[Experiences with plastic surgery in the therapy of skin neoplasms].
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14 very extensive skin cancer (T4) were treated with twice daily X-ray therapy (5 days per week, total dose 6,000 to 8,000 rads). 13 successful results were seen with follow-up for more than 14 months.
Recently, cornifin-alpha/SPPR1 has been identified as a putative precursor protein of the cornified cell envelope. In this study, the expression and localization of cornifin-alpha/SPPR1 was examined in untreated and tumor promoter-treated mouse skin, hair follicles, and skin neoplasms. Western analysis with antiserum (SQ37A) to a rabbit cornifin-alpha peptide or antiserum (SQ37C) to a human SPRR1 peptide demonstrated a 31-kDa immunoreactive protein in mouse epidermis and Northern analysis revealed the presence of a 1-kb mRNA. Immunohistochemical staining of mouse skin with SQ37A or SQ37C revealed intense and specific staining of the infundibulum, isthmus, and of Henle's layer of the inner root sheath of the lower anagen hair follicle and weak staining of the telogen follicle and the suprabasal layers of the epidermis. Treatment of mouse skin with 12-0-tetradecanoyl-phorbol-13-acetate (TPA) produced a large increase in cornifin-alpha/SPRR1 protein and mRNA. Immunohistochemical localization of cornifin-alpha/SPRR1 in TPA-treated skin indicated that cornifin-alpha/SPRR1 was increased in the suprabasal epidermis but not in the follicle. sn-1,2,-didecanoylglycerol, a model lipid second messenger, produced an increase in cornifin-alpha/SPRR1 protein similar to that of TPA, while mirex, a non-phorbol ester-type promoter had no effect. Topical doses of retinoic acid did not repress TPA-induced cornifin-alpha/SPRR1 expression. Papillomas demonstrated a 10- and 100-fold increase in cornifin-alpha/SPRR1 protein and mRNA, and expression was restricted to suprabasal cells. Squamous cell carcinomas exhibited an intermediate level of cornifin-alpha protein, and expression was restricted to keratinized areas. These data indicate: i) cornifin-alpha/SPRR1 is expressed in mouse skin; ii) cornifin-alpha/SPRR1 is localized to specific areas of the anagen hair follicle with weak staining in the telogen follicle and epidermis; iii) epidermal cornifin-alpha/SPRR1 expression is induced by phorbol ester and sn-1,2-didecanoylglycerol but not mirex, and iv) papillomas and squamous cell carcinomas demonstrate a constitutive increase in cornifin-alpha/SPRR1 in differentiated areas of the neoplasms.
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The present paper considers some of the problems linked to the surgical treatment of parotid metastases. The authors base these considerations on their limited personal cases and on the most accredited literature. In the presence of cutaneous malignancies of the upper portion of the face, accurate clinical-radiological evaluation must be made of the parotid and neck region. Elective parotidectomy is performed when the cutaneous carcinoma is quite extensive or located in proximity of the gland or when the case involves a melanoma. Depending on the oncological margins, a sub-total parotidectomy may be enough; however, the facial nerve must be sacrificed if there is a clinical deficit or if it is directly affected by the tumor. As the dimensions of the neoplasm increase, the feasibility of saving the nerve decreases. Prophylactic treatment of the neck is advisable in parotid metastases from cutaneous malignancies, particularly melanoma. Nevertheless, it is possible to perform a selective dissection, avoiding the V level of the neck as the incidence of its involvement is quite low. Prognosis for these tumors is extremely poor. Of the eleven patients surgically treated, only 4 (36%) survived: 2 passed away from other causes not involved in the base pathology; 2 for distant metastases but with no signs of local recurrence and 1 other for recurrence of the primary pathology in the maxillary sinus mucosa. There is no difference in the survival of the two main histological groups: 2 out of 3 of the patients with melanoma (67%) died as did 3 out of 5 (60%) of those with epidermal carcinoma. This does not, obviously, include the two patients who died from other causes.
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Neoplasms of preputial gland and skin were obtained from Fischer 344 male rats on lifetime drinking water studies of the benzidine congener 3,3'-dimethoxybenzidine, C.I. Direct Blue 15 or C.I. Acid Red 114, bisazobiphenyl dyes derived from 3,3'-dimethoxybenzidine and 3,3'-dimethylbenzidine. Portions of these well differentiated neoplasms were implanted into the left mammary fat pad of Fischer 344 male recipients. The rate of growth, presence of local invasion and distant metastases, and morphologic features were observed following 4 serial transplantations. All implants appeared early, grew rapidly, and were histomorphologically similar to the original neoplasms. Metastases from transplants were observed with both preputial gland and skin tumor lines in serial passages. The transplantation results confirm the malignant nature of these neoplasms.
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