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Sökning: WFRF:(Löfgren Burström Anna) > (2015-2019) > Metabolic factors a...

  • Myte, RobinUmeå universitet,Onkologi,Umea Univ, Dept Radiat Sci, Oncol, SE-90187 Umea, Sweden (författare)

Metabolic factors and the risk of colorectal cancer by KRAS and BRAF mutation status

  • Artikel/kapitelEngelska2019

Förlag, utgivningsår, omfång ...

  • 2019-01-24
  • John Wiley & Sons,2019
  • electronicrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:umu-158782
  • https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-158782URI
  • https://doi.org/10.1002/ijc.32104DOI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-385954URI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Originally included in thesis in manuscript form with title [Metabolic factors and colorectal cancer risk by KRAS and BRAF mutation status]
  • Factors related to energy metabolism and the metabolic syndrome, such as higher body mass index (BMI), blood glucose, or blood lipids, and blood pressure, are associated with an increased risk of colorectal cancer (CRC). However, CRC is a heterogeneous disease, developing through distinct pathways with differences in molecular characteristics and prognosis, and possibly also in risk factors. For subtypes defined by KRAS and BRAF mutation status, BMI is the only metabolic factor previously studied, with inconsistent findings. We investigated whether associations between BMI, blood glucose, blood lipids, and blood pressure and CRC risk differed by tumor KRAS and BRAF mutation status in 117,687 participants from two population-based cohorts within the Northern Sweden Health and Disease Study (NSHDS). Hazard ratios (HRs) for overall CRC and CRC subtypes by metabolic factors were estimated with Cox proportional hazards regression, using multiple imputation to handle missing exposure and tumor data. During a median follow-up of 15.6 years, we acquired 1,250 prospective CRC cases, of which 766 cases had complete baseline and molecular tumor data. Consistent with previous evidence, higher BMI, total cholesterol, triglyceride levels, and blood pressure were associated with an increased risk of overall CRC (HRs per 1 standard deviation increase: 1.07 to 1.12). These associations were similar regardless of CRC subtype by KRAS and BRAF mutation status (all pheterogeneity > 0.05). The same was true for subtypes based on microsatellite instability status. Poor metabolic health may therefore be a universal mechanism for colorectal cancer, acting across multiple developmental pathways.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Gylling, Björn,1978-Umeå universitet,Patologi,Umea Univ, Dept Med Biosci, Pathol, Umea, Sweden(Swepub:umu)bjgy0001 (författare)
  • Häggström, Jenny,1980-Umeå universitet,Statistik,Umea Univ, Umea Sch Business & Econ, Dept Stat, Umea, Sweden(Swepub:umu)jeyhom02 (författare)
  • Häggström, ChristelUppsala universitet,Umeå universitet,Enheten för biobanksforskning,Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.,Endokrinkirurgi,Umea Univ, Dept Biobank Res, Umea, Sweden(Swepub:uu)chrha650 (författare)
  • Zingmark, Carl,1975-Umeå universitet,Patologi,Umea Univ, Dept Med Biosci, Pathol, Umea, Sweden(Swepub:umu)cazi0001 (författare)
  • Löfgren Burström, AnnaUmeå universitet,Patologi,Umea Univ, Dept Med Biosci, Pathol, Umea, Sweden(Swepub:umu)anlo0002 (författare)
  • Palmqvist, RichardUmeå universitet,Patologi,Umea Univ, Dept Med Biosci, Pathol, Umea, Sweden(Swepub:umu)ripa0001 (författare)
  • van Guelpen, BethanyUmeå universitet,Onkologi,Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM),Umea Univ, Dept Radiat Sci, Oncol, SE-90187 Umea, Sweden;Umea Univ, Wallenberg Ctr Mol Med, Umea, Sweden(Swepub:umu)beyvan99 (författare)
  • Umeå universitetOnkologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:International Journal of Cancer: John Wiley & Sons145:2, s. 327-3370020-71361097-0215

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