胃肠道癌腹膜转移的核心病理机制

胃肠道癌腹膜转移是目前临床治疗的最大难题,解决该难题的根本之道在于临床医生准确把握胃肠道癌腹膜转移的核心细胞病理学机制,基本掌握分子病理学机制,并融会贯通地运用到每一例患者诊治的临床决策过程中,做到"防""治"并举,积极预防、主动治疗。与临床治疗决策密切相关的胃肠道癌腹膜转移的核心细胞病理学机制有4点:(1)腹腔游离癌细胞或微癌灶定植于腹膜,对腹膜间皮细胞造成不可逆病理性损害;(2)定植的癌细胞进一步侵袭腹膜特定结构乳斑,启动加速侵袭性生长过程;(3)腹膜间质纤维化过程加重腹膜的结构性破坏;(4)癌细胞与乳斑中免疫细胞的相互作用,形成促进腹膜转移癌生长的容受性免疫微环境。这4条核心细胞病理学机制互为因果,相互促进,构成腹膜转移发展的恶性循环。临床医生只要准确把握这4点,就有可能掌握临床诊治决策先机,将应对性被动治疗变为预防性主动治疗,改善胃肠道癌腹膜转移临床诊治现状。

Fundamental pathological mechanisms underlying gastro-intestinal cancer peritoneal metastasis

Gastrointestinal cancer peritoneal metastasis(GICPM)is one of the biggest challenges of clinical treatment.The ultimate solution to the problem requires the clinicians to accurately understand cytologic and molecular pathological mechanisms behind GICPM,and apply such knowledge in the clinical decision-making process for diagnosis and treatment of individual patient,so as to realize"prevention"and"treatment"proactively.The core cytopathological mechanisms behind GICPM,which are closely related to clinical treatment decisions,are as follows:(1)free cancer cells or clusters in peritoneal cavity colonize the peritoneum,resulting in irreversible pathological damage to peritoneal mesothelial cells;(2)the colonized cancer cells further invade the specific structure of the peritoneal milky spots and initiate an accelerated invasive growth process;(3)the process of peritoneal interstitial fibrosis aggravates the structural destruction of the peritoneum;(4)the interaction between cancer cells and immune cells in the milk spots forms a permissive immune microenvironment that promotes the growth of peritoneal metastatic cancer.These four core cytopathological mechanisms are mutually causal and promote each other,forming a vicious circle of GICPM development.As long as clinicians accurately understand these four points,it is possible to grasp the opportunity of clinical diagnosis and treatment,change reactive and passive treatment into preventive and proactive treatment,and improve the clinical diagnosis and treatment landscape of GICPM.