Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cutaneous metastases from internal malignancies are uncommon. Umbilical metastasis, also known as Sister Joseph nodule (SJN), develops in patients with carcinomatous peritonitis or superficial lymphadenopathy, while non-SJN skin metastases develop after surgery, injury, and lymphadenopathy. In this review, the possible mechanisms of skin metastases are discussed. SJNs develop by the contiguous or lymphatic spread of tumor cells. After surgery and injury, tumor cells spread by direct implantation or hematogenous metastasis, and after lymphadenopathy, they spread by extranodal extension. The inflammatory response occurring during wound healing is exploited by tumor cells and facilitates tumor growth. Macrophages are crucial drivers of tumor-promoting inflammation, which is a source of survival, growth and angiogenic factors. Angiogenesis is promoted by the vascular endothelial growth factor (VEGF), which also mediates tumor-associated immunodeficiency. In the subcutaneous tissues that surround metastatic lymph nodes, adipocytes promote tumor growth. In the elderly, age-associated immunosuppression may facilitate hematogenous metastasis. Anti-VEGF therapy affects recurrence patterns but at the same time, may increase the risk of skin metastases. Immune suppression associated with inflammation may play a key role in skin metastasis development. Thus, immune therapies, including immune checkpoint inhibitors reactivating cytotoxic T-cell function and inhibiting tumor-associated macrophage function, appear promising.
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PMID:Cutaneous Metastasis after Surgery, Injury, Lymphadenopathy, and Peritonitis: Possible Mechanisms. 3127 6

Ocular surface squamous neoplasia (OSSN) is a malignant or dysplastic lesion that has its origins in the epithelial cells at the ocular surface. The structures from which these lesions can arise are the conjunctiva, the limbus, and the cornea. Our study was conducted on a group of seven patients with ocular surface squamous cell carcinoma (SCC). Histopathologically diagnosed SCCs were then assessed as well, moderately and poorly differentiated, depending on which area of differentiation dominated in Hematoxylin-Eosin staining. For the immunohistochemical analysis, the following antibodies (markers) were used: Ki67, p53 and B-cell lymphoma 2 (Bcl-2), E-cadherin, and vascular endothelial growth factor (VEGF). Our study group was composed of seven cases of SCCs of the ocular surface. Three were below in T1 American Joint Committee on Cancer (AJCC) stage, two cases were in T2 AJCC stage, and two cases were in T3 AJCC stage. None of our cases were T4, N1 or M1 AJCC tumors. Four of the cases were histopathologically moderately differentiated SCCs of the ocular surface and three were poorly differentiated SCCs. None of the seven patients present human immunodeficiency virus (HIV) infection. P53 immunostaining was strongly present in our study. Bcl-2 overexpression is not a fact that our study highlights. The expression of Ki67 proliferation marker was low in our study. Our study on ocular surface SCC reveals negative assessment of VEGF immunostaining. E-cadherin expression in our study was positive. Ocular surface SCCs are slow growing tumors, with very low metastasis potential, when HIV-infection is not present.
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PMID:Behavior pattern of early-stage ocular surface squamous cell carcinoma in non-HIV patients. 3165 18


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