Emeraldmirror
New member
"SIKO
Actually many many countries including Canada and the UK have made many break through s when it comes to cf.. tons of breakthroughs for example i have copy pasted this from teh canadian cystic fibrosis website of their research history
Progress in Cystic Fibrosis Research Since 1985
* In 1985, Canadian scientists Drs. Lap-Chee Tsui and Manuel Buchwald trace the gene responsible for CF to chromosome 7. Over the following several years, the discovery of genetic "markers" helps researchers close in on the gene. The search is aided as well by an important new technique, developed by Dr. Francis Collins, called "chromosome jumping".
* In 1986, the CCFF launches its Research Development Program I (RDP I) in CF Genetics/Gene Expression, based at Toronto's Hospital for Sick Children.
* In 1988, the CCFF launches its Research Development Program II (RDP II) focused on Lung Infection in CF, based at the University of Calgary's Health Sciences Centre.
* In the 1980s, significant progress is made in exploring the potential of a new class of drugs for treating faulty secretion in CF. One such drug, amiloride, alters the characteristics of fluid secretion by reducing the ability of cells in the lung to reabsorb sodium. The result is that the exterior of cells remains moist.
* Pioneering work is done in the field of heart/lung and double lung transplantation, which has now emerged as a viable option for people with cystic fibrosis. In 1988, at the Toronto General Hospital, the first successful double lung transplant is done on a patient with cystic fibrosis.
* In August 1989, CF research takes a huge step forward as Drs. Lap-Chee Tsui and Jack Riordan of the RDP I team, in collaboration with Dr.Francis Collins, announce the discovery of the gene responsible for cystic fibrosis.
* In September 1990, scientists succeeded in correcting the CF defect,under laboratory conditions. Canadian investigators in the RDP I program once again lead the way, successfully building a normal version (cDNA)of the gene responsible for CF. Collaborators in the United States then use a virus to place this normal gene in cells affected by CF. When they do, chloride begins to move normally across the cell membranes, thereby corecting the major defect in the disease.
* In 1990, significant progress is made in experiments with a potential new CF treatment: the aerosol administration of DNase, an enzyme that breaks down human genetic material. When DNase is administered to CF lungs, it breaks down much of the "junk" DNA in lung secretions, and reduces the thickness of these secretions, which otherwise plug the airways and encourage infection. DNase aerosol therapy is now commercially available.
* A potential new therapy emerges in 1990, called alpha-1-antitrypsin. Delivered in the form of an aerosol, alpha-1-antitrypsin suppresses the activities of an enzyme called elastase, which is highly destructive of lung tissue in CF. This new treatment may be able to limit the damage caused by elastase, and improve the ability of the immune system to kill Pseudomonas aeruginosa bacteria.
* In 1991, over 30% of patients registered at Canadian CF clinics were adults.
* In February 1991, CCFF-funded investigators announce important insights into the function of the CF gene protein, called CFTR (cystic fibrosis transmembrane conductance regulator). By placing a normal version of the CF gene into cells which do not exhibit salt (chloride) channels like the one which is defective in CF, scientists are able to determine that the CF gene protein is, in all likelihood, itself the salt channel.
* Investigators at the University of North Carolina announce in August 1991 that certain naturally-occurring compounds, used in combination with amiloride, can increase the ability of epithelial cells to secrete chloride. This could significantly improve the ability of persons with CF to clear secretions from the lungs.
* In October 1991, CCFF-funded researchers identify precisely which cells in the body are affected by cystic fibrosis, showing that the normal counterpart of the gene responsible for CF is active in the cells lining the airways, and in the salivary glands, intestines, and reproductive tissues. The findings are of vital significance, since the development of effective pharmacological or genetic therapies for CF will depend upon knowing which cells represent the target for treatment.
* Two complementary papers in December 1991 demonstrate that the CF gene protein can be detected in the membranes of affected cells, and does have a limited ability to transport salt. These results overturn previous findings - according to which the CFTR protein did not reach the cell membrane and therefore could not transport chloride - and suggest that the defective protein may be prodded into service by chemical stimulation.
* In 1991, a significant step toward gene therapy for CF is reported. Researchers in the United States and France announce that they have modified an adenovirus, similar to the virus responsible for the common cold, so that it cannot reproduce, and then successfully used it to transport a normal version of the gene responsible for CF into the lungs of experimental rats. When this is done, the animals' respiratory cells began to produce a normal human CF protein, and continued to do so for two weeks. Subsequent studies suggest that the effect may last for more than a month.
* In February 1992, Drs. Christine Bear and Jack Riordan of Toronto's Hospital for Sick Children effectively close the gap between the gene responsible for cystic fibrosis and the basic defect in the disease. By successfully purifying the CF gene's protein product, they obtain direct proof that CFTR is a chloride channel. In addition, by reconstituting the protein in a synthetic system, Drs. Bear and Riordan bring the possibility of treating CF through protein therapy one step closer.
* In August 1992, scientists at the University of North Carolina announce the development of an animal model of cystic fibrosis: the "CF mouse". This animal model is expected to shed light on the disease process, and provide an effective way to test and refine potential new treatments for CF.
* In April 1993, Dr. Christine Bear publishes findings indicating that the protein produced by the major CF mutation is capable of functioning normally. However, the protein fails to move as it should to the cell membrane, and is therefore unable to move chloride across the cell wall. Dr. Bear hypothesizes that specially-targeted drugs may be able to escort the protein to its proper location, thereby correcting the defect in CF-affected cells.
* In April 1993, scientists at the National Institutes of Health in the United States use a modified virus to administer a normal version of the gene responsible for CF to a human subject, as a first step toward exploring the viability of gene therapy for cystic fibrosis.
* In July 1993, the Canadian Cystic Fibrosis Foundation formally launches Research Development Program III: Beyond the Gene - from theory to therapy.
* In October 1993, Dr. Michael Welsh of the University of Iowa College of Medicine announces, that, using gene therapy techniques, he and his colleagues have reversed the basic defect in the nasal epithelia of three individuals with cystic fibrosis. While not amounting to a cure, Dr. Welsh's accomplishment indicates that gene therapy may eventually alleviate or eliminate abnormal lung function in cystic fibrosis.
* In September 1994, Dr. Ron Crystal of the National Institutes of Health in the United States, reports on the successful administration of a modified adenovirus containing a normal version of the gene responsible for CF to the lungs of four individuals with cystic fibrosis.
* In January 1995, investigators in Great Britain and the United States report promising preliminary results in their efforts to use liposomes, or small bubbles of fat, to transfer a normal version of the CF gene to the epithelial cells of nine individuals with cystic fibrosis.
* In October 1995, Dr. Christine Bear and other investigators funded through the Foundation's RDP III initiative demonstrate, in the mouse model of CF, that protein replacement may be a viable treatment for cystic fibrosis.
* In 1996, the Canadian Cystic Fibrosis Foundation launches SPARX, the Special Programme in Applied Research and Therapy, a $5 million dollar initiative designed to bring new forms of therapy to the point of clinical application within five years.
* In December 1997, Dr. Jim Hu of Toronto's Hospital for Sick Children develops a novel way to 'turn on' the normal version of the gene responsible for CF, and control its activity, so that it will function properly. In order for genes to function, they need to be 'turned on' or expressed: Dr.Hu's "expression cassette" successfully turns on the CF gene in laboratory samples of human cells.
* In March 1998, Drs. Fred Zhang, Norbert Kartner, and Gergely Lukacs of the University of Toronto and The Hospital for Sick Children provide the first structural evidence that the defective cystic fibrosis gene leads to malformation of the protein that carries out the gene's specific function. Normally the protein acts as a channel, or pore at the cell surface, and permits the movement of salt and water across cell membranes. The most common defect in CF stops the protein from 'folding' normally; and consequently, the protein is retained in the cell, and fails to reach the cell surface to perform its function as a pore.
* In 1999, investigators with SPARX form an alliance with industry to bring DCF 987 (also known as dextran), a compound designed to combat lung infection, and enhance mucus clearance from lungs, to clinical trials.
* In 2000, SPARX realized major progress toward initiating Phase I clinical trials of aerosolized (inhaled) dextran.
* In 2000, thanks to improved clinical care and available treatments, over 45% of persons with CF in Canada are 18 years and older.
* In 2001, the CCFF announces a Special Initiative in CF Research - In Memory of Michael O'Reilly - a $1.05 million commitment over three years to explore and discover new approaches to treat cystic fibrosis patients who have Burkholderia cepacia and other multi-resistant bacteria in their airways.
* Dr. Shawn Aaron (University of Ottawa) initiates a clinical trial investigating whether patients with exacerbations of their cystic fibrosis lung disease will benefit from treatments with a combination of antibiotics used simultaneously. There are four CF centres in Canada participating in this study, which is partially funded by the CCFF.
* In 2002, SPARX realized successful completion of the Phase I clinical trial on dextran. The results indicated that inhaled dextran could be safely utilized in humans. Focus is now on initializing a Phase II clinical trial.
* In January 2002, the CCFF and the Institute of Circulatory and Respiratory Health of the Canadian Institutes of Health Research awarded a team of researchers led by Dr. Miguel Valvano (University of Western Ontario, London) over $1,000,000 in support of cystic fibrosis. The research is aimed at discovering new approaches for treating individuals with cystic fibrosis who have Burkholderia cepacia complex and other multi-resistant bacteria in their airways.
* In May 2002, the CCFF announced that the median age of survival for individuals with CF had risen from four years in 1960 to over 35 years(based on year 2000 data). The median age of survival is the age beyond which half of the affected population may be expected to live.
* In 2002, Genome Canada awarded Dr. Lap-Chee Tsui (The Hospital for Sick Children) and his colleagues $3.36 million over 3 years to supplement CCFF research funds (for a total grant of $7.01 million) to help researchers identify and understand the role of modifier genes in individuals with CF. Identification of genetic modifiers with various effects in CF will allow to more precisely determine CF disease outcome, and optimize the medical care and treatment.
* In January 2003, BCY LifeSciences Inc. reported that the first patients for the Phase II clinical trial of dextran were enrolled and treatment had started. This potential new treatment may prevent Pseudomonas aeruginosa and Burkholderia cepacia complex from adhering to lung cells, at the site of infection. Preliminary results of the trial were released in November 2003. Although dextran aerosol therapy was found to be very safe, and demonstrated trends towards improvements in lung function, more clinical trials are needed.The CCFF's Special Programme in Applied Research and Therapy (SPARX) funded the initial studies on dextran.
* In March 2003, the CCFF and the Canadian Institutes of Health Research announced the largest and most highly ambitious research program in the history of the Foundation. Breathe (Basic REsearch And THErapy), which is designed to target the basic defect in cystic fibrosis through the development of novel therapeutic approaches. This program intends to fund 1 or 2 groups in the range of $600,000 to $1,200,000 per year, for up to 5 years, beginning in April 2004.
* In December 2003, Dr. Jim Hu and colleagues in Toronto described a new gene delivery vehicle, or "vector", for CF lung gene therapy. This vector transfers a normal gene into targeted epithelial cells which line the airways, and produces a necessary protein, in place of a protein which is defective in CF. It may also have a positive, therapeutic effect in combatting a type of chronic lung infection that, in cystic fibrosis, can be life-threatening. This achievement was yet another "world first" for Canada, as this was the first time that CF gene therapy - albeit under laboratory conditions - had been observed to result in marked clinical benefit.
* In March 2003, the CCFF, together with the Institute of Circulatory and Respiratory Health and the Institute of Infection and Immunity of the Canadian Institutes of Health Research announced the two winning teams of a new, highly ambitious $6 million research program, Breathe (Basic Research and Therapy). The two teams, led by Dr. John Hanrahan (McGill University, Montreal) and Dr. Christine Bear (The Hospital for Sick Children, Toronto) plan to develop innovative approaches to altering the course of CF disease.
* In April 2004, two research teams led by Dr. John Hanrahan (Quebec) and Dr. Christine Bear (Ontario) began work on an ambitious $6 million research program, under the banner Breathe (for Basic Research and Therapy). While CF research is often focused on finding new treatments for the disease, Breathe is unique because it targets the basic defect in cystic fibrosis.
* In May 2004, the CCFF announced that the median age of survival for Canadians with CF had risen once again from 35.9 (in 2001) to 37 years (based on year 2002 data).
* In May 2004, Dr. Richard Boucher from The University of North Carolina at Chapel Hill reports, for the very first time, on the successful creation of a mouse with lung pathology similar to human cystic fibrosis. These mice should be useful for evaluating some therapeutic interventions to treat CF lung disease.
* In March 2005, Dr. Jim Hu at The Hospital for Sick Children was awarded the Foundation's Zellers Senior Scientist Award. The Zellers Senior Scientist Award recognizes outstanding contributions of an established CF investigator, and pays tribute to Hbc's tremendous support of the work of the Foundation. Dr. Hu is focusing his research on CF gene therapy, where the normal version of the gene responsible for CF will be delivered to lung cells. Dr. Hu has developed a novel viral vector that is effective in expressing Cftr in mice, and has been shown to protect the mice from lung infections. Dr. Hu plans to develop methods of delivering the vector to larger animals, whose airways are more similar to humans.
* In July 2005, Dr. Bob Hancock from The University of British Columbia demonstrates that a novel class of antibiotics called "antimicrobial peptides" has the potential to attack two of the components responsible for the progression of lung disease in cystic fibrosis: infection and inflammation.
* In August 2005, Dr. Rod Merrill from the University of Guelph discovers how the toxin produced by the bacteria Pseudomonas aeruginosa prevents CF-infected cells from synthesising proteins, and kills the cell. The toxin disguises itself as part of the ribosome, the structure that acts as the cell's protein factory, and shuts down the ribosome, stopping protein production in the cell. This insight into how the toxin works will give researchers a better chance of finding out how to disable it.
* In October 2005, an international team of investigators, including Canadian researchers (British Columbia, Ontario and Quebec) found a correlation between a variant of the modifier gene TGF-ß1 (which plays a role in lung inflammation) and individuals with CF who experience an accelerated rate of decline in lung function. Identification of modifier genes allows doctors to tailor more aggressive therapies for higher risk patients, and creates new potential therapies to help regulate the expression of modifier genes such as TGF-?1.
* In October 2005, the two Breathe teams reported that during the summer of 2005, more than 50,000 substances were tested to determine which could help "fix" the basic defect in CF. Of the 50,000 substances tested, the teams were able to identify several that were effective in "fixing" CF cells. These substances are being studied further for their therapeutic potential.
and that's just from canada and i can't tell the amount of times that i read articles about places abroad that have come out with new things
Ashley 23 w/cf
Actually many many countries including Canada and the UK have made many break through s when it comes to cf.. tons of breakthroughs for example i have copy pasted this from teh canadian cystic fibrosis website of their research history
Progress in Cystic Fibrosis Research Since 1985
* In 1985, Canadian scientists Drs. Lap-Chee Tsui and Manuel Buchwald trace the gene responsible for CF to chromosome 7. Over the following several years, the discovery of genetic "markers" helps researchers close in on the gene. The search is aided as well by an important new technique, developed by Dr. Francis Collins, called "chromosome jumping".
* In 1986, the CCFF launches its Research Development Program I (RDP I) in CF Genetics/Gene Expression, based at Toronto's Hospital for Sick Children.
* In 1988, the CCFF launches its Research Development Program II (RDP II) focused on Lung Infection in CF, based at the University of Calgary's Health Sciences Centre.
* In the 1980s, significant progress is made in exploring the potential of a new class of drugs for treating faulty secretion in CF. One such drug, amiloride, alters the characteristics of fluid secretion by reducing the ability of cells in the lung to reabsorb sodium. The result is that the exterior of cells remains moist.
* Pioneering work is done in the field of heart/lung and double lung transplantation, which has now emerged as a viable option for people with cystic fibrosis. In 1988, at the Toronto General Hospital, the first successful double lung transplant is done on a patient with cystic fibrosis.
* In August 1989, CF research takes a huge step forward as Drs. Lap-Chee Tsui and Jack Riordan of the RDP I team, in collaboration with Dr.Francis Collins, announce the discovery of the gene responsible for cystic fibrosis.
* In September 1990, scientists succeeded in correcting the CF defect,under laboratory conditions. Canadian investigators in the RDP I program once again lead the way, successfully building a normal version (cDNA)of the gene responsible for CF. Collaborators in the United States then use a virus to place this normal gene in cells affected by CF. When they do, chloride begins to move normally across the cell membranes, thereby corecting the major defect in the disease.
* In 1990, significant progress is made in experiments with a potential new CF treatment: the aerosol administration of DNase, an enzyme that breaks down human genetic material. When DNase is administered to CF lungs, it breaks down much of the "junk" DNA in lung secretions, and reduces the thickness of these secretions, which otherwise plug the airways and encourage infection. DNase aerosol therapy is now commercially available.
* A potential new therapy emerges in 1990, called alpha-1-antitrypsin. Delivered in the form of an aerosol, alpha-1-antitrypsin suppresses the activities of an enzyme called elastase, which is highly destructive of lung tissue in CF. This new treatment may be able to limit the damage caused by elastase, and improve the ability of the immune system to kill Pseudomonas aeruginosa bacteria.
* In 1991, over 30% of patients registered at Canadian CF clinics were adults.
* In February 1991, CCFF-funded investigators announce important insights into the function of the CF gene protein, called CFTR (cystic fibrosis transmembrane conductance regulator). By placing a normal version of the CF gene into cells which do not exhibit salt (chloride) channels like the one which is defective in CF, scientists are able to determine that the CF gene protein is, in all likelihood, itself the salt channel.
* Investigators at the University of North Carolina announce in August 1991 that certain naturally-occurring compounds, used in combination with amiloride, can increase the ability of epithelial cells to secrete chloride. This could significantly improve the ability of persons with CF to clear secretions from the lungs.
* In October 1991, CCFF-funded researchers identify precisely which cells in the body are affected by cystic fibrosis, showing that the normal counterpart of the gene responsible for CF is active in the cells lining the airways, and in the salivary glands, intestines, and reproductive tissues. The findings are of vital significance, since the development of effective pharmacological or genetic therapies for CF will depend upon knowing which cells represent the target for treatment.
* Two complementary papers in December 1991 demonstrate that the CF gene protein can be detected in the membranes of affected cells, and does have a limited ability to transport salt. These results overturn previous findings - according to which the CFTR protein did not reach the cell membrane and therefore could not transport chloride - and suggest that the defective protein may be prodded into service by chemical stimulation.
* In 1991, a significant step toward gene therapy for CF is reported. Researchers in the United States and France announce that they have modified an adenovirus, similar to the virus responsible for the common cold, so that it cannot reproduce, and then successfully used it to transport a normal version of the gene responsible for CF into the lungs of experimental rats. When this is done, the animals' respiratory cells began to produce a normal human CF protein, and continued to do so for two weeks. Subsequent studies suggest that the effect may last for more than a month.
* In February 1992, Drs. Christine Bear and Jack Riordan of Toronto's Hospital for Sick Children effectively close the gap between the gene responsible for cystic fibrosis and the basic defect in the disease. By successfully purifying the CF gene's protein product, they obtain direct proof that CFTR is a chloride channel. In addition, by reconstituting the protein in a synthetic system, Drs. Bear and Riordan bring the possibility of treating CF through protein therapy one step closer.
* In August 1992, scientists at the University of North Carolina announce the development of an animal model of cystic fibrosis: the "CF mouse". This animal model is expected to shed light on the disease process, and provide an effective way to test and refine potential new treatments for CF.
* In April 1993, Dr. Christine Bear publishes findings indicating that the protein produced by the major CF mutation is capable of functioning normally. However, the protein fails to move as it should to the cell membrane, and is therefore unable to move chloride across the cell wall. Dr. Bear hypothesizes that specially-targeted drugs may be able to escort the protein to its proper location, thereby correcting the defect in CF-affected cells.
* In April 1993, scientists at the National Institutes of Health in the United States use a modified virus to administer a normal version of the gene responsible for CF to a human subject, as a first step toward exploring the viability of gene therapy for cystic fibrosis.
* In July 1993, the Canadian Cystic Fibrosis Foundation formally launches Research Development Program III: Beyond the Gene - from theory to therapy.
* In October 1993, Dr. Michael Welsh of the University of Iowa College of Medicine announces, that, using gene therapy techniques, he and his colleagues have reversed the basic defect in the nasal epithelia of three individuals with cystic fibrosis. While not amounting to a cure, Dr. Welsh's accomplishment indicates that gene therapy may eventually alleviate or eliminate abnormal lung function in cystic fibrosis.
* In September 1994, Dr. Ron Crystal of the National Institutes of Health in the United States, reports on the successful administration of a modified adenovirus containing a normal version of the gene responsible for CF to the lungs of four individuals with cystic fibrosis.
* In January 1995, investigators in Great Britain and the United States report promising preliminary results in their efforts to use liposomes, or small bubbles of fat, to transfer a normal version of the CF gene to the epithelial cells of nine individuals with cystic fibrosis.
* In October 1995, Dr. Christine Bear and other investigators funded through the Foundation's RDP III initiative demonstrate, in the mouse model of CF, that protein replacement may be a viable treatment for cystic fibrosis.
* In 1996, the Canadian Cystic Fibrosis Foundation launches SPARX, the Special Programme in Applied Research and Therapy, a $5 million dollar initiative designed to bring new forms of therapy to the point of clinical application within five years.
* In December 1997, Dr. Jim Hu of Toronto's Hospital for Sick Children develops a novel way to 'turn on' the normal version of the gene responsible for CF, and control its activity, so that it will function properly. In order for genes to function, they need to be 'turned on' or expressed: Dr.Hu's "expression cassette" successfully turns on the CF gene in laboratory samples of human cells.
* In March 1998, Drs. Fred Zhang, Norbert Kartner, and Gergely Lukacs of the University of Toronto and The Hospital for Sick Children provide the first structural evidence that the defective cystic fibrosis gene leads to malformation of the protein that carries out the gene's specific function. Normally the protein acts as a channel, or pore at the cell surface, and permits the movement of salt and water across cell membranes. The most common defect in CF stops the protein from 'folding' normally; and consequently, the protein is retained in the cell, and fails to reach the cell surface to perform its function as a pore.
* In 1999, investigators with SPARX form an alliance with industry to bring DCF 987 (also known as dextran), a compound designed to combat lung infection, and enhance mucus clearance from lungs, to clinical trials.
* In 2000, SPARX realized major progress toward initiating Phase I clinical trials of aerosolized (inhaled) dextran.
* In 2000, thanks to improved clinical care and available treatments, over 45% of persons with CF in Canada are 18 years and older.
* In 2001, the CCFF announces a Special Initiative in CF Research - In Memory of Michael O'Reilly - a $1.05 million commitment over three years to explore and discover new approaches to treat cystic fibrosis patients who have Burkholderia cepacia and other multi-resistant bacteria in their airways.
* Dr. Shawn Aaron (University of Ottawa) initiates a clinical trial investigating whether patients with exacerbations of their cystic fibrosis lung disease will benefit from treatments with a combination of antibiotics used simultaneously. There are four CF centres in Canada participating in this study, which is partially funded by the CCFF.
* In 2002, SPARX realized successful completion of the Phase I clinical trial on dextran. The results indicated that inhaled dextran could be safely utilized in humans. Focus is now on initializing a Phase II clinical trial.
* In January 2002, the CCFF and the Institute of Circulatory and Respiratory Health of the Canadian Institutes of Health Research awarded a team of researchers led by Dr. Miguel Valvano (University of Western Ontario, London) over $1,000,000 in support of cystic fibrosis. The research is aimed at discovering new approaches for treating individuals with cystic fibrosis who have Burkholderia cepacia complex and other multi-resistant bacteria in their airways.
* In May 2002, the CCFF announced that the median age of survival for individuals with CF had risen from four years in 1960 to over 35 years(based on year 2000 data). The median age of survival is the age beyond which half of the affected population may be expected to live.
* In 2002, Genome Canada awarded Dr. Lap-Chee Tsui (The Hospital for Sick Children) and his colleagues $3.36 million over 3 years to supplement CCFF research funds (for a total grant of $7.01 million) to help researchers identify and understand the role of modifier genes in individuals with CF. Identification of genetic modifiers with various effects in CF will allow to more precisely determine CF disease outcome, and optimize the medical care and treatment.
* In January 2003, BCY LifeSciences Inc. reported that the first patients for the Phase II clinical trial of dextran were enrolled and treatment had started. This potential new treatment may prevent Pseudomonas aeruginosa and Burkholderia cepacia complex from adhering to lung cells, at the site of infection. Preliminary results of the trial were released in November 2003. Although dextran aerosol therapy was found to be very safe, and demonstrated trends towards improvements in lung function, more clinical trials are needed.The CCFF's Special Programme in Applied Research and Therapy (SPARX) funded the initial studies on dextran.
* In March 2003, the CCFF and the Canadian Institutes of Health Research announced the largest and most highly ambitious research program in the history of the Foundation. Breathe (Basic REsearch And THErapy), which is designed to target the basic defect in cystic fibrosis through the development of novel therapeutic approaches. This program intends to fund 1 or 2 groups in the range of $600,000 to $1,200,000 per year, for up to 5 years, beginning in April 2004.
* In December 2003, Dr. Jim Hu and colleagues in Toronto described a new gene delivery vehicle, or "vector", for CF lung gene therapy. This vector transfers a normal gene into targeted epithelial cells which line the airways, and produces a necessary protein, in place of a protein which is defective in CF. It may also have a positive, therapeutic effect in combatting a type of chronic lung infection that, in cystic fibrosis, can be life-threatening. This achievement was yet another "world first" for Canada, as this was the first time that CF gene therapy - albeit under laboratory conditions - had been observed to result in marked clinical benefit.
* In March 2003, the CCFF, together with the Institute of Circulatory and Respiratory Health and the Institute of Infection and Immunity of the Canadian Institutes of Health Research announced the two winning teams of a new, highly ambitious $6 million research program, Breathe (Basic Research and Therapy). The two teams, led by Dr. John Hanrahan (McGill University, Montreal) and Dr. Christine Bear (The Hospital for Sick Children, Toronto) plan to develop innovative approaches to altering the course of CF disease.
* In April 2004, two research teams led by Dr. John Hanrahan (Quebec) and Dr. Christine Bear (Ontario) began work on an ambitious $6 million research program, under the banner Breathe (for Basic Research and Therapy). While CF research is often focused on finding new treatments for the disease, Breathe is unique because it targets the basic defect in cystic fibrosis.
* In May 2004, the CCFF announced that the median age of survival for Canadians with CF had risen once again from 35.9 (in 2001) to 37 years (based on year 2002 data).
* In May 2004, Dr. Richard Boucher from The University of North Carolina at Chapel Hill reports, for the very first time, on the successful creation of a mouse with lung pathology similar to human cystic fibrosis. These mice should be useful for evaluating some therapeutic interventions to treat CF lung disease.
* In March 2005, Dr. Jim Hu at The Hospital for Sick Children was awarded the Foundation's Zellers Senior Scientist Award. The Zellers Senior Scientist Award recognizes outstanding contributions of an established CF investigator, and pays tribute to Hbc's tremendous support of the work of the Foundation. Dr. Hu is focusing his research on CF gene therapy, where the normal version of the gene responsible for CF will be delivered to lung cells. Dr. Hu has developed a novel viral vector that is effective in expressing Cftr in mice, and has been shown to protect the mice from lung infections. Dr. Hu plans to develop methods of delivering the vector to larger animals, whose airways are more similar to humans.
* In July 2005, Dr. Bob Hancock from The University of British Columbia demonstrates that a novel class of antibiotics called "antimicrobial peptides" has the potential to attack two of the components responsible for the progression of lung disease in cystic fibrosis: infection and inflammation.
* In August 2005, Dr. Rod Merrill from the University of Guelph discovers how the toxin produced by the bacteria Pseudomonas aeruginosa prevents CF-infected cells from synthesising proteins, and kills the cell. The toxin disguises itself as part of the ribosome, the structure that acts as the cell's protein factory, and shuts down the ribosome, stopping protein production in the cell. This insight into how the toxin works will give researchers a better chance of finding out how to disable it.
* In October 2005, an international team of investigators, including Canadian researchers (British Columbia, Ontario and Quebec) found a correlation between a variant of the modifier gene TGF-ß1 (which plays a role in lung inflammation) and individuals with CF who experience an accelerated rate of decline in lung function. Identification of modifier genes allows doctors to tailor more aggressive therapies for higher risk patients, and creates new potential therapies to help regulate the expression of modifier genes such as TGF-?1.
* In October 2005, the two Breathe teams reported that during the summer of 2005, more than 50,000 substances were tested to determine which could help "fix" the basic defect in CF. Of the 50,000 substances tested, the teams were able to identify several that were effective in "fixing" CF cells. These substances are being studied further for their therapeutic potential.
and that's just from canada and i can't tell the amount of times that i read articles about places abroad that have come out with new things
Ashley 23 w/cf