Circulating Leptin and Branched Chain Amino Acids—Correlation with Intraductal Papillary Mucinous Neoplasm Dysplastic Grade

Yip-Schneider, Michele; Simpson, Rachel E.; Carr, Rosalie A.; Wu, Hsin-Jung; Fan, Hao; Liu, Ziyue; Korc, Murray; Zhang, Jianjun; Schmidt, C. Max

doi:10.1007/s11605-018-3963-y

Cited by 11 publications

(5 citation statements)

References 29 publications

(31 reference statements)

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“…Multiple amino acids have been confirmed to be valuable in the identification of potential biomarkers and understanding the pathogenesis of various malignant tumors. Among these, the study of glutamine, serine, and glycine has been a primary focus (Jung et al, 2014;Yip-Schneider et al, 2019). Amino acid uptake, steady-state levels, and catabolism are all elevated in the leukemia stem cell (LSC) population (Jones et al, 2018).…”

Section: Amino Acid Metabolism Reprogramming In Tumor Growthmentioning

confidence: 99%

Recent Metabolomics Analysis in Tumor Metabolism Reprogramming

Han

Chen

et al. 2021

Front. Mol. Biosci.

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Metabolic reprogramming has been suggested as a hallmark of cancer progression. Metabolomic analysis of various metabolic profiles represents a powerful and technically feasible method to monitor dynamic changes in tumor metabolism and response to treatment over the course of the disease. To date, numerous original studies have highlighted the application of metabolomics to various aspects of tumor metabolic reprogramming research. In this review, we summarize how metabolomics techniques can help understand the effects that changes in the metabolic profile of the tumor microenvironment on the three major metabolic pathways of tumors. Various non-invasive biofluids are available that produce accurate and useful clinical information on tumor metabolism to identify early biomarkers of tumor development. Similarly, metabolomics can predict individual metabolic differences in response to tumor drugs, assess drug efficacy, and monitor drug resistance. On this basis, we also discuss the application of stable isotope tracer technology as a method for the study of tumor metabolism, which enables the tracking of metabolite activity in the body and deep metabolic pathways. We summarize the multifaceted application of metabolomics in cancer metabolic reprogramming to reveal its important role in cancer development and treatment.

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Section: Amino Acid Metabolism Reprogramming In Tumor Growthmentioning

confidence: 99%

Recent Metabolomics Analysis in Tumor Metabolism Reprogramming

Han

Chen

et al. 2021

Front. Mol. Biosci.

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“…It was shown in patients undergoing pancreatic resection that the circulating levels of branched-chain amino acids (BCAAs) were correlated with the dysplastic grades of IPNM, a high-risk precancerous lesion. 128 A recent study indicated that BCAA uptake promotes PDAC development, while BCAA catabolism is impeded in PDAC tissue, indicating that BCAA uptake could be a promising therapeutic target for the treatment of PDAC. 129 Isoleucine, one of the BCAAs, was associated with an increased risk of PC in women with long-term obesity.…”

Section: Mechanisms Of Obesity- and Dm-related Pancreatic Carcinogenesismentioning

confidence: 99%

Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review

Ruze

Song

Yin

et al. 2023

Sig Transduct Target Ther

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Research on obesity- and diabetes mellitus (DM)-related carcinogenesis has expanded exponentially since these two diseases were recognized as important risk factors for cancers. The growing interest in this area is prominently actuated by the increasing obesity and DM prevalence, which is partially responsible for the slight but constant increase in pancreatic cancer (PC) occurrence. PC is a highly lethal malignancy characterized by its insidious symptoms, delayed diagnosis, and devastating prognosis. The intricate process of obesity and DM promoting pancreatic carcinogenesis involves their local impact on the pancreas and concurrent whole-body systemic changes that are suitable for cancer initiation. The main mechanisms involved in this process include the excessive accumulation of various nutrients and metabolites promoting carcinogenesis directly while also aggravating mutagenic and carcinogenic metabolic disorders by affecting multiple pathways. Detrimental alterations in gastrointestinal and sex hormone levels and microbiome dysfunction further compromise immunometabolic regulation and contribute to the establishment of an immunosuppressive tumor microenvironment (TME) for carcinogenesis, which can be exacerbated by several crucial pathophysiological processes and TME components, such as autophagy, endoplasmic reticulum stress, oxidative stress, epithelial-mesenchymal transition, and exosome secretion. This review provides a comprehensive and critical analysis of the immunometabolic mechanisms of obesity- and DM-related pancreatic carcinogenesis and dissects how metabolic disorders impair anticancer immunity and influence pathophysiological processes to favor cancer initiation.

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“…Leptin may also be altered in the progression of IPMN to PDAC and was found to be actually decreased in higher grades of dysplasia and invasive cancer as compared to low-grade dysplasia. Lower leptin levels were associated with cancer cachexia [ 45 ] and this likely explains the decreased levels seen in the progression of IPMN to PDAC [ 46 ].…”

Section: Metabolic Alterationsmentioning

confidence: 99%

The Role of Genetic, Metabolic, Inflammatory, and Immunologic Mediators in the Progression of Intraductal Papillary Mucinous Neoplasms to Pancreatic Adenocarcinoma

Shockley

Chen

et al. 2023

Cancers

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Intraductal papillary mucinous neoplasms (IPMN) have the potential to progress to pancreatic ductal adenocarcinoma (PDAC). As with any progression to malignancy, there are a variety of genetic and metabolic changes, as well as other disruptions to the cellular microenvironment including immune alterations and inflammation, that can contribute to tumorigenesis. Previous studies further characterized these alterations, revealing changes in lipid and glucose metabolism, and signaling pathways that mediate the progression of IPMN to PDAC. With the increased diagnosis of IPMNs and pancreatic cysts on imaging, the opportunity to attenuate risk with the removal of high-risk lesions is possible with the understanding of what factors accelerate malignant progression and how they can be clinically utilized to determine the level of dysplasia and stratify the risk of progression. Here, we reviewed the genetic, metabolic, inflammatory, and immunologic pathways regulating the progression of IPMN to PDAC.

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Circulating Leptin and Branched Chain Amino Acids—Correlation with Intraductal Papillary Mucinous Neoplasm Dysplastic Grade

Abstract: Circulating leptin in females and BCAA correlates with IPMN dysplastic grade and, if combined with clinical characteristics, have the potential to improve clinical decision-making.

Cited by 11 publications

References 29 publications

Recent Metabolomics Analysis in Tumor Metabolism Reprogramming

Recent Metabolomics Analysis in Tumor Metabolism Reprogramming

Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review

The Role of Genetic, Metabolic, Inflammatory, and Immunologic Mediators in the Progression of Intraductal Papillary Mucinous Neoplasms to Pancreatic Adenocarcinoma

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