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아무쪼록 빨리 성공해서 싸게 나오길 ㅜ

http://news.chosun.com/site/data/html_dir/2012/12/11/2012121100706.html

AIDS 바이러스(HIV)로 백혈병 치료 성공

에이즈(AIDS·후천성 면역 결핍증)를 일으키는 인체면역결핍바이러스(HIV)를 이용해 어린이 백혈병 환자를 치료하는 방법이 성공을 거뒀다고 미국 뉴욕타임스(NYT)가 9일 보도했다.

뉴욕타임스에 따르면 올해 7세인 에마 화이트헤드(여)는 2년 전 림프구성 백혈병 판정을 받고 두 차례 항암치료를 받았으나 별다른 효과를 보지 못했다. 더는 치료 방법이 없는 상태였다. 

펜실베이니아대 연구팀은 지난 4월 화이트헤드에게 비활성화시킨 HIV를 투입해 치료하는 임상시험을 제안했다. 연구팀은 부모와 본인 동의 아래 몸에 에이즈를 일으키는 바이러스를 주입했고, 화이트헤드는 한동안 높은 열과 오한으로 괴로워했다. 하지만 7개월이 지난 현재 화이트헤드의 몸에선 암세포가 없어졌고 완전한 회복세를 보이고 있다.

연구팀은 현재까지 화이트헤드를 비롯해 환자 11명에게 이 같은 임상시험 치료를 실시했다. 그 중 화이트헤드 등 4명은 완치됐고 4명은 호전됐다. 2명은 효과를 보지 못했으며 1명은 호전된 뒤 재발했다.

백혈병을 치료하려면 백혈병 환자의 몸에서 제기능을 못하는 T세포를 제거하고 새로운 T세포로 대체해야 한다. 그러려면 T세포에 특정 유전물질을 주입해 증식해야 하는데, 이때 비활성화된 HIV가 그 역할을 한다. HIV는 유전 물질을 세포 내에 전달하는 기능이 매우 뛰어나기 때문이다. 과정이 잘 진행되면 T세포가 증식하면서 암세포를 공격해 제거한다.

환자가 고열과 함께 고통스러워하는 과정은 백혈병이 호전되는 징조다. 치료법이 제대로 진행되면 체내 면역 세포가 활성화하면서 고열과 혈압 강하 등의 현상이 나타난다. 화이트헤드가 겪었던 증상은 사이토카인-릴리즈(cytokine-release)라고 한다.

존스홉킨스대 이반 보렐로 교수는 “이 치료법은 백혈병 치료에 커다란 돌파구”라고 평가했다. 치료법이 개발된 지 얼마 되지 않았음을 고려하면 놀라운 성과라는 것이다. 거대 제약 회사들 역시 이 치료법에 관심을 보이고 있다고 펜실베니아대 연구팀은 말했다.

In Girl’s Last Hope, Altered Immune Cells Beat Leukemia

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 afterchemotherapy, 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.

Emma had been ill with acute lymphoblastic leukemia since 2010, when she was 5, said her parents, Kari and Tom. She is their only child.

She is among just a dozen patients with advanced leukemiato have received the experimental treatment, which was developed at the University of Pennsylvania. Similar approaches are also being tried at other centers, including the National Cancer Institute and Memorial Sloan-Kettering Cancer Center in New York.

“Our goal is to have a cure, but we can’t say that word,” said Dr. Carl June, who leads the research team at the University of Pennsylvania. He hopes the new treatment will eventually replace bone-marrow transplantation, an even more arduous, risky and expensive procedure that is now the last hope when other treatments fail in leukemia and related diseases.

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 theAmerican 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.

Dr. John Wagner, the director of pediatric blood and marrow transplantation at the University of Minnesota, called the Pennsylvania results “phenomenal” and said they were “what we’ve all been working and hoping for but not seeing to this extent.”

A major drug company, Novartis, is betting on the Pennsylvania team and has committed $20 million to building a research center on the university’s campus to bring the treatment to market.

Hervé Hoppenot, the president of Novartis Oncology, called the research “fantastic” and said it had the potential — if the early results held up — to revolutionize the treatment of leukemia and related blood cancers. Researchers say the same approach, reprogramming the patient’s immune system, may also eventually be used against tumors like breast andprostate cancer.

To perform the treatment, doctors remove millions of the patient’s T-cells — a type of white blood cell — and insert new genes that enable the T-cells to kill cancer cells. The technique employs a disabled form of H.I.V. because it is very good at carrying genetic material into T-cells. The new genes program the T-cells to attack B-cells, a normal part of the immune system that turn malignant in leukemia.

The altered T-cells — called chimeric antigen receptor cells — are then dripped back into the patient’s veins, and if all goes well they multiply and start destroying the cancer.

The T-cells home in on a protein called CD-19 that is found on the surface of most B-cells, whether they are healthy or malignant.

A sign that the treatment is working is that the patient becomes terribly ill, with raging fevers and chills — a reaction that oncologists call “shake and bake,” Dr. June said. Its medical name is cytokine-release syndrome, or cytokine storm, referring to the natural chemicals that pour out of cells in the immune system as they are being activated, causing fevers and other symptoms. The storm can also flood the lungs and cause perilous drops inblood pressure — effects that nearly killed Emma.

Steroids sometimes ease the reaction, but they did not help Emma. Her temperature hit 105. She wound up on a ventilator, unconscious and swollen almost beyond recognition, surrounded by friends and family who had come to say goodbye.

But at the 11th hour, a battery of blood tests gave the researchers a clue as to what might help save Emma: her level of one of the cytokines, interleukin-6 or IL-6, had shot up a thousandfold. Doctors had never seen such a spike before and thought it might be what was making her so sick.

Dr. June knew that a drug could lower IL-6 — his daughter takes it for rheumatoid arthritis. It had never been used for a crisis like Emma’s, but there was little to lose. Her oncologist, Dr. Stephan A. Grupp, ordered the drug. The response, he said, was “amazing.”

Within hours, Emma began to stabilize. She woke up a week later, on May 2, the day she turned 7; the intensive-care staff sang “Happy Birthday.”

Since then, the research team has used the same drug, tocilizumab, in several other patients.

In patients with lasting remissions after the treatment, the altered T-cells persist in the bloodstream, though in smaller numbers than when they were fighting the disease. Some patients have had the cells for years.

Dr. Michel Sadelain, who conducts similar studies at the Sloan-Kettering Institute, said: “These T-cells are living drugs. With a pill, you take it, it’s eliminated from your body and you have to take it again.” But T-cells, he said, “could potentially be given only once, maybe only once or twice or three times.”

The Pennsylvania researchers said they were surprised to find any big drug company interested in their work, because a new batch of T-cells must be created for each patient — a far cry from the familiar commercial strategy of developing products like Viagra orcholesterol medicines, in which millions of people take the same drug.