Racial disparity in metabolic regulation of cancer

Abstract

Genetic mutations and metabolic reprogramming are two key hallmarks of cancer, required for proliferation, invasion, and metastasis of the disease. While genetic mutations, whether inherited or acquired, are critical for the initiation of tumor development, metabolic reprogramming is an effector mechanism imperative for adaptational transition during the progression of cancer. Recent findings in the literature emphasize the significance of molecular cross-talk between these two cellular processes in regulating signaling and differentiation of cancer cells. Genome-wide sequencing analyses of cancer genomes have highlighted the association of various gene mutations in predicting cancer risk and survival. Oncogenic mutational frequency is heterogeneously distributed among various cancer types in different populations, resulting in varying susceptibility to cancer risk. In this review, we explore and discuss the role of genetic mutations in metabolic enzymes and metabolic oncoregulators to stratify cancer risk in people from different racial backgrounds.

Phosphoinositide 3-Kinase Signaling Pathway in Pancreatic Ductal Adenocarcinoma Progression, Pathogenesis, and Therapeutics

“…Pancreatic cancer is the third-leading cause of cancer-related morbidity in the United States, owing largely to the short-term survival rates observed for pancreatic cancer patients despite a low incidence rate (Mazure et al, 1997 ; Siegel et al, 2016 ; Attri et al, 2017 ). Pancreatic adenocarcinoma (PDAC), characterized by a strong desmoplastic stromal formation around the cancerous tissues, accounts for more than 90% of pancreatic cancer cases (Mosdell and Doberneck, 1991 ).…”

“…Pancreatic adenocarcinoma (PDAC), characterized by a strong desmoplastic stromal formation around the cancerous tissues, accounts for more than 90% of pancreatic cancer cases (Mosdell and Doberneck, 1991 ). In advanced stages of pancreatic cancer development, the primary tumor reaches the surrounding lymph nodes and then disseminates into the distal metastatic organs like liver, lung, and diaphragm (Pour et al, 1991 ; Attri et al, 2017 ). The sudden onset of pancreatic cancer combined with rapid progression of the disease accounts for the lack of robust prognostic markers and early-stage diagnostic markers (Kaur et al, 2012 ; Le et al, 2016 ).…”

Clinical metabolomics characteristics of diabetic kidney disease: A meta‐analysis of 1875 cases with diabetic kidney disease and 4503 controls

“…In all the studies included in this paper, the age distribution is 27–71 years old, and the proportion of males is 0.4%–1%, which is the reason for the great heterogeneity 34–36 . In addition, due to environmental exposure, lifestyle (food intake, exercise) and health status, there are substantial differences in metabolic patterns among different races 37,38 . The purpose of this study is to provide more comprehensive information about the correlation between metabolites and DKD.…”

“…[34][35][36] In addition, due to environmental exposure, lifestyle (food intake, exercise) and health status, there are substantial differences in metabolic patterns among different races. 37,38 The purpose of this study is to provide more comprehensive information about the correlation between metabolites and DKD. The recruited areas of the included studies are extensive, and their living habits and exposure environment are different, which have become the factors leading to the heterogeneity of meta-analysis results.…”

PTGES Expression Is Associated with Metabolic and Immune Reprogramming in Pancreatic Ductal Adenocarcinoma

“…Interestingly, our analysis identifies associations between PTGES and glycolytic metabolism and hypoxia signaling. Cancer cells activate HIF-1α signaling to manage hypoxic stress in the TME and directly regulate glycolysis [ 38 , 39 ]. Previously, PTGES was shown to be an HIF-inducible gene in esophageal cancer.…”