It is likely that the obesity epidemic explains, at least in part, the increasing incidence of esophageal adenocarcinoma observed in Western countries over the past few decades (13). Moreover, the male predominance of this tumor might be partly explained by its strong association with body fat distribution typical to men. It is becoming increasingly apparent that insulin resistance, disturbed adipokine homeostasis secondary to central adiposity,
and sex hormones all lead to activation of carcinogenic molecular pathways and may explain the gender Inhibitors,research,lifescience,medical and ethnic differences seen in this cancer. There are still uncertainties regarding the role of obesity in the increased incidence of esophageal adenocarcinoma. Much research remains to be carried out XAV 939 before the mechanisms that explain the strong link between obesity and esophageal adenocarcinoma are fully understood. The interactions between
obesity and other environmental exposures including tobacco smoking, Inhibitors,research,lifescience,medical infection with Helicobacter pylori and dietary factors also deserve attention (9). Dietary and lifestyle modiﬁcation aimed at avoidance of central obesity will likely provide the Inhibitors,research,lifescience,medical most beneﬁt in the prevention of esophageal and other cancers. Acknowledgements We appreciate Dr. Qi Cao and Dr. Jun Wang for the critical reading. The work was supported by National Natural Science Foundation of China (Grant No. 81172244). Inhibitors,research,lifescience,medical Disclosure: The authors declare no conflict of interest.
Stromal tumors arising from the GI tract were initially classified as smooth muscle neoplasms including leiomyomas (5), leiomyoblastomas or sarcomas (6), following description by Stout and colleagues in 1940 (7). These descriptions were widely used until the 1970s when electron microscope found little evidence of the smooth muscle origin of these tumors (8,9). With the Inhibitors,research,lifescience,medical advent of immunohistochemistry during the 1980’s it was soon appreciated that a large number of these tumors did not have immunophenotypic features of smooth muscle, and conversely, expressed antigens related to neural crest cells (10). The term of “stromal
tumors” was first described as a separate entity by Mazur and Clark (11) in 1983 and Schaldenbrand and Appleman however in 1984 (12). However, this term was not widely accepted. In 1989, a distinctive subset of these stromal tumors revealing autonomic neural features was recognized and named “plexosarcoma” (13) and subsequently as gastrointestinal autonomic nerve tumor (GANT) (14). There was considerable confusion regarding the origin, differentiation and even clinical behavior of these tumors. In 1994, it was discovered that a significant proportion of GANTs were immunopositive for CD34 (15,16), which was the first relatively specific marker of GISTs during the mid-1990s. Based on the CD34 immunopositivity the possibility that GIST might be related to the interstitial cells of Cajal was raised by investigators (17).