Overview of esophageal cancer pathology

By | March 24, 2012

Overview of esophageal pathology, esophageal mucosa in a variety of factors, long-term effect of cancer, can cause chronic inflammation of esophageal mucosa and epithelial hyperplasia, from simple hyperplasia to dysplasia and ultimately cancer, carcinoma in situ into by the invasive carcinoma. It is reported that of 46,161 cases of esophageal epithelial hyperplasia in normal and cancerous time, cancer rates show that the average time of severe proliferative cancer was 41 months, 64 months with mild hyperplasia, normal epithelium to 106 months, the cancer rate was 38.9% , 5.8%, 1.4%. Another 82 cases of esophageal epithelial severe dysplasia were found in long-term follow-up 6 years of cumulative cancer rate of 39.3%. From the pathological findings of early esophageal cancer, most patients had adjacent dysplasia of epithelial cells, cancer and non-cancerous transitional epithelium transition. Comparison of 80 cases of carcinoma in situ and 51 cases of severe atypical hyperplasia in biopsy specimens K-67 and p53 protein expression in seven and found no significant difference between the two groups, the study showed that from the perspective of the pathophysiology of severe atypical hyperplasia and in situ between the cancer is difficult to define. This shows the current pathology profession severe atypical hyperplasia and carcinoma in situ of the diagnostic criteria and treatment there are considerable differences, but accepted the point is that at least severe dysplasia should be used as pre-cancer lesions, treatment and positively close follow-up, thereby reducing the incidence of esophageal cancer to improve rates of early diagnosis and treatment.
Esophageal pathology outlined, with the incidence of esophageal adenocarcinoma increased year by year, Barrett esophagus as precancerous lesions more and more attention. Barrett esophagus has been named the first time since 1950, with the histological evolution of the development has gone through many, 1975 is defined as "directly observed a wide range of columnar metaplasia," in 2003 Chicago, American College of Gastroenterology meeting is given New definition: "abnormal endoscopic appearance of the distal esophagus epithelium, and histologically confirmed intestinal metaplasia of esophageal mucosa." Numerous clinical studies shows that in 10% -40% in esophageal cancer patients associated with Barrett esophagus, 64% of patients with esophageal adenocarcinoma associated with Barrett esophagus. According to the Tenth World Conference on Digestive Diseases information, Barrett esophagus is the probability of occurrence of esophageal cancer 30-125 times the normal esophagus.
Cytological studies have shown that atypical hyperplasia cells decreased glycogen content, and DNA in the carcinogenesis of esophageal epithelium progressively increased. Electron microscopy the cytoplasm of adjacent epithelial or stroma reduced mitochondrial swelling, the spinal disorder. By molecular biology studies, p53 protein has been shown to participate in a variety of tumors, including esophageal cancer, including the occurrence and development, p53 gene alterations in esophageal squamous cell carcinoma is an early biological changes, which is currently one of the most a tumor suppressor gene. P53 gene mutation in esophageal cancer 10% -70% in premalignant Barrett epithelium and esophageal adenocarcinoma had p53 mutations, 93% of esophageal cancer with p53 protein accumulation. Studies have found that p53 protein in normal mucosa, esophagitis, mild dysplasia, moderate and severe dysplasia, carcinoma in situ and invasive carcinoma in ascending order of 2.9%, 6.7%, 38.8%, 52.0%, 61.1 % and 62.5%, that the abnormal p53 protein expression may precede the appearance of invasive cancer.
Zhengzhou University School of Medicine Research and precancerous First Affiliated Hospital of Zhengzhou University, Department of Pathology, detected by immunohistochemistry p53 protein in normal esophageal mucosa, simple hyperplasia, atypical hyperplasia, carcinoma in situ and invasive carcinoma cases, location of these proteins in esophageal cancer in different regions in the distribution of lesions, to investigate the occurrence and development of esophageal cancer provides a theoretical basis for the mechanism. The results showed: p53 protein expression mainly in the nucleus; in all cases of normal esophageal mucosa was no positive expression of p53 protein; p53 protein was increased from normal mucosa to invasive carcinoma and no expression gradually increased to 71% when ; in simple hyperplasia and atypical hyperplasia were significantly different expression (P <0.0l). Experiments show that the p53 gene in esophageal cancer in natural history presented with progressive, high expression, and in simple hyperplasia and atypical hyperplasia in a significant difference, indicating that changes in p53 gene occur in early esophageal cancer has emerged. p53 protein expression and cell differentiation and relevance of depth of invasion, indicating that p53 gene alterations in esophageal cancer in the entire history of sustained accumulation. 31 cases of invasive cervical cancer positive cases in grade I in 7 cases (7 / 16, 44%), H grade in 20 cases (20/25, 80%), field 4 cases (4 / 4, 100%), p53 protein expression and organization histologic grade was correlated (P <0.01); invasion into the cases of Greece in the lower film 1 (25%) positive to the muscular layer in 16 cases (67%) positive to the outer membrane of 14 patients (88 %) positive, p53 protein expression also correlated with depth of invasion (P <0.08), lymph node metastasis but no correlation.
Overview of esophageal pathology, in recent years have more people find the origin of esophageal cancer (esophageal cancer multi-center hypothesis.) Guo Chunrong of 669 cases of esophageal cancer patients and other (male 573 cases, female 96 cases, male to female ratio was 5.97:1, age 32–88 years of age, clinical symptoms of progressive dysphagia to the main course for 2 weeks to 10 months are not etc., have different degrees of endoscopic esophageal stricture) in endoscopic pathological analysis. Endoscopic results: 669 cases in 13 patients detected multiple sources 0.94%), a total of 27 foci, 12 cases of dual-source cancer, and 1 carcinoma of the three sources; esophageal cancer, four cases of multi-source, multi-source esophagus of a cardiac 4 cases of cancer, esophageal cancer, a stomach, 3 cases of multi-source, multi-source carcinoma of the esophagus of a throat in 2 cases. Multi-source cancer in the microscope as follows: the tumor exist in isolation, between the mucosal lesions smooth, intact, continuous with no lesions. For many cancers of the esophagus often occur because of lack of knowledge of it, only to meet the lesions occurred in a missed diagnosis, or tumor caused by living on the endoscope can not narrow the lead agent or through the poor, resulting in missed diagnosis, the tumor residence . Xiao Yang reported 5 cases before 1988, more than all cancers of preoperative misdiagnosis, since 1989 more than 8 cases of all cancers of the preoperative diagnosis. Clinically, patients with esophageal cancer should be suspected of endoscopic and X-ray bar meal and then come to cross-reference photos diagnosed during endoscopy should be possible through the tumor stenosis, check the following esophagus cancer, cardia and stomach duodenal whether the presence of intestinal lesions suspicious. With the emphasis on multi-source cancer and endoscopic equipment, improvements, multi-source in recent years gradually increased the detection rate of cancer.

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