Haynes Talaijha, Oprea-Ilies Gabriela, Manne Upender, Singh Rajesh, Singh Shailesh, Mir Hina
Department of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine, Atlanta, GA, USA; Cancer Health Equity Institute, Morehouse School of Medicine, Atlanta, GA, USA.
Department of Pathology & Laboratory Medicine, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, USA.
Transl Oncol. 2022 Feb;16:101330. doi: 10.1016/j.tranon.2021.101330. Epub 2022 Jan 3.
Colorectal cancer (CRC) is the third leading cause of cancer-related deaths in the United States. Despite increased screening options and state-of-art treatments offered in clinics, racial differences remain in CRC. African Americans (AAs) are disproportionately affected by the disease; the incidence and mortality are higher in AAs than Caucasian Americans (CAs). At the time of diagnosis, AAs more often present with advanced stages and aggressive CRCs, primarily accounting for the racial differences in therapeutic outcomes and mortality. The early incidence of CRC in AAs could be attributed to race-specific gene polymorphisms and lifestyle choices associated with socioeconomic status (SES). Altered melatonin-serotonin signaling, besides the established CRC risk factors (age, diet, obesity, alcoholism, and tobacco use), steered by SES, glucocorticoid, and Vitamin D status in AAs could also account for the early incidence in this racial group. This review focuses on how the lifestyle factors, diet, allelic variants, and altered expression of specific genes could lead to atypical serotonin and melatonin signaling by modulating the synthesis, secretion, and signaling of these pineal hormones in AAs and predisposing them to develop more aggressive CRC earlier than CAs. Crosstalk between gut microbiota and pineal hormones and its impact on CRC pathobiology is addressed from a race-specific perspective. Lastly, the status of melatonin-focused CRC treatments, the need to better understand the perturbed melatonin signaling, and the potential of pineal hormone-directed therapeutic interventions to reduce CRC-associated disparity are discussed.
结直肠癌(CRC)是美国癌症相关死亡的第三大主要原因。尽管临床上提供了更多的筛查选择和先进的治疗方法,但CRC中的种族差异仍然存在。非裔美国人(AAs)受该疾病的影响尤为严重;非裔美国人的发病率和死亡率高于美国白人(CAs)。在诊断时,非裔美国人更常表现为晚期和侵袭性CRC,这主要是治疗结果和死亡率存在种族差异的原因。非裔美国人中CRC的早期发病率可能归因于种族特异性基因多态性以及与社会经济地位(SES)相关的生活方式选择。除了已确定的CRC风险因素(年龄、饮食、肥胖、酗酒和吸烟)外,由SES、糖皮质激素和维生素D状态所驱动的褪黑素 - 血清素信号改变,也可能是该种族群体早期发病的原因。本综述重点关注生活方式因素、饮食、等位基因变体以及特定基因表达的改变如何通过调节这些松果体激素在非裔美国人中的合成、分泌和信号传导,导致非典型的血清素和褪黑素信号,使他们比白人更容易更早地发展出更具侵袭性的CRC。从种族特异性角度探讨了肠道微生物群与松果体激素之间的相互作用及其对CRC病理生物学的影响。最后,讨论了以褪黑素为重点的CRC治疗现状、更好地理解受干扰的褪黑素信号的必要性,以及松果体激素导向的治疗干预措施减少CRC相关差异的潜力。