Overview of reported facilitators and barriers of adherence to recommendations for cancer prevention that were perceived as most important by Lynch Syndrome mutation carriers and the frequency and the proportion with which they were mentioned.

<p>Overview of reported facilitators and barriers of adherence to recommendations for cancer prevention that were perceived as most important by Lynch Syndrome mutation carriers and the frequency and the proportion with which they were mentioned.</p

Determinants of adherence to recommendations for cancer prevention among Lynch Syndrome mutation carriers: A qualitative exploration

<div><p>Background</p><p>Lynch Syndrome (LS) mutation carriers are at high risk for various cancer types, particularly colorectal cancer. Adherence to lifestyle and body weight recommendations for cancer prevention may lower this risk. To promote adherence to these recommendations, knowledge on determinants of adherence in LS mutation carriers is needed. Therefore, this study aimed to identify determinants of adherence to lifestyle recommendations for cancer prevention in LS mutation carriers.</p><p>Methods</p><p>Five focus groups were conducted with DNA confirmed LS mutation carriers (n = 29). Transcripts were analyzed by thematic analysis, using the Health Belief Model (HBM) as a theoretical framework.</p><p>Results</p><p>Tolerance of an unhealthy lifestyle because of the desire to enjoy life and avoidance of LS dominating their life were most frequently reported as important barriers of adherence to the recommendations. Most important facilitators of adherence to the recommendations were enhancement of wellbeing and intolerance of unhealthy foods due to colon surgery.</p><p>Conclusions</p><p>This study provided a comprehensive overview of determinants of adherence to recommendations for cancer prevention. These determinants, of which some are typically and unique for LS mutation carriers, can be used to design a lifestyle intervention that meets the needs of LS mutation carriers.</p></div

Characteristics of Lynch Syndrome mutation carriers who participated in the focus groups (n = 29).

<p>Characteristics of Lynch Syndrome mutation carriers who participated in the focus groups (n = 29).</p

Linkage on chromosome 4 for the families in which multiple tumours showed the “22-gain-like” aCGH profile.

<p>The LOD-score was calculated under the assumption of homogeneity. The dashed lines indicate the maximum LOD-score -1interval. The X-axis shows the position on chromosome 4 in centimorgan and the markers with a LOD score >0 are indicated. The highest LOD score of 2.49 was located at marker D4S405.</p

Pedigrees of the families in which multiple tumours showed the “22-gain-like” aCGH profile.

<p>Individuals affected with breast cancer are represented by a filled square or circle. Individuals affected by another type of cancer are represented by a square or circle with a vertical black stripe. Below the age at diagnosis and type of cancer can be found: B stands for breast cancer, Li or liver cancer, S for stomach cancer, Oes for oesophagus cancer, C for colon cancer, M for melanoma, Cvx for Cervix cancer, K for kidney cancer, P for prostate cancer and U for type of cancer unknown. Arrows point at the individuals at whose DNA was used for exome sequence. Individuals with tumours with and without the “22-gain-like profile” are represented by “22+”and “22−”.</p

Possibly damaging or well conserved variants in genes encoding proteins involved in DNA integrity maintaince.

<p>Variants were selected if either of these criteria was met: Grantham score>100, GERP conservation score>3, PhastCons conservation score>0.7, or a “Probably damaging” Polyphen2 prediction.</p>1<p>Phastcons and GERP are both regional conservation algorithms ranging from 0 to 1 and −12.3 to 6.17 respectively (1 and 6.17 being most conserved).</p

Well conserved or coding variants in the linkage region on chromosome 4.

1<p>Phastcons and GERP are both regional conservation algorithms ranging from 0 to 1 and −12.3 to 6.17 respectively (1 and 6.17 being most conserved).</p>2<p>Grantham = 45, PolyPhen prediction = Benign.</p

Genomewide high-density SNP linkage analysis of non-BRCA1/2 breast cancer families identifies various candidate regions and has greater power than microsatellite studies-2

<p><b>Copyright information:</b></p><p>Taken from "Genomewide high-density SNP linkage analysis of non-BRCA1/2 breast cancer families identifies various candidate regions and has greater power than microsatellite studies"</p><p>http://www.biomedcentral.com/1471-2164/8/299</p><p>BMC Genomics 2007;8():299-299.</p><p>Published online 30 Aug 2007</p><p>PMCID:PMC2072960.</p><p></p> bottom of each panel

Genomewide high-density SNP linkage analysis of non-BRCA1/2 breast cancer families identifies various candidate regions and has greater power than microsatellite studies-3

<p><b>Copyright information:</b></p><p>Taken from "Genomewide high-density SNP linkage analysis of non-BRCA1/2 breast cancer families identifies various candidate regions and has greater power than microsatellite studies"</p><p>http://www.biomedcentral.com/1471-2164/8/299</p><p>BMC Genomics 2007;8():299-299.</p><p>Published online 30 Aug 2007</p><p>PMCID:PMC2072960.</p><p></p

Genomewide high-density SNP linkage analysis of non-BRCA1/2 breast cancer families identifies various candidate regions and has greater power than microsatellite studies-0

<p><b>Copyright information:</b></p><p>Taken from "Genomewide high-density SNP linkage analysis of non-BRCA1/2 breast cancer families identifies various candidate regions and has greater power than microsatellite studies"</p><p>http://www.biomedcentral.com/1471-2164/8/299</p><p>BMC Genomics 2007;8():299-299.</p><p>Published online 30 Aug 2007</p><p>PMCID:PMC2072960.</p><p></p