Thursday, October 08, 2009
He Went Not Gently: The Daily Transit
He went not gently
Published June 4, 2007
It is perhaps one of the saddest things in life to lose touch with a person only to later find that they have passed away – the understanding that there will never be a reconnection bears a heavy weight.
This morning, I felt the brunt of this sadness as I tried to look up a former professor of mine from the University of Washington. It was strange; when I failed to find his email in the directory I simply assumed he had moved on to another school – he was a young guy and, as far as I knew, in good health.
I decided to Google his name just to see where he might have wound up, only to come upon the ominous subtext of the first link, from the UW Department of Asian Languages: “The department mourns the passing of…”
I clicked the link anxiously, eyes wide as they jumped between the text and the black and white photograph of my former professor. I spoke aloud and disbelievingly to myself and to the silence of my apartment. Everything was making horrible sense – the emails that were never returned, and in front of me, the glaring fact that he had died last year.
Professor Scott Swaner was not someone I could call a personal friend, which seems quite obvious given my obliviousness to his death. But to me he was somewhat of a kindred spirit. He was my adviser and professor in 2005, and a great scholar of Korean literature.
We shared a common bond in our passion for the culture of the peninsular nation, and I always smile when I think of the comedy of two tall white guys with somewhat outlandish facial hair sitting in an office speaking in Korean. Professor Swaner always pushed me (and all of his students) towards a deeper understanding of Korean culture through literature and towards sharper language skills. He was one of the first professors to really teach me how to think, and he encouraged and further inspired my ambition to be a journalist in Seoul.
I remember fondly other things about him – the Korean movie poster covering his office door, the John Coltrane poster hanging on his wall, and the time we ran into each other at an anti-war rally in downtown Seattle. Professor Swaner was a confident, complex and wise man, and I regret that I didn’t take more time to visit his office hours, to just chat, to listen and learn.
While in subtle mix of disbelief and sorrow this morning, I followed the internet hypertext trail to a comment on an NPR segment on cancer about Professor Swaner, and from there to the blog that he ran from his diagnosis to his death. It’s called Do Not Go Gentle, the title inspired by the poem by Dylan Thomas.
Though I hardly have the heart to backtrack through his battle with the disease, his first post is perhaps one of the most sobering – I’ll re-post a bit of it here:
Imagine you’re moving through your life, beginning your career, enjoying some success and good health, and like anyone else you’re making plans. You’re 38–in many senses it’s the prime of your life. In any event, you’re young still. You liked reading and writing so you went to graduate school, you traveled a bit, in 2003 you started teaching poetry in a university in Seattle. You get halfway through your second year, gearing up to finish that “first book,” when your doctor calls to follow up on some tests about stomach pains you’ve had: “You’ve got cancer of the pancreas.” [...]
It is both an unimaginable nightmare and a stark reality – that life, one day, ends. It is always sad, but for Professor Swaner and all good-hearted people who face death young, it is a tragedy.
Professor Swaner died of pancreatic cancer on December 20, 2006.
He was 38 years-old.
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Responses to “He went not gently”
Sheri Swaner
June 5, 2007 at 9:12 pm
My thanks to you for your recognizing
and your writing about my brother, Scott Swaner.
It is always good to her from those who knew him in a different context then that of family.
He was a brilliant writer, insightful teacher–
who loved Korea; its people, language and culture.
I miss him dearly.
And you are correct–
He “did not go gentle .. ” — he fought and raged against this senseless and tragic disease until the day he died.
He is my hero, my best friend–
I’m so glad you two were aqauainted
and I appreciate your caring enough about Scott,
to write about him.
If it is okay- can I pass along your blog to the rest of my family?
Thank you so much.
Sincerely,
Sheri Swaner
Salt Lake City, UT
http://thedailytransit.wordpress.com/2007/06/04/he-went-not-gently/
Pancreatic Cancer News: Rx Reverses Resistance to Chemotherapy
Pancreatic Cancer: Researchers Find Drug That Reverses Resistance To Chemotherapy
NewsRx.com
October 1, 2009
For the first time researchers have shown that by inhibiting the action of an enzyme called TAK-1, it is possible to make pancreatic cancer cells sensitive to chemotherapy, opening the way for the development of a new drug to treat the disease.
Dr Davide Melisi told Europe's largest cancer congress, ECCO 15 - ESMO 34 [1], in Berlin today (Thursday 24 September) that resistance to chemotherapy was the greatest challenge to treating pancreatic cancer.
"Pancreatic cancer is an incurable malignancy, resistant to every anti-cancer treatment. Targeting TAK-1 could be a strategy to revert this resistance, increasing the efficacy of chemotherapy," said Dr Melisi, who until the start of September was a Fellow at the M.D. Anderson Center in Houston (Texas, USA); he has now moved to a staff position at the National Cancer Institute in Naples (Italy). "During the past few years we have been studying the role played by a cytokine or regulatory protein called Transforming Growth Factor beta (TGFbeta) in the development of pancreatic cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance."
Dr Melisi and his colleagues investigated the expression of TAK-1 (TGFbeta-Activated Kinase-1) in pancreatic cell lines and developed a drug that was capable of inhibiting TAK-1. They tested the activity of the TAK-1 inhibitor on its own and in combination with the anti-cancer drugs gemcitabine, oxaliplatin and SN-38 (a metabolite of the anti-cancer drug irinotecan) in cell lines, and the activity of the TAK-1 inhibitor combined with gemcitabine against pancreatic cancer in mice.
"The use of this TAK-1 inhibitor increased the sensitivity of pancreatic cells to all three chemotherapeutic drugs. By combining it with classic anti-cancer drugs, we were able to use doses of drugs up to 70 times lower in comparison with the control to kill the same number of cancer cells. In mice, we were able to reduce significantly the tumour volume, to prolong the mice survival, and to reduce the toxicity by combining the TAK-1 inhibitor with very low doses of a classic chemotherapeutic drug, gemcitabine, that would have been ineffective otherwise," said Dr Melisi.
The use of gemcitabine on its own against the cancer in mice was ineffective because of the drug resistant nature of the disease. However, once it was combined with the TAK-1 inhibitor, Dr Melisi and his colleagues saw a 78% reduction in tumour volumes. "The median average survival for the control, TAK-1 inhibitor, gemcitabine on its own, or TAK-1 inhibitor combined with gemcitabine was 68, 87, 82 and 122 days respectively," he said.
"This is the first time that TAK-1 has been indicated as a relevant target for the treatment of a solid tumour and that it is a valid approach to reverting the intrinsic drug resistance of pancreatic cancer. The TAK-1 inhibitor used in this study is an exciting drug that warrants further development for the treatment of pancreatic cancer. In the near future, we will study whether it is also able to make other chemotherapeutic agents, such as oxaliplatin, 5-FU or irinotecan, work against pancreatic cancer in mice.
"Our main goal is to translate this combination approach from the bench to the bedside, conducting a clinical trial that could demonstrate the safety of this TAK-1 inhibitor in combination with gemcitabine, and its efficacy, in pancreatic cancer patients."
Copyright 2009, Anti-Infectives Week via NewsRx.com
NewsRx.com
October 1, 2009
For the first time researchers have shown that by inhibiting the action of an enzyme called TAK-1, it is possible to make pancreatic cancer cells sensitive to chemotherapy, opening the way for the development of a new drug to treat the disease.
Dr Davide Melisi told Europe's largest cancer congress, ECCO 15 - ESMO 34 [1], in Berlin today (Thursday 24 September) that resistance to chemotherapy was the greatest challenge to treating pancreatic cancer.
"Pancreatic cancer is an incurable malignancy, resistant to every anti-cancer treatment. Targeting TAK-1 could be a strategy to revert this resistance, increasing the efficacy of chemotherapy," said Dr Melisi, who until the start of September was a Fellow at the M.D. Anderson Center in Houston (Texas, USA); he has now moved to a staff position at the National Cancer Institute in Naples (Italy). "During the past few years we have been studying the role played by a cytokine or regulatory protein called Transforming Growth Factor beta (TGFbeta) in the development of pancreatic cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance."
Dr Melisi and his colleagues investigated the expression of TAK-1 (TGFbeta-Activated Kinase-1) in pancreatic cell lines and developed a drug that was capable of inhibiting TAK-1. They tested the activity of the TAK-1 inhibitor on its own and in combination with the anti-cancer drugs gemcitabine, oxaliplatin and SN-38 (a metabolite of the anti-cancer drug irinotecan) in cell lines, and the activity of the TAK-1 inhibitor combined with gemcitabine against pancreatic cancer in mice.
"The use of this TAK-1 inhibitor increased the sensitivity of pancreatic cells to all three chemotherapeutic drugs. By combining it with classic anti-cancer drugs, we were able to use doses of drugs up to 70 times lower in comparison with the control to kill the same number of cancer cells. In mice, we were able to reduce significantly the tumour volume, to prolong the mice survival, and to reduce the toxicity by combining the TAK-1 inhibitor with very low doses of a classic chemotherapeutic drug, gemcitabine, that would have been ineffective otherwise," said Dr Melisi.
The use of gemcitabine on its own against the cancer in mice was ineffective because of the drug resistant nature of the disease. However, once it was combined with the TAK-1 inhibitor, Dr Melisi and his colleagues saw a 78% reduction in tumour volumes. "The median average survival for the control, TAK-1 inhibitor, gemcitabine on its own, or TAK-1 inhibitor combined with gemcitabine was 68, 87, 82 and 122 days respectively," he said.
"This is the first time that TAK-1 has been indicated as a relevant target for the treatment of a solid tumour and that it is a valid approach to reverting the intrinsic drug resistance of pancreatic cancer. The TAK-1 inhibitor used in this study is an exciting drug that warrants further development for the treatment of pancreatic cancer. In the near future, we will study whether it is also able to make other chemotherapeutic agents, such as oxaliplatin, 5-FU or irinotecan, work against pancreatic cancer in mice.
"Our main goal is to translate this combination approach from the bench to the bedside, conducting a clinical trial that could demonstrate the safety of this TAK-1 inhibitor in combination with gemcitabine, and its efficacy, in pancreatic cancer patients."
Copyright 2009, Anti-Infectives Week via NewsRx.com
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