Local skin tumors

For subcutaneous injections a large skin surface area is available for daily applications. It is recommended to change the site of injections continuously because repeated injection to the same site can cause fibrotic reactions and, in case of treatments for a period of 1 year and longer, induce subcutaneous tumors especially in small rodents. The risk of inducing local skin tumors is high if the pH value of the administration solution is below 5. 

Chrysene produced skin tumors after skin application to mice and has been shown to be active as a tumor initiator. Local tumors were observed after its subcutaneous injection in mice. Perinatal administration of chrysene to male mice by intraperitoneal injection increased the incidence of liver tumors, malignant lymphoma, and lung tumors. ... 

The International Agency for Research on Cancer (lARC) (1974, 1979, 1982, 1987) reported that there is sufficient evidence of carcinogenicity of BCME. When BCME is administered through subcutaneous route to mice of both sexes, it induced pulmonary tumors, papillomas, and firbrosarcomas local sarcomas in female mice and fibromas and fibrosarcomas in female rats. BCME is also an initiator of skin tumors in mice. It produced low incidence of tumors of respiratory tract in rats and hamsters after exposure by inhalation. When administered by inhalation, BCME induced lung tumors in mice and squamous cell carcinoma of the lung and est-hesioneuroepitheliomas of the nasal cavity in rats. When applied topically, BCME induced papillomas, most of which developed into squamous cell carcinoma in female mice. 

Phorbol esters were first detected in oil prepared from seeds of Croton tiglium, and are the most widely studied skin tumor promoters however, many other chemical compounds have been shown to possess skin tumor-promoting properties, for example, phenobarbitol, DDT, and the peroxisomal prolifera-tors. Within a few hours after application of a single effective dose of phorbol 12-myristate 13-acetate (also known as TPA and 12-O-tetradecanoyTphor-boTl3-acetate, CAS 16561-29-8) to mouse skin, localized edema and erythema characteristic of inflammation and irritation are evident, and within 24 h there is leukocytic infiltration of the dermis. Within 1 or 2 days after a single promoter treatment, stimulation of mitotic activity in the basal cell layer of the epidermis is evident and continues for several days. This results in an increased number of... 

Steigleder, G. K., and Fissher, I., Localization of ribonuclease and deoxyribonuclease activity in normal skin, skin altered by inflammation and in skin tumors. Arch. Klin. Expil. Dermatol. 217, 653-562 (1963). 

Exposure to UV radiation from sunlight is the major cause of human skin cancer. Skin tumors from patients with Xeroderma pigmentosum, a DNA-repair deficiency associated with increased sensitivity to UV, show a particularly high frequency of these CC to TT transitions (Dumaz et al., 1993). Mutations at dipyrimidines have been observed in the normal skin of sun-exposed skin cancer patients (Jonason et al., 1996 Nakazawa et al., 1994 Ren et al., 1996a). The localization of mutations in skin shows striking differences with other types of cancers, with hotspots at codons 177-179 and... 

HUMAN HEALTH RISKS EPA group B2 probable human carcinogen Acute Risks skin irritation damage to mucous membranes of nose throat and lungs conjunctivitis keratitis Chronic Risks alters genetic material local sarcomas liver disturbance skin tumors. 

To perform photodynamic therapy (PDT) in skin tumors, the most often used substance is ALA. The porphyrin precursor is topically applied under occlusive foil as described above. Irradiation should be performed when the optimal ratio of photosensitizer levels between tumor and normal tissue is reached (in the case of ALA 2-6 h after application Figures 2, 5, 7) [16]. The type of light source (laser or incoherent light) and the required fluence depend on the photosensitizer used as well as on the type and localization of the lesion. 

Mueller DK, Kopp SA, Marks F, Seibert K, Fuerstenberger G. Localization of prostaglandin H synthase isoenzymes in murine epidermal tumors suppression of skin tumor promotion by inhibition of prostagalndin H synthase-2. Mol Carcinog 1998 23 36-44. 

Andronova, N.V, Bokhyan, B.Yu., Nikolaev, A.L., Treschahna, E.M., Aliev, M.D., Kovalevskiy, E.E., Filonenko, D.V, Gopin, A.V., Bozhevolnov, V.E., Kogan, B.Ya., Vorozhtsov, G.N. Rationale for clinical study of preoperative treatment of soft hssue sarcomas with local ultrasound hyperthermia and chemotherapy with cisplatin and/or doxorubicin. Sarcoma of bone, soft tissue and skin tumors, 2011, 1, 28-33 (in Russian). 

Radiation is an important modality in the treatment of symptomatic metastatic disease. The most common indication for treatment with radiation therapy is painful bone metastases or other localized sites of disease refractory to systemic therapy. Radiation therapy gives significant pain relief to approximately 90% of patients who are treated for painful bone metastases. Radiation is also an important modality in the palliative treatment of metastatic brain lesions and spinal cord lesions, which respond poorly to systemic therapy, as well as eye or orbit lesions and other sites where significant accumulation of tumor cells occurs. Skin and/or lymph node metastases confined to the chest wall area also may be treated with radiation therapy for palliation (e.g., open wounds or painful lesions). 

Once T cells are activated, they migrate from lymph nodes and the bloodstream into skin and secrete various cytokines (e.g., interferon % interleukin 2 [IL-2]) that induce the pathologic changes of psoriasis. Local keratinocytes and neutrophils are induced to produce other cytokines, such as tumor necrosis factor-a (TNF-a), IL-8, and others. 

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