Background: Primary basal cell carcinoma (BCC) is a rare prostate cancer. Currently, a standard treatment regime for BCC of the prostate is lacking and most patients have a poor prognosis. We reported on a patient with BCC of the prostate whose cancer metastasized after undergoing a radical prostatectomy and whose prognosis improved after treatment with etoposide. Case Presentation: A 62-year-old male with a history of seminoma was admitted complaining of intermittent gross hematuria for 1 month. Following a prostate biopsy, the patient was diagnosed with BCC of the prostate and received radical prostatectomy and radiotherapy. Initially, the patient's symptoms improved; however, 2 years later, a chest computed tomography (CT) scan revealed lung nodules. The patient did not exhibit any symptoms of BCC of the prostate; however, pathological examination and immunohistochemical staining of the nodules confirmed metastatic BCC of the prostate. Chemotherapy with docetaxel and cisplatin was well-tolerated but did not slow disease progression. Next-generation sequencing revealed mutations in the ataxia telangiectasia-mutated (ATM), SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily b-member 1 (SMARCB1), and phosphoinositide-3kinase regulatory subunit 1 (PIK3R1) genes. The patient did not receive targeted therapy owing to financial limitations and instead, etoposide was administered. A 9-month followup chest CT scan showed an 80% reduction in existing lung nodules and no new nodules had developed. Conclusion: Our patient, diagnosed with recurrent prostate BCC after receiving a radical prostatectomy, responded to treatment with etoposide. Radical prostatectomy and radiotherapy should remain first-line therapy; however, etoposide may be an alternative second-line therapy when other options are not available. Consensus regarding treatment plans, and the molecular mechanisms behind prostate BBC, must be elucidated.

Background Renal cell carcinoma (RCC) contributed to 403,262 new cases worldwide in 2018, which constitutes 2.2% of global cancer, nevertheless, sunitinib, one of the major targeted therapeutic agent for RCC, often developed invalid due to resistance. Emerging evidences suggested sunitinib can impact tumor environment which has been proven to be a vital factor for tumor progression. Methods In the present study, we used ssGSEA to extract the immune infiltrating abundance of clear cell RCC (ccRCC) and normal control samples from http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE65615, TCGA, and GTEx; key immune cells were determined by Student's t‐test and univariable Cox analysis. Co‐expression network combined with differentially expressed analysis was then applied to derive key immune‐related genes for ccRCC, followed by the identification of hub genes using differential expression analysis. Subsequently, explorations and validations of the biological function and the immune‐related and sunitinib‐related characteristics were conducted in KEGG, TISIDB, Oncomine, ICGC, and GEO databases. Results We refined immature dendritic cells and central memory CD4 T cells which showed associations with sunitinib and ccRCC. Following, five hub genes (CRYBB1, RIMBP3C, CEACAM4, HAMP, and LYL1) were identified for their strong relationships with sunitinib and immune infiltration in ccRCC. Further validations in external data refined CRYBB1, CEACAM4, and HAMP which play a vital role in sunitinib resistance, immune infiltrations in ccRCC, and the development and progression of ccRCC. In conclusion, our findings could shed light on the resistance of sunitinib in ccRCC and provide novel biomarkers or drug targets for ccRCC.

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Microtubule-interacting and trafficking domain containing 1 (MITD1) is associated with abscission during cytokinesis. However, systematic investigation into its role in cancer is lacking. Therefore, we explored the pan-cancer role of MITD1 using multiple databases. Expression and clinical survival, immunological, and enrichment analyses were performed using R packages and online tools. For breast cancer, single-cell level analysis, immunochemistry, and in vitro experiments were performed to explore the mechanism of MITD1. A nomogram was established to predict the prognosis of patients with breast cancer and evaluate the immunotherapy biomarker based on two datasets. In some cancers, high MITD1 expression was associated with a more favorable prognosis. For instance, it inhibited tumor cell proliferation and migration in breast cancer. MITD1 may regulate cancer development by altering the tumor microenvironment, and MITD1 expression may predict the response to immune checkpoint blockade, platinum, and poly ADP-ribose polymerase inhibitor therapies. Our nomogram was used to determine the prognosis of patients with breast cancer. MITD1 can also predict the response to immunotherapy. Our first pan-cancer study of MITD1 has shown that it plays different roles in cancer development and therapy. In breast cancer, MITD1 inhibited cell proliferation and migration and serves as a new biomarker.