Monday, October 5, 2009
This video was made by a junior high student and his principal watched the video. The principal was a smoker for the past 42 years. He was so moved by the pic of the grandfather dying, he stopped smoking that day and called his daughter who had just “given” him his first grandchild and told her she would not have to watch him die….
Each one … reach one… we make the difference!
Sunday, September 27, 2009
New Avenues
Primary lung cancer shifts to metastatic disease by suppressing a family of small molecules that normally locks the tumor in a noinvasive state.
“Existing treatments have little success against cancer that has spread to other organs, so finding a way to prevent metastasis could have a huge impact on survival,” said senior author Jonathan Kurie, M.D., professor in M. D. Anderson ’s Department of Thoracic/Head and Neck Medical Oncology.
For this to be done researchers/doctors will need to understand what initiates metastasis. In the following information they show that microRNA-200 is one of those central cues that initiate metastasis. MicroRNAs are single-stranded bits of RNA that regulate messenger RNA expressed by genes to order the creation of a specific protein.
All primary tumors in a strain of mice prone to metastatic lung cancer became invasive and spread when miR-200 was suppressed. Protecting miR-200 from blockade completely prevented metastasis in another group of the mice, the researchers found.
Tumors shift between noninvasive and invasive state
The team found that miR-200 needs to be shut down for the primary tumor to change from stationary epithelial cells to mobile mesenchymal cells. This epithelial-to-mesenchymal transition (EMT) is recognized as a crucial step in metastasis, which causes 90 percent of all cancer deaths.
An estimated 80 percent of all solid tumors originate in the epithelial cells, which line an organ or its cavities and are generally immobile. Mesenchymal cells are mobile and can differentiate into many different cell types.
When the team profiled a panel of 40 human lung cancer cell lines that had been characterized on the basis of EMT features (epithelial versus mesenchmyal) and site of origin (primary lung tumor versus metastasis), miR-200 expression was highest in those cells with epithelial features and was the best of more than 700 microRNAs tested as an indicator of metastatic or primary origin.
“Highly metastatic lung cancer cells had completely shutdown miR-200 expression, that’s what triggered EMT in those cells,” Kurie said. “When we went back and forced overexpression of miR-200, the cells remained locked in the epithelial state and could no longer metastasize.”
The team also found that the cancer cells could shift from epithelial to mesenchymal and back depending on the cell’s context. The same cells that remain epithelial in Matrigel become “blatantly mesenchymal” when moved to the mouse model and assume an intermediate state when growing in plastic dishes.
Matrigel is a gelatinous mixture that is designed to simulate the complex environment that cells occupy called the extracellular matrix.
“If you take the tumors out of the mice and back to the matrigel, they revert to epithelial cells,” Kurie said. “These cells are highly plastic and responsive to the extracellular environment.
“The idea that these highly plastic cells are the source of metastasis indicates that metastatic capacity is a regulatable tumor cell function. That’s new,” Kurie said. “Identifying the signals that govern plasticity could lead to a novel way of targeting and preventing metastasis.”
Kurie and colleagues continue to work on identifying upstream regulators of miR-200 that might provide targets for therapy.
The researchers started with a strain of mice that develops metastatic lung cancer based on mutations in the Kras oncogene and the tumor-suppressing p53 gene. Cell lines isolated from these mice were introduced in wild type mice and the resultant tumors characterized for metastatic potential.
All tumor cell lines were profiled for gene expression. “The thing that popped out strongly was an EMT signal present in the metastatic cells but not in the non-metastatic cells,” Kurie said.
The team then profiled the tumors for microRNA expression. Out of thousands of miRNAs, only the miR-200 family of five miRNAs, along with three others, emerged as differentially expressed. The other three are being studied.
More information can be found @ www.mdanderson.org/newsroom
Reference info:
Co-authors with Kurie were first author Don Gibbons, M.D., Ph.D., Wei Lin, M.D., Zain Rizvi, and Nishan Thilaganathan, all of the Department of Thoracic/Head and Neck Medical Oncology; Chad Creighton, Ph.D., and Yiqun Zhang of the Dan L. Duncan Cancer Center at Baylor College of Medicine; Philip Gregory, Ph.D., and Gregory Goodall, Ph.D., of the Centre for Cancer Biology, Hanson Institute in Adelaide, Australia; and Alexander Pertsemlidis, PH.D., and Liqin Du, Ph.D., of the Eugene McDermott Center for Human Growth and Development at The University of Texas Southwestern Medical Center in Dallas.
The research was funded by grants from the National Cancer Institute, including the Lung Cancer Specialized Program of Research Excellence; the David M. Sather Memorial Fund, the Armour Family Lung Cancer Research Fund and the Dan L. Duncan Cancer Center at Baylor College of Medicine. Gibbons also was supported by a Young Investigator Award from The ASCO Cancer Foundation and an International Association for the Study of Lung Cancer (IASLC) Fellow Grant.
“Existing treatments have little success against cancer that has spread to other organs, so finding a way to prevent metastasis could have a huge impact on survival,” said senior author Jonathan Kurie, M.D., professor in M. D. Anderson ’s Department of Thoracic/Head and Neck Medical Oncology.
For this to be done researchers/doctors will need to understand what initiates metastasis. In the following information they show that microRNA-200 is one of those central cues that initiate metastasis. MicroRNAs are single-stranded bits of RNA that regulate messenger RNA expressed by genes to order the creation of a specific protein.
All primary tumors in a strain of mice prone to metastatic lung cancer became invasive and spread when miR-200 was suppressed. Protecting miR-200 from blockade completely prevented metastasis in another group of the mice, the researchers found.
Tumors shift between noninvasive and invasive state
The team found that miR-200 needs to be shut down for the primary tumor to change from stationary epithelial cells to mobile mesenchymal cells. This epithelial-to-mesenchymal transition (EMT) is recognized as a crucial step in metastasis, which causes 90 percent of all cancer deaths.
An estimated 80 percent of all solid tumors originate in the epithelial cells, which line an organ or its cavities and are generally immobile. Mesenchymal cells are mobile and can differentiate into many different cell types.
When the team profiled a panel of 40 human lung cancer cell lines that had been characterized on the basis of EMT features (epithelial versus mesenchmyal) and site of origin (primary lung tumor versus metastasis), miR-200 expression was highest in those cells with epithelial features and was the best of more than 700 microRNAs tested as an indicator of metastatic or primary origin.
“Highly metastatic lung cancer cells had completely shutdown miR-200 expression, that’s what triggered EMT in those cells,” Kurie said. “When we went back and forced overexpression of miR-200, the cells remained locked in the epithelial state and could no longer metastasize.”
The team also found that the cancer cells could shift from epithelial to mesenchymal and back depending on the cell’s context. The same cells that remain epithelial in Matrigel become “blatantly mesenchymal” when moved to the mouse model and assume an intermediate state when growing in plastic dishes.
Matrigel is a gelatinous mixture that is designed to simulate the complex environment that cells occupy called the extracellular matrix.
“If you take the tumors out of the mice and back to the matrigel, they revert to epithelial cells,” Kurie said. “These cells are highly plastic and responsive to the extracellular environment.
“The idea that these highly plastic cells are the source of metastasis indicates that metastatic capacity is a regulatable tumor cell function. That’s new,” Kurie said. “Identifying the signals that govern plasticity could lead to a novel way of targeting and preventing metastasis.”
Kurie and colleagues continue to work on identifying upstream regulators of miR-200 that might provide targets for therapy.
The researchers started with a strain of mice that develops metastatic lung cancer based on mutations in the Kras oncogene and the tumor-suppressing p53 gene. Cell lines isolated from these mice were introduced in wild type mice and the resultant tumors characterized for metastatic potential.
All tumor cell lines were profiled for gene expression. “The thing that popped out strongly was an EMT signal present in the metastatic cells but not in the non-metastatic cells,” Kurie said.
The team then profiled the tumors for microRNA expression. Out of thousands of miRNAs, only the miR-200 family of five miRNAs, along with three others, emerged as differentially expressed. The other three are being studied.
More information can be found @ www.mdanderson.org/newsroom
Reference info:
Co-authors with Kurie were first author Don Gibbons, M.D., Ph.D., Wei Lin, M.D., Zain Rizvi, and Nishan Thilaganathan, all of the Department of Thoracic/Head and Neck Medical Oncology; Chad Creighton, Ph.D., and Yiqun Zhang of the Dan L. Duncan Cancer Center at Baylor College of Medicine; Philip Gregory, Ph.D., and Gregory Goodall, Ph.D., of the Centre for Cancer Biology, Hanson Institute in Adelaide, Australia; and Alexander Pertsemlidis, PH.D., and Liqin Du, Ph.D., of the Eugene McDermott Center for Human Growth and Development at The University of Texas Southwestern Medical Center in Dallas.
The research was funded by grants from the National Cancer Institute, including the Lung Cancer Specialized Program of Research Excellence; the David M. Sather Memorial Fund, the Armour Family Lung Cancer Research Fund and the Dan L. Duncan Cancer Center at Baylor College of Medicine. Gibbons also was supported by a Young Investigator Award from The ASCO Cancer Foundation and an International Association for the Study of Lung Cancer (IASLC) Fellow Grant.
Monday, September 7, 2009
Calling all Volunteers!
If you are interested in volunteering with Rexanna's Foundation for Fighting Lung Cancer, let us know! We would love to hear from you and love to hear where you would like to help serve. We have space for you! You can email us at Lindsey.Vaughn@hotmail.com
Friday, August 21, 2009
Save the Date!!!
It is getting to be that time of the year again....LONE STAR HUDDLE UP!!!
Who: YOU
What: Live auction, silent auction, good food, good music(Rick Trevino!), fun people
When: November 14th, 2009
Where: Salt Lick Pavilion in Driftwood, Texas
Let us know if you have any questions or would like to help with this event. You an email at: lindsey.vaughn@hotmail.com
Who: YOU
What: Live auction, silent auction, good food, good music(Rick Trevino!), fun people
When: November 14th, 2009
Where: Salt Lick Pavilion in Driftwood, Texas
Let us know if you have any questions or would like to help with this event. You an email at: lindsey.vaughn@hotmail.com
Tuesday, August 4, 2009
T.E.A.M Blast Off!!
Kristen Alex shares about coaching school experience!
I wanted to send a quick note to give you a small taste of what we have been experiencing with T.E.A.M. at the two conventions this week. While in San Antonio at TAHPERD, we singed up over 90 schools and passed on Rexanna's story to hundreds of people. Lisa, Bertha and I were totally jazzed by the reception and excitement this project is generating. We were riding that high all the way to and through girls coaching school . We started off the set up morning with Kevin Halfmann appearing out of the blue to help us unload and we termed him our "angel"! The conference began with excitement as Sheri, Stephanie, and Sandy all roped in people based on past knowledge of who they were or the town shirts they were wearing. We stole moments here and there to tell our own Rexanna stories and renewed our passion for why we do what we do. At girls, we took in another 80 schools!!! So we are about double where we were last year and still have two more to go!!
I just can not say thank you enough to all of you who came together to get this thing rolling. We have two more weeks and I just can't tell you how pumped I am about this project. THANK YOU THANK YOU THANK YOU!!!
Lisa, Bertha, Kristen
Bertha & Kristen
Sheri, Sandy, Kristen, Stephanie
I wanted to send a quick note to give you a small taste of what we have been experiencing with T.E.A.M. at the two conventions this week. While in San Antonio at TAHPERD, we singed up over 90 schools and passed on Rexanna's story to hundreds of people. Lisa, Bertha and I were totally jazzed by the reception and excitement this project is generating. We were riding that high all the way to and through girls coaching school . We started off the set up morning with Kevin Halfmann appearing out of the blue to help us unload and we termed him our "angel"! The conference began with excitement as Sheri, Stephanie, and Sandy all roped in people based on past knowledge of who they were or the town shirts they were wearing. We stole moments here and there to tell our own Rexanna stories and renewed our passion for why we do what we do. At girls, we took in another 80 schools!!! So we are about double where we were last year and still have two more to go!!
I just can not say thank you enough to all of you who came together to get this thing rolling. We have two more weeks and I just can't tell you how pumped I am about this project. THANK YOU THANK YOU THANK YOU!!!
Lisa, Bertha, Kristen
Bertha & Kristen
Sheri, Sandy, Kristen, Stephanie
Thursday, July 9, 2009
200 Letter Challenge
The 200 Letter Challenge is Still ON!!!
Alright Foundation members, blog readers, friends and family. We need your help! Our goal is 200 hundred letters and we believe that we can do that and MORE. We have an opportunity to make people aware of Lung Cancer and its effects, through Oprah.(cool) The Bonnie J. Addario Lung Cancer Foundation has begun writing letters to Oprah asking her to do a show on "Lung Cancer Matters." We can do our part to help make society aware of this disease by sending letters and representing our foundation.
All you have to do is click here
Let us know if you have written a letter by commenting!
Thanks for all you do in getting the word out.
Alright Foundation members, blog readers, friends and family. We need your help! Our goal is 200 hundred letters and we believe that we can do that and MORE. We have an opportunity to make people aware of Lung Cancer and its effects, through Oprah.(cool) The Bonnie J. Addario Lung Cancer Foundation has begun writing letters to Oprah asking her to do a show on "Lung Cancer Matters." We can do our part to help make society aware of this disease by sending letters and representing our foundation.
All you have to do is click here
Let us know if you have written a letter by commenting!
Thanks for all you do in getting the word out.
Monday, July 6, 2009
GIANT STEPS
A GREAT VICTORY IN PROTECTING KIDS FROM TOBACCO!
It is my great pleasure to tell you that the US Senate just passed the Family Smoking Prevention and Tobacco Control Act (S 982/HR ), which gives the Food and Drug Administration (FDA) the authority to regulate the manufacture, marketing, and sales of tobacco products. The bill was approved in a bipartisan vote of 79 to 17. After more than 10 years of hard work, this lifesaving legislation will soon become law!
This is a major achievement and one that would not have been possible without the hard work and persistence of volunteers and staff nationwide. In the past few weeks alone, more than 5,000 phone calls were placed to members of Congress.
Today history has been made. Thanks to this legislation, we can make cancer history too!
It is my great pleasure to tell you that the US Senate just passed the Family Smoking Prevention and Tobacco Control Act (S 982/HR ), which gives the Food and Drug Administration (FDA) the authority to regulate the manufacture, marketing, and sales of tobacco products. The bill was approved in a bipartisan vote of 79 to 17. After more than 10 years of hard work, this lifesaving legislation will soon become law!
This is a major achievement and one that would not have been possible without the hard work and persistence of volunteers and staff nationwide. In the past few weeks alone, more than 5,000 phone calls were placed to members of Congress.
Today history has been made. Thanks to this legislation, we can make cancer history too!
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