Giant condyloma acuminatum (GCA) or Buschke-Loewenstein tumor is a rare disease, with an estimated prevalence of 0.1%. It was initially described in 1896 by Buschke and later in 1925 by Buschke and Loewenstein. Classic condyloma acuminata (CCA) and squamous cell carcinoma (SCC) were initially described as different entities. These three entities are currently considered to correspond to the same spectrum of different but not exclusive malignant transformations, associated with multiple risk factors such infection by human papilloma virus (HPV), immunodeficiencies, poor hygiene, multiple sexual partners, and chronic genital infections. HPV subtypes 6 and 11 are associated with 90% of GCA. It presents as a cauliflower-like tumor in the genital region with bad odor, bleeding, and local infection, differential diagnosis with multiple conditions should be considered, and sexually transmitted diseases should always be investigated. GCA has a higher rate of malignant transformation than CCA and tends to infiltrate adjacent soft tissues. The therapeutic approach is controversial but is considered that the resection with free edges is the gold standard and can be combined with adjuncts. The recurrence rate is high. Overall mortality is 21% and is associated with morbidity caused by recurrences. Imiquimod cream 5% has recently shown good results as monotherapy and in combination with ablative and surgical treatments. The quality of life is diminished in patients with this condition. In this review, we address the different aspects of this rare entity including the therapeutic approach.
Despite having a favorable response to platinum-based chemotherapies, ~15% of Testicular Germ-Cell Tumor (TGCT) patients are platinum-resistant. Mortality rates among Latin American countries have remained constant over time, which makes the study of this population of particular interest. To gain insight into this phenomenon, we conducted whole-exome sequencing, microarray-based comparative genomic hybridization, and copy number analysis of 32 tumors from a Mexican cohort, of which 18 were platinum-sensitive and 14 were platinum-resistant. We incorporated analyses of mutational burden, driver mutations, and SNV and CNV signatures. DNA breakpoints in genes were also investigated and might represent an interesting research opportunity. We observed that sensitivity to chemotherapy does not seem to be explained by any of the mutations detected. Instead, we uncovered CNVs, particularly amplifications on segment 2q11.1 as a novel variant with chemosensitivity biomarker potential. Our data shed light into understanding platinum resistance in a Latin-origin population.
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