Esophagus Tumors

Swallowing. If it is sufficiently irritant or caustic, a swallowed material may cause local effects on the mouth, pharynx, esophagus, and stomach. Additionally, carcinogenic materials may induce tumor formation in the alimentary tract. Also, the gastrointestinal tract is an important route by which toxic materials are absorbed. The sites of absorption and factors regulating absorption have been reviewed (42,43). 

AIDS (acquired immunodeficiency syndrome) is the final stage of disease caused by infection with HIV. In this stage, the vims infection has severely affected the immune system, causing a depletion of CD4+ T-helper cells. AIDS is characterized by the manifestation of typical diseases caused by opportunistic infections (Pneumocystis carinii pneumonia, CMV retinitis, candidiasis of the esophagus, cerebral toxoplasmosis), neurological manifestations, cachexia, or certain tumors (Kaposi sarcoma of the skin, B-cell lymphoma). 

NHEX is a potent carcinogen which induces tumors of the liver and esophagus in rats, and tumors of the trachea in Syrian golden hamsters (50, 51). It has not been detected in the environment. ... 

It appears that considerable metabolism of nitrosamines takes place in the liver, from the finding that most of them are activated by rat liver microsomes to bacterial mutagens. However, relatively few nitrosamines induce liver tumors in rats. The most common target is the esophagus and a wide variety of nitrosamines induce tumors in this organ of rats, some only tumors of the esophagus, others tumors of other organs also. 

Croton f lavens. Analysis of the leaf extract shows the presence of diterpene di- and triesters that are structurally related to TPA (49). The diesters exhibit strong tumor promoting activity in dorsal mouse skin. Each cup of tea contains more tumor promoter than is required to maintain chronic irritation of the human esophagus, a necessary requirement for the promotion of esophageal cancer. 

Tumors of the lower thoracic esophagus Mia Metastasis in celiac lymph nodes Mlb Other distant metastasis Tumors of the midthoracic esophagus Mia Not applicable... 

Type I tumor Adenocarcinoma of the distal esophagus, which usually arises from an area with specialized intestinal metaplasia of the esophagus (i.e., Barrett s esophagus) and which may infiltrate the esophagogastric junction from above. 

Type III tumor Subcardial gastric carcinoma, which infiltrates the esophagogastric junction and distal esophagus from below. 

Fig. 2. Example of FDG-PET/CT studies (fused images) in a patient with adenocarcinomas of the esophagus and metabolic non-response. High focal initial FDG uptake in the tumor (A) which is almost unchanged 14 days (B) after initiation of chemotherapy. (See Colour Plate Section at the end of this book.)...

FU remains the most widely used agent in the treatment of colorectal cancer, both as adjuvant therapy and for advanced disease. It also has activity against a wide variety of solid tumors, including cancers of the breast, stomach, pancreas, esophagus, liver, head and neck, and anus. Major toxicities include myelosuppression, gastrointestinal toxicity in the form of mucositis and diarrhea, skin toxicity manifested by the hand-foot syndrome, and neurotoxicity. 

Oldenlandia diffusa L. Bai Hua Shi Shi Cao (aerial part) Asperuloside, palderoside, desacetylasperuloside, beta-sitosterol, stigmasterol, ursolic acid, oldenlandoside.33 Treats mahgnant tumors, hepatomas, hepatomegaly, cancer of the cervix, esophagus, stimulates reticuloendothelial system. 

Hao D, Ritter MA, Oliver T, Browman GP. Platinum-based concurrent hemoradiotherapy for tumors of the head and neck and the esophagus. Semin Radiat Oncol. 2006 16 10-19. 

Cancer of the esophagus is not amenable to satisfactory surgical or chemical intervention and must therefore be addressed by searching for preventative measures. This type of neoplasm provides a unique epidemiologic model for the study of cancer causation and offers a means to learn more about initiation and promotion of this unique tumor. 

Table III lists results of carcinogenicity studies associated with zinc deficiency. These rats were given 17 doses of MBN, beginning at seven weeks of age. Fifty eight days after the first dose of MBN, all zinc-deficient rats had developed tumors of the esophagus, 83% of which were invasive carcinomas. Five weeks later, all deficient rats had tumors, 33% of which were invasive, clearly, a marked enhancement of carcinogenesis by zinc deficiency.

Additional studies have further supported a role for zinc in the etiology of cancer of the esophagus (24,25). In the presence of a zinc deficit, the precursors of methylbenzylnitrosamine (MBN) more readily induced both esophageal and forestomach tumors in rats, compared to zinc-supplemented control rats. Table VII illustrates these effects. 

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