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END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20330313T030000 RDATE:20331106T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20340312T030000 RDATE:20341105T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20350311T030000 RDATE:20351104T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20360309T030000 RDATE:20361102T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20370308T030000 RDATE:20371101T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT END:VTIMEZONE BEGIN:VEVENT UID:468b0935d7b7307db1303cb9cc0abb53 CATEGORIES:LSDM CREATED:20150523T101039 SUMMARY:Shawnie Bray DESCRIPTION:  \n  \n  \n    "I believed I was living a truncated life... so, I never took a new day for granted."   Travis Bray Founder, FAPFoundation     Above:  Travis Bray speaks to La Societe Deux Magots (LSDM) on 18 Feb 2014, Wasatch Bagel, Park City, UT.   Travis H. Bray is a third ge neration familial adenomatours polyposis (F.A.P) survivor and understands f irsthand the long-reaching physical and emotional effects living with this disease has on both the patient and their loved ones. By drawing upon both personal experiences with F.A.P. and those of his extended family, he is mo tivated to developing a support net for those born or affected by F.A.P. Tr avis graduate with top honors for his graduate work in Actinide Chemistry a t Auburn University in 2008. He continued his research for two years as the Berkeley Actinide Postdoctoral Fellow at Lawrence Berkeley National Labora tory, and a third year of post-doctoral research at Argonne National Labora tory. Travis stepped away from his career as a chemistry researcher (June, 2012) to found the F.A.P. Foundation.   Hat tip: Event     Abo ve:  Travis Bray presses a point as he educates LSDM members on familial ad enomatours polyposis, a congenital colon cancer.  Wasatch Bagel, 18 Februar y 2014.     http://ghr.nlm.nih.gov/condition/familial-adenomatous-pol yposis (http://ghr.nlm.nih.gov/condition/familial-adenomatous-polyposis) What is familial adenomatous polyposis? Familial adenomatou s polyposis (FAP) is an inherited disorder characterized by cancer of the l arge intestine (colon) and rectum. People with the classic type of familial adenomatous polyposis may begin to develop multiple noncancerous (benign) growths (polyps) in the colon as early as their teenage years. Unless the c olon is removed, these polyps will become malignant (cancerous). The averag e age at which an individual develops colon cancer in classic familial aden omatous polyposis is 39 years. Some people have a variant of the disorder, called attenuated familial adenomatous polyposis, in which polyp growth is delayed. The average age of colorectal cancer onset for attenuated familial adenomatous polyposis is 55 years.\n In people with classic famili al adenomatous polyposis, the number of polyps increases with age, and hund reds to thousands of polyps can develop in the colon. Also of particular si gnificance are noncancerous growths called desmoid tumors. These fibrous tu mors usually occur in the tissue covering the intestines and may be provoke d by surgery to remove the colon. Desmoid tumors tend to recur after they a re surgically removed. In both classic familial adenomatous polyposis and i ts attenuated variant, benign and malignant tumors are sometimes found in o ther places in the body, including the duodenum (a section of the small int estine), stomach, bones, skin, and other tissues. People who have colon pol yps as well as growths outside the colon are sometimes described as having Gardner syndrome.\n A milder type of familial adenomatous polyposis , called autosomal recessive familial adenomatous polyposis, has also been identified. People with the autosomal recessive type of this disorder have fewer polyps than those with the classic type. Fewer than 100 polyps typica lly develop, rather than hundreds or thousands. The autosomal recessive typ e of this disorder is caused by mutations in a different gene than the clas sic and attenuated types of familial adenomatous polyposis.\n Ho w common is familial adenomatous polyposis? The reported incid ence of familial adenomatous polyposis varies from 1 in 7,000 to 1 in 22,00 0 individuals.\n What genes are related to familial adenomatous polyposis? Mutations in the APC gene cause both classic and at tenuated familial adenomatous polyposis. These mutations affect the ability of the cell to maintain normal growth and function. Cell overgrowth result ing from mutations in the APC gene leads to the colon polyps seen in famili al adenomatous polyposis. Although most people with mutations in the APC ge ne will develop colorectal cancer, the number of polyps and the time frame in which they become malignant depend on the location of the mutation in th e gene.\n Mutations in the MUTYH gene cause autosomal recessive fam ilial adenomatous polyposis (also called MYH-associated polyposis). Mutatio ns in this gene prevent cells from correcting mistakes that are made when D NA is copied (DNA replication) in preparation for cell division. As these m istakes build up in a person's DNA, the likelihood of cell overgrowth incre ases, leading to colon polyps and the possibility of colon cancer.\n Read more about the APC (http://ghr.nlm.nih.gov/gene/APC) and MUTYH (http ://ghr.nlm.nih.gov/gene/MUTYH) genes.\n How do people inherit fa milial adenomatous polyposis? Familial adenomatous polyposis c an have different inheritance patterns.\n When familial adenomatous polyposis results from mutations in the APC gene, it is inherited in an au tosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In most cases, an affected person has one parent with the condition.\n When familial adenomatous pol yposis results from mutations in the MUTYH gene, it is inherited in an auto somal recessive pattern, which means both copies of the gene in each cell h ave mutations. Most often, the parents of an individual with an autosomal r ecessive condition each carry one copy of the mutated gene, but do not show signs and symptoms of the condition.\n     Takeaways...   One cure.  Total colonectomy.    33% of those contracting are de nov o... ie. gene mutation in parent.   In last 90 days, six individual s with F.A.P. have died.   2013. 144k deaths from colon cancer... o f which, 5% are hereditary (1% F.A.P.).   Travis diagnosed at 15 years of age.  Colon removed replaced by "J patch" fashioned by removed section of small intestine.  "J patch" is one of seven surgical procedures used for disease.   In his early 30's Travis relapsed... effects of the cancer spread to duodenum.    "I believed I was living a truncated life... so, I never took a new day for granted."    Travis left a promising career in chemical and nuclear research to form FAPFoundation.  http://www.hcctak esguts.org/ (http://www.hcctakesguts.org/)   Travis, a trained research er, was amazed at the significant amount of scientific research on F.A.P.  But, none of the research was available in easy to understand, synthesized form for the average afflicted person.  Because of the diseases rarity, the average physician had little knowledge.  The condition was often diagnosed as hemorrhoids or some such...   Drawn from Argonne National Laborator y in Illinois, to Huntsman Cancer Center, Salt Lake City where the world's top experts in F.A.P. work... Randy Burt, Deb Meckelson... they have connec ted F.A.P. "to the 5th gene..."  they are the best at hereditary cancers in the world.  Their scientific progress was facilitated by their extensive u se of LDS church familial and hereditary records.   "I learned from Mec kelson that there was no reason I couldn't live a long life. I was virtuall y given a new life by my connection with the people at Huntsman.   "I have found my niche."   FAPFoundation is located in Park City, UT and is run by Travis and his wife.   Supporters of FAPFoundation are 60% individu als and 40% corporations.  We have a good network of friends and family.   The National Society of Genetic Counselors has 700 members.  We work cl osely to educate genetic counselors on F.A.P.   Five scientists/researc hers at Huntsman are on the board of FAPFoundation.     Thank-you.   LSDM thanks Travis Bray for his very informative presentation about the little understood colon affliction, familial adenomatours polyposis, and c ongratulates him for his dedication making this affliction better known.     La Societe Deux Magots (LSDM) is a non-partisan ROMEO (retired old men eating out) group which meets daily, at 7:00 AM at Wasatch Bagel in Par k City, UT. LSDM members are the rightful intellectual heirs of a group of authors (Hemingway, Sartre, Camus, deBouvoir) who met daily at Cafe Deux Ma gots, in Paris, France in the 1930's.    \n  \n  \n La Societe Deux Ma gots (LSDM) is a non-partisan ROMEO (retired old men eating out) group whic h meets daily, at 7:00 AM at Wasatch Bagel in Park City, UT. LSDM members a re the rightful intellectual heirs of a group of authors (Hemingway, Sartre , Camus, deBouvoir) who met daily at Cafe Deux Magots, in Paris, France in the 1930's.) www.lsdm-parkcity.com (http://www.lsdm-parkcity.c om/)\n   X-ALT-DESC;FMTTYPE=text/html:

 

 

 

  
< strong>"I believed I was living a truncated life... so, I never took a new day for granted."
 
Travis Bray
Founder, FAPFoundation
 
 
Above:  Travis Bra y speaks to La Societe Deux Magots (LSDM) on 18 Feb 2014, Wasatch Bagel, Pa rk City, UT.
 
Travis H. Bray is a third generation familial adenomatours polyposi s (F.A.P) survivor and understands firsthand the long-reachi ng physical and emotional effects living with this disease has on both the patient and their loved ones. By drawing upon both personal experiences wit h F.A.P. and those of his extended family, he is motivated to developing a support net for those born or affected by F.A.P. Travis graduate with top h onors for his graduate work in Actinide Chemistry at Auburn University in 2 008. He continued his research for two years as the Berkeley Actinide Postd octoral Fellow at Lawrence Berkeley National Laboratory, and a third year o f post-doctoral research at Argonne National Laboratory. Travis stepped awa y from his career as a chemistry researcher (June, 2012) to found the F.A.P . Foundation.
 
Ha t tip: Event
 
 
Above:  Travis Bray pres ses a point as he educates LSDM members on familial adenomatours polyposis, a congenital colon cancer.  Wasatch Bagel, 18 February 2014.
 
 
http://ghr.nlm.nih.gov/condition/familial-adenoma tous-polyposis

What is familial adenomatous polyposis?

< p style="margin-bottom: 0pt; margin-top: 1ex; "> Familial adenomatous p olyposis (FAP) is an inherited disorder characterized by cancer of the larg e intestine (colon) and rectum. People with the classic type of familial ad enomatous polyposis may begin to develop multiple noncancerous (benign) gro wths (polyps) in the colon as early as their teenage years. Unless the colo n is removed, these polyps will become malignant (cancerous). The average a ge at which an individual develops colon cancer in classic familial adenoma tous polyposis is 39 years. Some people have a variant of the disorder, cal led attenuated familial adenomatous polyposis, in which polyp growth is del ayed. The average age of colorectal cancer onset for attenuated familial ad enomatous polyposis is 55 years.

In people with classic familial adenomatous polyposis, t he number of polyps increases with age, and hundreds to thousands of polyps can develop in the colon. Also of particular significance are noncancerous growths called desmoid tumors. These fibrous tumors usually occur in the t issue covering the intestines and may be provoked by surgery to remove the colon. Desmoid tumors tend to recur after they are surgically removed. In b oth classic familial adenomatous polyposis and its attenuated variant, beni gn and malignant tumors are sometimes found in other places in the body, in cluding the duodenum (a section of the small intestine), stomach, bones, sk in, and other tissues. People who have colon polyps as well as growths outs ide the colon are sometimes described as having Gardner syndrome.

A milder type of famili al adenomatous polyposis, called autosomal recessive familial adenomatous p olyposis, has also been identified. People with the autosomal recessive typ e of this disorder have fewer polyps than those with the classic type. Fewe r than 100 polyps typically develop, rather than hundreds or thousands. The autosomal recessive type of this disorder is caused by mutations in a diff erent gene than the classic and attenuated types of familial adenomatous po lyposis.

How common is familial adenomatous polyposis?

The reported inciden ce of familial adenomatous polyposis varies from 1 in 7,000 to 1 in 22,000 individuals.

What genes are related to familial adenomatous polyposis?

Mutations in the APC gene cause both classic and attenuated familial adenomatous polyposis. These mu tations affect the ability of the cell to maintain normal growth and functi on. Cell overgrowth resulting from mutations in the APC gene leads to the colon polyps seen in familial adenomatous polyposis. Although most people with mutations in the APC gene wil l develop colorectal cancer, the number of polyps and the time frame in whi ch they become malignant depend on the location of the mutation in the gene .

Mutations in the MUTYH gene cause autosomal recessive familial adenomatous polyposis (also called MYH-a ssociated polyposis). Mutations in this gene prevent cells from correcting mistakes that are made when DNA is copied (DNA replication) in preparation for cell division. As these mistakes build up in a person's DNA, the likeli hood of cell overgrowth increases, leading to colon polyps and the possibil ity of colon cancer.

Read more about the APC and MUTYH genes.

How do people inherit fa milial adenomatous polyposis?

Familial adenomatous polyposis can have different inheritance patterns.

When familial adenomatous polyposis results from mutations in the < span class="geneSymbol" style="FONT-STYLE: italic">APC gene, it is i nherited in an autosomal dominant pattern, which means one copy of the alte red gene in each cell is sufficient to cause the disorder. In most cases, a n affected person has one parent with the condition.

When familial adenomatous polyposis results from mutations in the MUTYH gene, it is inherited in an autosomal recessive pattern , which means both copies of the gene in each cell have mutations. Most oft en, the parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but do not show signs and symptoms of the condition.

 
 
Takeaways...
 
One cure.  Total colonectomy. 
 
33% of those contracting are de novo... ie. gene mutation in parent.
 
In last 90 days, six individuals with F.A.P. ha ve died.
 
2013. 144k deaths from colon cance r... of which, 5% are hereditary (1% F.A.P.).
 
< div> Travis diagnosed at 15 years of age.  Colon removed replaced by "J pa tch" fashioned by removed section of small intestine.  "J patch" is one of seven surgical procedures used for disease.
 
In his early 30's Travis relapsed... effects of the cancer spread to duodenum.  
 
"I believed I was living a truncated life... so, I never took a new day for granted." 
 
Travi s left a promising career in chemical and nuclear research to form FAPFound ation.  http://www.hcctakesguts.org/
 
Travi s, a trained researcher, was amazed at the significant amount of scientific research on F.A.P.  But, none of the research was available in easy to und erstand, synthesized form for the average afflicted person.  Because of the diseases rarity, the average physician had little knowledge.  The conditio n was often diagnosed as hemorrhoids or some such...
 
< div> Drawn from Argonne National Laboratory in Illinois, to Huntsman Cance r Center, Salt Lake City where the world's top experts in F.A.P. work... Ra ndy Burt, Deb Meckelson... they have connected F.A.P. "to the 5th gene..."  they are the best at hereditary cancers in the world.  Their scientific pr ogress was facilitated by their extensive use of LDS church familial and he reditary records.
 
"I learned from Meckelson tha t there was no reason I couldn't live a long life. I was virtually given a new life by my connection with the people at Huntsman.   "I have found my n iche."
 
FAPFoundation is located in Park City, U T and is run by Travis and his wife.
 
Supporters of FAPFoundation are 60% individuals and 40% corporations.  We have a good network of friends and family.
 
The National So ciety of Genetic Counselors has 700 members.  We work closely to educate ge netic counselors on F.A.P.
 
Five scientists/rese archers at Huntsman are on the board of FAPFoundation.
 
 
Thank-you.
 
LSDM thanks Travis Bray for his very informative presentation about the little understood colon affliction, familial adenoma tours polyposis, and congratulates him for his dedication making this affli ction better known.
 
 
La Societe Deux Mago ts (LSDM) is a non-partisan ROMEO (retired old men eating out) group which meets daily, at 7:00 AM at Wasatch Bagel in Park City, UT. LSDM members are the rightful intellectual heirs of a group of authors (Hemingway, Sartre, Camus, deBouvoir) who met daily at Cafe Deux Magots, in Paris, France in th e 1930's.
 

 

 

 

La Societe Deux Magots (LSDM ) is a non-partisan ROMEO (retired old men eating out) group which meets da ily, at 7:00 AM at Wasatch Bagel in Park City, UT. LSDM members are the rig htful intellectual heirs of a group of authors (Hemingway, Sartre, Camus, d eBouvoir) who met daily at Cafe Deux Magots, in Paris, France in the 1930's .)

www.lsdm-parkcity.com

 
DTSTAMP:20260424T165855 DTSTART;TZID=America/Denver:20150526T070000 DTEND;TZID=America/Denver:20150526T080000 SEQUENCE:0 TRANSP:OPAQUE END:VEVENT END:VCALENDAR