BEGIN:VCALENDAR VERSION:2.0 PRODID:-//jEvents 2.0 for Joomla//EN CALSCALE:GREGORIAN METHOD:PUBLISH BEGIN:VTIMEZONE TZID:America/Denver BEGIN:STANDARD DTSTART:20141102T010000 RDATE:20150308T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20151101T010000 RDATE:20160313T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20161106T010000 RDATE:20170312T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20171105T010000 RDATE:20180311T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20181104T010000 RDATE:20190310T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20191103T010000 RDATE:20200308T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20201101T010000 RDATE:20210314T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20211107T010000 RDATE:20220313T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20221106T010000 RDATE:20230312T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20231105T010000 RDATE:20240310T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20241103T010000 RDATE:20250309T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20251102T010000 RDATE:20260308T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20261101T010000 RDATE:20270314T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20271107T010000 RDATE:20280312T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20281105T010000 RDATE:20290311T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20291104T010000 RDATE:20300310T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20301103T010000 RDATE:20310309T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20311102T010000 RDATE:20320314T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20321107T010000 RDATE:20330313T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20331106T010000 RDATE:20340312T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20341105T010000 RDATE:20350311T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20351104T010000 RDATE:20360309T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20361102T010000 RDATE:20370308T030000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:STANDARD DTSTART:20371101T010000 TZOFFSETFROM:-0600 TZOFFSETTO:-0700 TZNAME:America/Denver MST END:STANDARD BEGIN:DAYLIGHT DTSTART:20140525T070000 RDATE:20141102T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20150308T030000 RDATE:20151101T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20160313T030000 RDATE:20161106T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20170312T030000 RDATE:20171105T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20180311T030000 RDATE:20181104T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20190310T030000 RDATE:20191103T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20200308T030000 RDATE:20201101T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20210314T030000 RDATE:20211107T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20220313T030000 RDATE:20221106T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20230312T030000 RDATE:20231105T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20240310T030000 RDATE:20241103T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20250309T030000 RDATE:20251102T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20260308T030000 RDATE:20261101T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20270314T030000 RDATE:20271107T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20280312T030000 RDATE:20281105T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20290311T030000 RDATE:20291104T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20300310T030000 RDATE:20301103T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20310309T030000 RDATE:20311102T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT END:DAYLIGHT BEGIN:DAYLIGHT DTSTART:20320314T030000 RDATE:20321107T010000 TZOFFSETFROM:-0700 TZOFFSETTO:-0600 TZNAME:America/Denver MDT 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 Bray s peaks to La Societe Deux Magots (LSDM) on 18 Feb 2014, Wasatch Bagel, Park City, UT.
 
Travis H. Bray is a third generation familial adenomatours polyposis < font size="2">(F.A.P) survivor and understands firsthand the long-reaching physical and emotional effects living with this disease has on both the pat ient and their loved ones. By drawing upon both personal experiences with F .A.P. and those of his extended family, he is motivated to developing a sup port net for those born or affected by F.A.P. Travis graduate with top hono rs for his graduate work in Actinide Chemistry at Auburn University in 2008 . He continued his research for two years as the Berkeley Actinide Postdoct oral Fellow at Lawrence Berkeley National Laboratory, and a third year of p ost-doctoral research at Argonne National Laboratory. Travis stepped away f rom his career as a chemistry researcher (June, 2012) to found the F.A.P. F oundation.
 
< font color="#000000" face="Arial" size="2" style="BACKGROUND-COLOR: transpa rent">Hat t ip: Event
 
 
Above:  Travis Bray presses a point as he educates LSDM members on familial adenomatours polyposis, a con genital colon cancer.  Wasatch Bagel, 18 February 2014.
 
 
http://ghr.nlm.nih.gov/condition/familial-adenomatous-p olyposis

What is familial adenomatous polyposis?

Familial adenomatous polypos is (FAP) is an inherited disorder characterized by cancer of the large inte stine (colon) and rectum. People with the classic type of familial adenomat ous polyposis may begin to develop multiple noncancerous (benign) growths ( polyps) in the colon as early as their teenage years. Unless the colon is r emoved, these polyps will become malignant (cancerous). The average age at which an individual develops colon cancer in classic familial adenomatous p olyposis is 39 years. Some people have a variant of the disorder, called at tenuated familial adenomatous polyposis, in which polyp growth is delayed. The average age of colorectal cancer onset for attenuated familial adenomat ous polyposis is 55 years.

In people with classic familial adenomatous polyposis, the num ber of polyps increases with age, and hundreds to thousands of polyps can d evelop in the colon. Also of particular significance are noncancerous growt hs called desmoid tumors. These fibrous tumors usually occur in the tissue covering the intestines and may be provoked by surgery to remove the colon. Desmoid tumors tend to recur after they are surgically removed. In both cl assic familial adenomatous polyposis and its attenuated variant, benign and malignant tumors are sometimes found in other places in the body, includin g the duodenum (a section of the small intestine), stomach, bones, skin, an d other tissues. People who have colon polyps as well as growths outside th e colon are sometimes described as having Gardner syndrome.

A milder type of familial ade nomatous polyposis, called autosomal recessive familial adenomatous polypos is, has also been identified. People with the autosomal recessive type of t his disorder have fewer polyps than those with the classic type. Fewer than 100 polyps typically develop, rather than hundreds or thousands. The autos omal recessive type of this disorder is caused by mutations in a different gene than the classic and attenuated types of familial adenomatous polyposi s.

How common is familial adenomatous polyposis?

The reported incidence of familial adenomatous polyposis varies from 1 in 7,000 to 1 in 22,000 indivi duals.

What genes are related to familial adenomatous polyposis?

Mutations in th e APC gene cause both classic and attenuated familial adenomatous polyposis. These mutation s affect the ability of the cell to maintain normal growth and function. Ce ll overgrowth resulting from mutations in the APC gene leads to the colon polyps seen in fa milial adenomatous polyposis. Although most people with mutations in the APC gene will deve lop colorectal cancer, the number of polyps and the time frame in which the y become malignant depend on the location of the mutation in the gene.

Mutations in the < span class="geneSymbol" style="FONT-STYLE: italic">MUTYH gene cause autosomal recessive familial adenomatous polyposis (also called MYH-associa ted polyposis). Mutations in this gene prevent cells from correcting mistak es that are made when DNA is copied (DNA replication) in preparation for ce ll division. As these mistakes build up in a person's DNA, the likelihood o f cell overgrowth increases, leading to colon polyps and the possibility of colon cancer.

Read more about the APC and MUTYH genes.

How do people inherit familial adenomatous polyposis?

Familial adenomatous polyposis can have different inheri tance patterns.

When familial adenomatous polyposis results from mutations in the APC gene, it is inherit ed in an autosomal dominant pattern, which means one copy of the altered ge ne in each cell is sufficient to cause the disorder. In most cases, an affe cted person has one parent with the condition.

When familial adenomatous polyposis result s from mutations in the MUTYH gene, it is inherited in an autosomal recessive pattern, whic h means both copies of the gene in each cell have mutations. Most often, th e 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 co ndition.

 
 
< font size="4">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. have die d.
 
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" f ashioned by removed section of small intestine.  "J patch" is one of seven surgical procedures used for disease.
 
In his ea rly 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.hcctakesguts.org/
 
Travis, a t rained researcher, was amazed at the significant amount of scientific resea rch on F.A.P.  But, none of the research was available in easy to understan d, synthesized form for the average afflicted person.  Because of the disea ses rarity, the average physician had little knowledge.  The condition was often diagnosed as hemorrhoids or some such...
 
Drawn from Argonne National Laboratory in Illinois, to Huntsman Cancer Cent er, Salt Lake City where the world's top experts in F.A.P. work... Randy Bu rt, Deb Meckelson... they have connected 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 use of LDS church familial and heredita ry records.
 
"I learned from Meckelson that ther e was no reason I couldn't live a long life. I was virtually given a new li fe 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 FA PFoundation are 60% individuals and 40% corporations.  We have a good netwo rk of friends and family.
 
The National Society of Genetic Counselors has 700 members.  We work closely to educate genetic counselors on F.A.P.
 
Five scientists/researcher s at Huntsman are on the board of FAPFoundation.
 
 
Thank-you.
 
LSDM thanks Travis Bray for his very informative presen tation about the little understood colon affliction, familial adenomatours polyposis, and congratulates him for his dedication making this affliction better known.
 
 
La Societe Deux Magots (LS DM) 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 r ightful 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.
 

 

 

< p>  

La Societe Deux Magots (LSDM) is a non-partisan ROMEO (retired old men eating out) group which meets daily, a t 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, deBouvo ir) who met daily at Cafe Deux Magots, in Paris, France in the 1930's.)
  DTSTAMP:20260505T061726 DTSTART;TZID=America/Denver:20150526T070000 DTEND;TZID=America/Denver:20150526T080000 SEQUENCE:0 TRANSP:OPAQUE END:VEVENT END:VCALENDAR