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Metabolic profiles are principally different between cancers of the liver, pancreas and breast.

ABSTRACT: Molecular profiling of primary tumors may facilitate the classification of patients with cancer into more homogenous biological groups to aid clinical management. Metabolomic profiling has been shown to be a powerful tool in characterizing the biological mechanisms underlying a disease but has not been evaluated for its ability to classify cancers by their tissue of origin. Thus, we assessed metabolomic profiling as a novel tool for multiclass cancer characterization. Global metabolic profiling was employed to identify metabolites in paired tumor and non-tumor liver (n=60), breast (n=130) and pancreatic (n=76) tissue specimens. Unsupervised principal component analysis showed that metabolites are principally unique to each tissue and cancer type. Such a difference can also be observed even among early stage cancers, suggesting a significant and unique alteration of global metabolic pathways associated with each cancer type. Our global high-throughput metabolomic profiling study shows that specific biochemical alterations distinguish liver, pancreatic and breast cancer and could be applied as cancer classification tools to differentiate tumors based on tissue of origin.

SUBMITTER: Budhu A

PROVIDER: S-EPMC4159687 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Metabolic profiles are principally different between cancers of the liver, pancreas and breast.

Budhu Anuradha A Terunuma Atsushi A Zhang Geng G Hussain S Perwez SP Ambs Stefan S Wang Xin Wei XW

International journal of biological sciences 20140830 9

Molecular profiling of primary tumors may facilitate the classification of patients with cancer into more homogenous biological groups to aid clinical management. Metabolomic profiling has been shown to be a powerful tool in characterizing the biological mechanisms underlying a disease but has not been evaluated for its ability to classify cancers by their tissue of origin. Thus, we assessed metabolomic profiling as a novel tool for multiclass cancer characterization. Global metabolic profiling ...[more]

PMID: 25210494

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Project description:IntroductionAberrant DNA methylation has been found frequently in human breast cancers, associated with the loss of expression of a number of regulatory genes for growth and correlated to clinical outcomes. The present study was undertaken to determine whether methylation of a set of growth-suppressor genes would correlate to the expression of estrogen receptors (ERs) and progesterone receptors (PRs).MethodsWe used a pyrosequencing methylation analysis to study the methylation of 12 known growth-suppressor genes in 90 pairs of malignant/normal breast tissues. We also examined the expression of ERs and PRs in those specimens by immunohistochemistry. Mutations of p53 in tumor cells were detected by direct sequencing.ResultsTwelve tumor-suppressor genes: ARHI, RASSF1A, HIN-1, RARbeta2, hMLH1, 14-3-3 sigma, RIZ1, p16, E-cadherin, RIL, CDH13, and NKD2 were selected for this methylation study. Five of them (RIL, HIN-1, RASSF1A, CDH13, and RARbeta2) were frequently methylated in breast cancers (57%, 49%, 58%, 44%, and 17%, respectively) but not the normal breast (0-4%). Two panels of methylation profiles were defined. The methylation of the HIN-1/RASSFIA panel strongly correlated to the expression of ERs, PRs, and hormone receptors (HRs; which were defined as 'positive' if ERs and/or PRs were positive; p < 0.001). Conversely, the methylation of the RIL/CDH13 panel strongly correlated to negative ER, PR, and HR expression (p = 0.001, 0.025, and 0.001, respectively). The subset of triple-negative breast cancers (in other words, those with negative ER, PR, and HER-2/neu status) was positively associated with the methylation of the RIL/CDH13 panel and negatively associated with the HIN-1/RASSF1A panel. Mutations of p53 were found in nine breast tumors (11%), seven of which lacked methylation in both panels.ConclusionWe have defined two panels (HIN-1/RASSFIA, and RIL/CDH13) of methylation profiles, which correlated, either positively or negatively, to HR status.

Project description:BackgroundTo evaluate the associations between a new definition of metabolic dysfunction-associated fatty liver disease (MAFLD) and extrahepatic cancers and compare with nonalcoholic fatty liver disease (NAFLD).MethodsWe enrolled 151,391 Chinese participants in the Kailuan cohort. Hepatic steatosis was detected by abdominal ultrasound. Fine and Gray competing risk regression models were used to estimate hazard ratios (HRs) and 95% confidence interval (CI) between MAFLD and extrahepatic cancers.ResultsMAFLD was associated with increased risk of prostate (HR =1.49, 95% CI: 1.07-2.08) and obesity-related cancers, including thyroid (HR =1.47, 95% CI: 1.01-2.12), kidney (HR =1.54, 95% CI: 1.18-2.00), colorectal (HR =1.15, 95% CI: 0.98-1.34) and breast cancer (HR =1.31, 95% CI: 1.04-1.66). The results were consistent in NAFLD vs. non-NAFLD and MAFLD-NAFLD vs. neither FLD. Compared with the neither FLD group, the NAFLD-only group had a higher risk of extrahepatic cancers (HR =1.57, 95% CI: 1.18-2.09), esophageal (HR =5.11, 95% CI: 2.25-11.62), and bladder cancer (HR =3.36, 95% CI: 1.23-9.17). The additional risk of extrahepatic cancers (HR =1.42, 95% CI: 1.17-1.73), esophageal (HR =4.37, 95% CI: 2.55-7.49), and breast cancer (HR =1.99, 95% CI: 1.01-3.92) was observed in MAFLD with metabolic dysregulation, and kidney (HR =1.83, 95% CI: 1.38-2.43), prostate (HR =1.46, 95% CI: 1.00-2.14) and breast cancer (HR =1.33, 95% CI: 1.02-1.74) was observed in MAFLD with overweight and metabolic dysregulation, as well as colorectal (HR =1.45, 95% CI: 1.07-1.96) and prostate cancer (HR =2.44, 95% CI: 1.42-4.21) in MAFLD with three risk factors. Additionally, MAFLD with excessive alcohol consumption would increase extrahepatic cancers (HR =1.14, 95% CI: 1.01-1.29) and breast cancer (HR =7.27, 95% CI: 2.33-22.69) risk.ConclusionsMAFLD and NAFLD shared similar excessive risks of obesity-related cancers, suggesting a driving role of FLD in these cancers. Metabolic dysregulation beyond obesity may play additional kidney, colorectal, and prostate cancer risks in MAFLD patients. It may be helpful in the clinic to relieve symptoms by treating metabolic disorders and preventing adverse outcomes of extrahepatic cancers.

Dataset Information

Metabolic profiles are principally different between cancers of the liver, pancreas and breast.

Publications

Metabolic profiles are principally different between cancers of the liver, pancreas and breast.

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