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@ARTICLE{Bull:287441,
author = {C. J. Bull and E. Hazelwood and D. N. Legge and L. J.
Corbin and T. G. Richardson and M. Lee and J. Yarmolinsky
and K. Smith-Byrne and D. A. Hughes and M. Johansson and U.
Peters and S. I. Berndt and H. Brenner$^*$ and A.
Burnett-Hartman and I. Cheng and S.-S. Kweon and L. Le
Marchand and L. Li and P. A. Newcomb and R. Pearlman and A.
McConnachie and P. Welsh and R. Taylor and M. E. J. Lean and
N. Sattar and N. Murphy and M. J. Gunter and N. J. Timpson
and E. E. Vincent},
title = {{I}mpact of weight loss on cancer-related proteins in
serum: results from a cluster randomised controlled trial of
individuals with type 2 diabetes.},
journal = {EBioMedicine},
volume = {100},
issn = {2352-3964},
address = {Amsterdam [u.a.]},
publisher = {Elsevier},
reportid = {DKFZ-2024-00244},
pages = {104977},
year = {2024},
abstract = {Type 2 diabetes is associated with higher risk of several
cancer types. However, the biological intermediates driving
this relationship are not fully understood. As novel
interventions for treating and managing type 2 diabetes
become increasingly available, whether they also disrupt the
pathways leading to increased cancer risk is currently
unknown. We investigated the effect of a type 2 diabetes
intervention, in the form of intentional weight loss, on
circulating proteins associated with cancer risk to gain
insight into potential mechanisms linking type 2 diabetes
and adiposity with cancer development.Fasting serum samples
from participants with diabetes enrolled in the Diabetes
Remission Clinical Trial (DiRECT) receiving the
Counterweight-Plus weight-loss programme (intervention, N =
117, mean weight-loss 10 kg, $46\%$ diabetes remission) or
best-practice care by guidelines (control, N = 143, mean
weight-loss 1 kg, $4\%$ diabetes remission) were subject to
proteomic analysis using the Olink Oncology-II platform
$(48\%$ of participants were female; $52\%$ male). To
identify proteins which may be altered by the weight-loss
intervention, the difference in protein levels between
groups at baseline and 1 year was examined using linear
regression. Mendelian randomization (MR) was performed to
extend these results to evaluate cancer risk and elucidate
possible biological mechanisms linking type 2 diabetes and
cancer development. MR analyses were conducted using
independent datasets, including large cancer meta-analyses,
UK Biobank, and FinnGen, to estimate potential causal
relationships between proteins modified during intentional
weight loss and the risk of colorectal, breast, endometrial,
gallbladder, liver, and pancreatic cancers.Nine proteins
were modified by the intervention: glycoprotein Nmb; furin;
Wnt inhibitory factor 1; toll-like receptor 3; pancreatic
prohormone; erb-b2 receptor tyrosine kinase 2; hepatocyte
growth factor; endothelial cell specific molecule 1 and Ret
proto-oncogene (Holm corrected P-value <0.05). Mendelian
randomization analyses indicated a causal relationship
between predicted circulating furin and glycoprotein Nmb on
breast cancer risk (odds ratio (OR) = 0.81, $95\%$
confidence interval (CI) = 0.67-0.99, P-value = 0.03; and OR
= 0.88, $95\%$ CI = 0.78-0.99, P-value = 0.04 respectively),
though these results were not supported in sensitivity
analyses examining violations of MR assumptions.Intentional
weight loss among individuals with recently diagnosed
diabetes may modify levels of cancer-related proteins in
serum. Further evaluation of the proteins identified in this
analysis could reveal molecular pathways that mediate the
effect of adiposity and type 2 diabetes on cancer risk.The
main sources of funding for this work were Diabetes UK,
Cancer Research UK, World Cancer Research Fund, and
Wellcome.},
keywords = {Cancer (Other) / DiRECT (Other) / Diabetes (Other) /
Mendelian randomization (Other) / Obesity (Other) / Weight
loss (Other)},
cin = {C070 / C120 / HD01},
ddc = {610},
cid = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
I:(DE-He78)HD01-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:38290287},
doi = {10.1016/j.ebiom.2024.104977},
url = {https://inrepo02.dkfz.de/record/287441},
}