Pancreatic tumor metastasis from colorectal cancer is very rare. This study evaluated the significance of an endoscopic ultrasound-guided fine-needle aspiration biopsy (EUS-FNAB) and surgical treatment. Case 1 was a 67-year-old male with a history of rectal cancer (6 years ago) and lung metastases (5 years ago) who had two masses in the pancreatic head and body. Case 2 was a 58-year-old male with the history of rectal cancer and simultaneous lung metastasis (7 years ago) who had a mass in the pancreatic body. Imaging studies showed stenosis of the pancreatic duct with distal dilatation in both cases, mimicking primary pancreatic cancer. An EUS-FNAB with immunohistochemical staining made a definitive diagnosis of pancreatic metastasis from rectal cancer. Both patients received margin-negative limited resection, middle-segment-preserving pancreatectomy and distal pancreatectomy, respectively, and were alive 16 and 6 months after pancreatectomy, respectively. An EUS-FNAB is helpful to make a definitive diagnosis of pancreatic metastasis and in determining the subsequent therapeutic approach.

Gastric carcinoma is thought to develop via the actions of inducers and promoters of carcinogenesis. Tryptophan in charred fish or animal meat, ultraviolet rays, and irradiation, which damage genes of normal cells, have long been regarded as inducers of carcinoma, and agents such as alcohol, tobacco, aflatoxin, and nitrosoamine as promoters, with tobacco having both activities. The interaction between these environmental factors, principally diet, and Helicobacter pylori (Hp) is important in the genesis of gastric carcinoma. In this report, the histopathological feature of the Hp gastritis-carcinoma sequence is outlined, and the pathological characteristics of gastroesophageal reflux disease (GERD) and endoscopically negative reflux disease (ENRD) and the risk factors for lower esophageal carcinoma after Hp eradicated status in particular are discussed regarding aspects of cell cycle-associated factors. We conclude that (1) Infection with Hp increases the risk of gastric cancer in two histological phenotypes (i.e., diffuse undifferentiated type and intestinal differentiated type). Excessive cell replication and interrupting the mucus secretion mechanism may result in a large proportion of cells with genetic abnormalities. (2) Genetic alterations in gastric carcinogenesis may differ from those in colonic carcinogenesis. (3) The degree of GERD in Japanese patients is milder than that in patients from Western countries, although the incidence of GERD increases the status after successful eradication of Hp. It is also possible that accumulation of genetic abnormalities increases the number of cardiac and lower esophageal cancers. Investigation of cell cycle factors in GERD including ENRD can be expected to reveal the risk of carcinogenesis.

No abstract

No abstract

No abstract