Epithelial-mesenchymal cell interactions and participation of the neuroendocrine markers in tumor development. Immunohistochemical study.
Existence of the organ stem cell population seems to decide on ability of the tissue to regenerate and, likewise, on carcinogenesis. The source of the organ specific stem cells may be perivascular mesenchyma of thin-walled vascular channels. Our previous study on the breast cancer indicates that the perivascular mesenchyma of thin-walled vessels appears to be source of myoid cells (myofibroblasts) from which cancer cells arise. Similar results have been observed in the cancers of lung, salivary gland and colon, investigated in the current study. The perivascular cells of thin-walled channels are the source of myoid cells with expression of synaptophysin (Syn) and/or chromogranin A (Chg A), and from these cells neoplastic cells could originate. Syn and/or Chg A positive neoplastic cells were particularly well visible in connection with the vascular channels on the peripheries of tumors while other parts of tumors were only weak positive or negative for those neuroendocrine markers. Similarly as in breast cancers, the S100-protein positive dendritic cells with various of distribution were seen, expressing intimate connection with neoplastic cells. The epithelial pearls especially abundant in non-small cell lung carcinomas demonstrated immunohistochemical analogy to Hassall's bodies: they had monocytogenic cell inside and they displayed thymosin alpha 1 (TA1), as well as mucin secretion and minute calcification. Some epithelial cells expressed desmin and Syn. All types of investigated cancers demonstrated TA1. Results of our present study suggest that the perivascular cells have a differentiation defect. Such defect may initiate abnormal stromal environment, commonly observed in neogenesis, however, the presence of thymic growth factors may favor tumor growth.
Department of Immunopathology, University Medical School, Gdańsk, Poland.
A
A
Zółtowska
J
J
Stepiński
J
J
Kuczkowski
M
M
Kamiński
B
B
Cynowska
W
W
Kruszewski
D000199:Actins / Q000378:metabolism; D014408:Biomarkers, Tumor / Q000378:metabolism*; D002450:Cell Communication / Q000502:physiology*; D053379:Chromogranin A; D002864:Chromogranins / Q000378:metabolism; D003110:Colonic Neoplasms / Q000378:metabolism / Q000473:pathology; D004847:Epithelial Cells / Q000166:cytology; D006801:Humans; D007150:Immunohistochemistry; D008175:Lung Neoplasms / Q000378:metabolism / Q000473:pathology; D008648:Mesoderm / Q000166:cytology; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology*; D009418:S100 Proteins / Q000378:metabolism; D012468:Salivary Gland Neoplasms / Q000378:metabolism / Q000473:pathology; D017154:Stromal Cells / Q000166:cytology; D016708:Synaptophysin / Q000378:metabolism
D000199:Actins; D014408:Biomarkers, Tumor; D053379:Chromogranin A; D002864:Chromogranins; D009418:S100 Proteins; D016708:Synaptophysin