Prostate cancer (PCa) is the most frequently diagnosed malignancy in men worldwide. Chemotherapy response is very poor and resistance to hormone-based treatments is frequent in advances stages. Recently, tumor-initiating cells or cancer stem cells (CSCs) have been identified in several cancers, including PCa. These cells are thought to be responsible for therapy resistance, relapse and metastasis. In the present work, enriched populations of CSCs were obtained using a mixed procedure that included differential clone-forming ability, sphere growing induction (prostatospheres) and magnetic-associated cell sorting (MACS). Also, stem marker expression was determined in PCa biopsies of different histological grades and metastasis samples. The signature for stem markers of the isolated CSCs was CD133+/CD44+/ABCG2+/ CD24-. Expression of stem markers (CD133, CD44, and ABCG2) was higher in medium Gleason biopsies than in lower and higher grades, and lymph-node and bone metastasis samples. These results suggest that the CSCs in PCa reach an important number in medium Gleason grades, when the tumor is still confined into the gland. At this stage, the surgical treatment is usually with curative intention. However, an important percentage of patients relapse after treatment. Number and signature of CSCs may be a prognosis factor for PCa recurrence.

AJA publishes new findings in basic and clinical (including modern, traditional and epidemiological) research on Andrology.

Next-generation sequencing (NGS) is progressively being used in clinical practice. However, several barriers preclude using this technology for precision oncology in most Latin American countries. To overcome some of these barriers, we have designed a 25-gene panel that contains predictive biomarkers for most current and near-future available therapies in Chile and Latin America. Library preparation was optimized to account for low DNA integrity observed in formalin-fixed paraffin-embedded tissue. The workflow includes an automated bioinformatic pipeline that accounts for the underrepresentation of Latin Americans in genome databases. The panel detected small insertions, deletions, and single nucleotide variants down to allelic frequencies of 0.05 with high sensitivity, specificity, and reproducibility. The workflow was validated in 272 clinical samples from several solid tumor types, including gallbladder (GBC). More than 50 biomarkers were detected in these samples, mainly in BRCA1/2, KRAS, and PIK3CA genes. In GBC, biomarkers for PARP, EGFR, PIK3CA, mTOR, and Hedgehog signaling inhibitors were found. Thus, this small NGS panel is an accurate and sensitive method that may constitute a more cost-efficient alternative to multiple non-NGS assays and costly, large NGS panels. This kind of streamlined assay with automated bioinformatics analysis may facilitate the implementation of precision medicine in Latin America.

Introduction We evaluated the immunohistochemical expression of p53, Ki67, CD30, and CD117 and correlated it with histological features and presence of clinical metastasis at diagnosis of testicular seminomas. Materials and Methods A retrospective study of 62 patients was performed in patients with pure seminoma. The retroperitoneum was staged with computed tomography scan and the thorax with simple x-rays and/or computed tomography scan. Pathologists were unaware of the clinical stage of the patients. Manual microarrays were created from a tissue representative of tumor. The expression of p53, Ki67, CD30, and CD117 was evaluated as negative, any degree of expression, and expression in more than 50% of neoplastic cells. Univariate and multivariate analysis were performed. Results Sixty-two cases were analyzed: 43 cases were in clinical stage I (69.4%), 17 were in clinical stage II (27.4%), and 2 were in clinical stage III (3.2%). Fifty-six cases expressed CD117 (90%), 42 p53 (68%), 8 CD30 (13%), and all cases Ki67. There were no differences in p53, Ki67, CD30, and CD117 expression between testicular seminoma with and without clinical metastasis at diagnosis, regardless of the magnitude of expression. Neither of them found positive association between these marker expressions and morphologic risk factors such as tumor size greater than 6 cm and rete testis invasion. Conclusions This study shows that expression of p53, Ki67, and CD30 and loss of CD117 expression fail to predict the presence of clinical metastasis at diagnosis of testicular seminoma and do not correlate with other histopathological risk factors in clinical stage I patients.