ABSTRACT
Rare histologic variants of esophageal cancer account for about 5% of cases. As its name suggests, polypoid spindle cell carcinoma of the esophagus (carcinosarcoma, pseudosarcoma) is comprised of both epithelial and spindle cell elements. The nomenclature reflects both the historical controversy over the lesion's cell of origin as well as its characteristic fungating intraluminal growth pattern. The authors report a case of polypoid spindle cell carcinoma of the esophagus that was preoperatively diagnosed as a visceral sarcoma.
Subject(s)
Carcinosarcoma/diagnosis , Esophageal Neoplasms/diagnosis , Aged , Biopsy , Carcinosarcoma/surgery , Diagnosis, Differential , Endoscopy, Gastrointestinal , Esophageal Neoplasms/surgery , Esophagectomy , Follow-Up Studies , Gastrectomy , Humans , Male , Tomography, X-Ray ComputedSubject(s)
Antineoplastic Agents/adverse effects , Antineoplastic Agents/therapeutic use , Carcinoma, Non-Small-Cell Lung/drug therapy , Lung Diseases, Interstitial/chemically induced , Lung Neoplasms/drug therapy , Pulmonary Fibrosis/chemically induced , Quinazolines/adverse effects , Quinazolines/therapeutic use , Cough/etiology , Dyspnea/etiology , Fatal Outcome , Gefitinib , Humans , Male , Middle AgedABSTRACT
The interferon-inducible, double-stranded RNA (dsRNA)-activated protein kinase, PKR, plays key roles in regulation of cell growth and differentiation, and has been postulated as a tumor suppressor. Downstream effectors of PKR include the translation initiation factor, eIF2alpha, and the transcription factor, NF-kappaB. We found elevated levels of PKR protein, dsRNA-dependent PKR autophosphorylation activity, and phosphorylated eIF2alpha in melanoma cells compared to nontransformed melanocytes in culture. Treatment with interferon-alpha2b further induced PKR expression and activity. Immunohistochemical analysis of primary melanomas demonstrated minimal PKR immunoreactivity, but melanoma lymph node metastases expressed a high level of PKR protein. Furthermore, analysis of colon cancer specimens revealed that transformation from normal mucosa to adenomas and carcinomas was coincident with an increase in PKR expression. These data do not support the concept of PKR as a classic tumor suppressor but instead suggest that PKR upregulation occurs at defined steps in cancer progression, probably as a cellular response to neoplasia.