beautiful, honey,” Cindy said. For a moment, the crowded shop went quiet.
“I should take it off,” Erin said reluctantly, breaking the silence. “I’m sweating all over it.”
A call from her sister
For the second time that day, Erin arrived at OHSU. No weigh-in or blood draw awaited her. Instead, she would speak at a donor reception for the Portland chapter of the Leukemia & Lymphoma Society, an organization that helped pay for Gleevec’s development.
Dr. Mauro took the lectern and introduced Erin to the crowd. “Erin is a very special patient of mine,” he said, “but she’s more than that. She’s a shining example of where we’re going with cancer research.”
As Erin related her story, starting with her diagnosis, the crowd — many directly affected by cancer — listened attentively. Cindy, sitting at the back of the room, watched her daughter with the same pride she displayed at the bridal shop. But tears rolled down her face when Erin began talking about her sister Melissa.
In 2003, “three hours after I got the news that I was basically cancer-free, my sister Melissa called me with news of her own: She had just been diagnosed with Hodgkin’s lymphoma. She was 27 and seven months’ pregnant.
“Everyone immediately assumed that we must be living on a toxic-waste dump, but our doctors assured us that it was more likely bad luck than bad genes or bad water.”
Melissa, now 29, went on to deliver a healthy boy, Andrew, now 2. Five months after her diagnosis, she went into remission, only to relapse 10 months later. Today, after a stem-cell transplant, Melissa is again cancer-free.
“Through my column for Glamour, I get a ton of letters from readers,” Erin continued. “And the one thing I’ve realized is that not everyone has the support of their family or access to the best doctors and information or the means to get it. Not everyone is as lucky as my sister and I have been.”
The crowd gave Erin a standing ovation, and she beamed. Then, as the reception neared an end, Katie Knudson, a 10-year-old with CML, presented Erin with a ceramic wine chiller she had painted. Dotted with pink crowns, it read, “A pretty princess is a healthy princess.”
Erin flew back to New York three days later. On July 14, Dr. Mauro e-mailed the test results from her June visit. Her blood showed no trace of leukemia. On Aug. 5, her 13th column will appear in Glamour. On Saturday, she married longtime love Nick Ruddy in her hometown of Huntington, N.Y.
Chris Hunt: 503-412-7078; christinehunt@news.oregonian.com
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He doesn’t try to hide the emotion. The excitement for this day has been building inside him for more than a year.
“This is a once-in-a-lifetime opportunity,” Adam McFadden said Friday before departing for Chicago. “I’m so happy. Every time I think about it, I’m almost in tears.”
In Chicago, the Rochester city councilman will meet an 18-year-old named Lamar Adams. McFadden saved Adams’ life last year, or as McFadden says, extended it, by donating his blood stem cells.
Most patients must search for a match from an unrelated donor. There are 5.5 million potential donors on the National Marrow Donor Registry, resulting in 20,000 transplants since 1987. A match is more likely among people of the same heritage, the program’s Pat Thompson said, explaining why it’s trying to attract minority donors. About 450,000 potential donors are African American.
McFadden signed up five years ago Friday at a recruitment drive at James Madison High School of Excellence. A friend’s son had leukemia, but McFadden wasn’t a match.
Then, in late fall 2003 and more than 300 miles away in the Bronx, Adams went for a physical so he could play high school basketball and was diagnosed with chronic myelogenous leukemia.
“I was scared a little,” Adams said. “But I wasn’t thinking how bad it was going to get.”
A month or so later, he was matched to McFadden, who began a pre-donation drug regimen that boosted his white blood cell count. He said it made his bones hurt so even a handshake was painful.
Under program rules, donor and recipient must remain anonymous for at least a year. McFadden said he thought about it every day, then started making inquiries when the year was up in March.
Eleven days ago, he got the call. The donor program would pay their way to the TriCaucus Minority Health Summit this weekend at the University of Illinois-Chicago.
“I don’t know what to say, still,” Adams said from Chicago, adding he feels 100 percent but remains on medication.
As for McFadden: “I’m just probably going to hug the kid and probably cry a little bit, I’m not going to lie. It’s not every day that you know you can sacrifice a small piece of yourself to help someone live. I was given that chance.”
Posted by rob on July 24, 2005 under Uncategorized | Be the First to Comment
A polar bear tries to break a block of ice containing fish at Tokyo’s Ueno Zoo as part of the zoo’s annual summer presents to animals to keep them cool.
Posted by rob on July 23, 2005 under Uncategorized | Be the First to Comment
Orenstein JM, Russo P, Didier ES, Bowers C, Bunin N, Teachey DT
Ultrastruct Pathol. 2005 May-Aug ; 29(3): 269-76
Microsporidia are ubiquitous obligate eukaryotic intracellular parasites that are now felt to be more akin to degenerate fungi than to protozoa. Microsporidia can be highly pathogenic, causing a broad range of symptoms in humans, especially individuals who are immunocompromised. The vast majority of human cases of microsporidiosis have been reported during the past 20 years, in patients with HIV/AIDS, while only relatively rare cases have been described in immunocompetent individuals. However, microsporidia infections are being increasingly reported in patients following solid-organ transplanation, where the main symptom has been diarrhea. The authors report the first case of pulmonary microsporidial infection in an allogeneic bone marrow transplant recipient in the United States and only the second case in the world. The patient, with a history of Hodgkin disease followed by acute myelogenous leukemia received a T-cell-depleted graft, but succumbed to respiratory failure 63 days post transplantation. An open lung biopsy, taken just before death, was originally thought to show toxoplasmosis. The correct diagnosis of microsporidiosis was made postmortem by light and electron microscopy. DNA polymerase chain reaction analysis confirmed the diagnosis and furthermore revealed it to be the dog strain of the microsporidia species Encephalitozoon cuniculi. Although to date rarely diagnosed, microsporidial infection should also be considered in the differential diagnosis of, e.g., unexplained pulmonary infection in bone marrow transplant patients.
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Jelinek J, Oki Y, Gharibyan V, Bueso-Ramos C, Prchal JT, Verstovsek S, Beran M, Estey E, Kantarjian HM, Issa JP
Blood. 2005 Jul 21;
An activating 1849G>T mutation of JAK2 tyrosine kinase was recently described in chronic myeloproliferative disorders (MPD). Its role in other hematological neoplasms is unclear. We developed a quantitative pyrosequencing assay and analyzed 374 samples of hematological neoplasms. The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in acute myeloid leukemia (AML) with an antecedent PV or myelofibrosis (5/14 patients or 36%). JAK2 mutation was also detected in 3/16 (19%) patients with Philadelphia-chromosome (Ph)-negative chronic myelogenous leukemia (CML), 2/11 (18%) patients with megakaryocytic AML, 7/52 (13%) patients with chronic myelomonocytic leukemia, and in 1/68 (1%) patients with myelodysplastic syndromes. No mutation was found in Ph-positive CML (99 patients), AML M0-M6 (28 patients) and acute lymphoblastic leukemia (20 patients). We conclude that JAK2 1849G>T mutation is common in Ph-negative MPD but not critical for transformation to the acute phase of these diseases, and generally rare in aggressive leukemias.
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Manoharan A
IDrugs. 2000 Dec ; 3(12): 1525-33
Decitabine, a potent DNA methyltransferase inhibitor, which was originally under development by Pharmachemie, is being developed by SuperGen [341375]. Pharmachemie had been studying decitabine in phase II clinical trials for several leukemia indications in Europe and the US [328658,218338]. Preliminary results indicated that the compound was active in the treatment of myelodysplasia, relapsed leukemia, acute myeloid leukemia and postallogeneic progenitor cell transplant relapse [240549]. The compound is in phase II clinical trials with phase III trials scheduled to begin shortly [389367]. Decitabine has been used to treat myelodysplastic syndrome in a total of 125 patients, with an overall response rate of 49%. In a study using decitabine to treat chronic myelogenous leukemia in 81 patients, a response rate of 62% among patients in chronic phase of the disease was achieved [388947]. In a phase I/II trial designed to establish safety and efficacy in the treatment of sickle cell anemias treatment with decitabine generated a response in 100% of the patients tested: a total of eight patients were enrolled, each experienced elevated levels of fetal hemaglobin. Side effects were minimal and the drug was well tolerated. Plans for additional clinical studies of decitabine as a treatment for sickle cell anemia are underway [388307]. A phase II trial using a low dose of decitabine in patients with myelodysplastic syndrome has been completed. Of 66 patients entered, 62 were evaluable. The response rate was 48%, with a median response duration of 40 weeks. The mean survival from the start of therapy was 13 months [309098]. In a study with 37 CML patients, a 25% overall response rate was seen in those patients in the blastic phase of the disease, and a 52% response rate was observed in the accelerated phase patients. The most significant side effect was prolonged myelosuppression [278488]. The drug suppresses cellular growth in seven human tumor cell lines, possibly by reactivation of certain growth suppressor genes [278485].
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The full moon rises behind the ancient temple of Posseidon, in Sounio.
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Crossman LC, Druker BJ, Deininger MW, Pirmohamed M, Wang L, Clark RE
Blood. 2005 Aug 1; 106(3): 1133-4
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The golden crosses of the Novodevichy Monastery in Moscow are silhouetted against the full moon.
Posted by rob on July 21, 2005 under Uncategorized | Be the First to Comment
Protesters rallying against corruption raise their painted hands in the air in Lima.
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Tartaglia M, Gelb BD
Annu Rev Genomics Hum Genet. 2005 Apr 13;
Noonan syndrome is a pleiomorphic autosomal dominant disorder with short stature, facial dysmorphia, webbed neck, and heart defects. In the past decade, progress has been made in elucidating the pathogenesis of this disorder using a positional cloning approach. Noonan syndrome is now known to be a genetically heterogeneous disorder with nearly one half of cases caused by gain-of-function mutations in PTPN11, the gene encoding the protein tyrosine phosphatase SHP-2. Similar germ line mutations cause two related genetic disorders, Noonan-like disorder with multiple giant cell lesion syndrome and LEOPARD syndrome, and somatic PTPN11 mutations can underlie certain pediatric hematopoietic malignancies, including juvenile myelomonocytic, acute lymphoblastic, and acute myelogenous leukemias. A mouse model of PTPN11-related Noonan syndrome was recently generated, providing a reagent for studying disease pathogenesis in greater depth as well as experimenting with novel therapeutic strategies. Expected online publication date for the Annual Review of Genomics and Human Genetics Volume 6 is August 30, 2005. Please see http://www.annualreviews.org/catalog/pub_dates.asp for revised estimates.
Noonan Syndrome and Related Disorders: Genetics and Pathogenesis.
