When the two men met 13 years ago, they both managed to get their way. Logan entered one of the first imatinib trials and is still thriving. His success makes him a perfect example of what Druker set out to do when he buried himself in laboratory research in the early s, pledging not to emerge until he had a better way to treat patients with the deadly disease. It was during a brief phone call in that Druker told a newly diagnosed Logan he could not participate in phase I trials of imatinib because his disease was not advanced enough.
Their conversation with the doctor stretched past the minute mark, beyond an hour, and through a second and then a third hour. The upshot was that Logan was accepted into a phase I trial of imatinib, becoming the first patient to enroll. The trial, one of several early-phase looks at the drug, tested imatinib in combination with cytarabine, and, later, interferon.
While the drugs did not prove valuable in combination, Logan remains forever grateful that he was given the chance to participate. Logan found out he had CML after his family doctor conducted a routine blood test. On the job for the video production company he owns with his wife, Logan was getting ready to fly from Chicago to Europe when he got an alarming call from the practitioner.
Logan asked if he would be dead within the next couple of weeks. When the doctor said he would not, the videographer boarded the plane. His first visit to the Internet turned up a website full of memorials to people who had died from CML. Later, his doctor told him he would live 42 months unless he received a bone marrow transplant from someone considered an appropriate match.
So the patient contacted his attorney, whose former college roommate, also a lawyer, represented some staff members at OHSU. When Logan finally heard from the doctor, he was elbows-deep in a video job at the Grand Ole Opry, and had been inundated, to the point of annoyance, by local friends calling to say hello.
But when I failed on these drugs, it was miraculous that each time a door has opened. In fact, Logan participated in phase I clinical trials of every TKI currently approved for the treatment of CML, developed by a variety of researchers and pharmaceutical companies. The drug, recently approved by the FDA, is designed to overcome all forms of resistance that can arise in CML, including the bedeviling TI mutation. January 17, It was the first time that doctors observed such a response by administering only one anti-cancer drug to their patients, instead of many different, nasty ones!
Five years later, the patients still did not have any cancer cells in their blood Figure 4. These results were impressive!
Imatinib was a ground-breaking discovery, not only because of the results it achieved and because it saved the lives of thousands of patients, but also because of the way this drug was developed and what scientists have learned from its development. This approach has since been used to develop drugs for other cancers, such as some forms of ovarian, skin, and lung cancer. Scientific progress is accelerating the speed of drug development. As scientists, we hope that this progress will more rapidly lead to successful stories, such as that of imatinib.
Stay tuned! It is the material that carries all the information needed for the life and death of a cell. In CML patients, the blood is full of cancer cells that occupy all the space normally taken up by functional blood cells.
Inside human cells, the DNA is organized into 46 chromosomes. Each chromosome contains hundreds of genes. Each gene codes for a protein with a specific function.
The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Gleevec: the breakthrough in cancer treatment. Chronic myeloid leukemia: reminiscences and dreams. Haematologica — A structure for deoxyribose nucleic acid. Nature —8. A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining.
Nature —3. J, Talpaz, M. Share on Facebook. Abstract Some say it is a magic bullet. Cancers by Body Location. Late Effects of Childhood Cancer Treatment. Pediatric Supportive Care. Rare Cancers of Childhood Treatment. Childhood Cancer Genomics. Study Findings. Metastatic Cancer Research.
Intramural Research. Extramural Research. Cancer Research Workforce. Partners in Cancer Research. What Are Cancer Research Studies. Research Studies. Get Involved. Cancer Biology Research. Cancer Genomics Research. Research on Causes of Cancer. Cancer Prevention Research.
Cancer Treatment Research. Cancer Health Disparities. Childhood Cancers Research. Global Cancer Research. Cancer Research Infrastructure.
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Driving Discovery. Highlighted Scientific Opportunities. Research Grants. Medical Careers: Genetic Screening and Diagnostics. Pray, Ph. Citation: Pray, L. Nature Education 1 1 How do scientists develop new treatments for disease? With Gleevec, a remarkable cancer drug, the approach was to target the disease at the cellular and subcellular level. Aa Aa Aa. Some say it's a miracle drug.
Others call it a silver bullet. Gleevec, also marketed internationally as Glivec and sometimes referred to by its chemical name imatinib, entered the medical world with a bang. This medication was initially approved for use by the U.
Food and Drug Administration FDA in for the treatment of chronic myelogenous leukemia CML , a rare form of cancer that affects certain types of white blood cells. Since its initial approval, Gleevec has also been approved for use in patients with several types of gastrointestinal tumors. Currently, scientists continue to study the drug's effectiveness not only in various cancers, but also in other diseases, such as stroke Su et al.
But just how effective is Gleevec, especially when it comes to CML, and what is its mechanism of action? Gleevec Statistics. As Nowell recounts: I knew nothing about cytogenetics at this time but felt that the chromosomal preparations of the leukemic cells warranted investigation for any abnormalities. Details of the Philadelphia Chromosome Begin to Emerge.
Figure 1: The Philadelphia chromosome. Discovered in , the diagnostic karyotypic abnormality for chronic myelogenous leukemia is shown in this picture of the banded chromosomes 9 and Shown is the result of the reciprocal translocation of 22q to the lower arm of 9 and 9q c-abl to a specific breakpoint cluster region [bcr] of chromosome 22 indicated by the arrows.
Nowell Courtesy of Peter C. All rights reserved. References and Recommended Reading Cameron, D. Cell 36 , 93—99 Heisterkamp, N. Journal of Clinical Investigation , — Rowley, J. Article History Close. Share Cancel. Revoke Cancel. Keywords Keywords for this Article.
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