{'fraction_non_alphanumeric': 0.019313304721030045, 'fraction_numerical': 0.0, 'mean_word_length': 5.537383177570093, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Lipoatrophy associated with interferon alfa adjuvant therapy for melanoma.

Comment. In our patient, the clinical cutaneous alterations, as well as the histologic and serologic findings, were indistinguishable from those encountered in LCSSc. Paclitaxel functions as an antineoplastic agent by disrupting the microtubular network that is essential for normal mitotic processes. The drug binds to free tubulin and promotes the formation of microtubules. This process leads to the stabilization of microtubule bundles and prevents their disassembly during normal phases of the cell cycle. The centromere, involved in the genesis of autoantibodies in LCSSc, also plays an important role in cell division. Although the mechanisms have not been clarified, the onset of LCSSc with positive ACA findings could indicate an effect of paclitaxel. Various case reports describe scleroderma secondary to malignant neoplasm. Especially in breast cancer, a close relationship between this carcinoma and SSc has been described several times. Many factors have been suggested to be pathogenetic for SSc in patients with neoplasia: cytokines, growth factors, hormones, antigen presentation, antibody genesis, and cell immunologic disturbances. Along with these factors, cancer therapy may have an additional effect. Our case suggests a possible association between taxanes and SSc and between SSc and breast cancer.