Basal Cell Carcinoma Of Prostate Research Articles

Genomic Characterization of Prostatic Basal Cell Carcinoma

Basal cell carcinoma (BCC) of the prostate is a rare tumor. Compared with the more common acinar adenocarcinoma (AAC) of the prostate, BCCs show features of basal cell differentiation and are thought to be biologically distinct from AAC. The spectrum of molecular alterations of BCC has not been comprehensively described, and genomic studies are lacking. Herein, whole genome sequencing was performed on archival formalin-fixed, paraffin-embedded specimens of two cases with BCC. Prostatic BCCs were characterized by an overall low copy number and mutational burden. Recurrent copy number loss of chromosome 16 was observed. In addition, putative driver gene alterations in KIT, DENND3, PTPRU, MGA, and CYLD were identified. Mechanistically, depletion of the CYLD protein resulted in increased proliferation of prostatic basal cells invitro. Collectively, these studies show that prostatic BCC displays distinct genomic alterations from AAC and highlight a potential role for loss of chromosome 16 in the pathogenesis of this rare tumor type.

Prostatic basal cell carcinoma treated by chemoradiation with weekly cisplatine: case report and literature review

BackgroundBasal cell carcinoma of the prostate is a relatively rare entity. Their evolution is characterized by the frequency of local and/or distant relapses. Due to their rarity, the treatment is not consensual in the literature. We report here a case of Basal cell carcinoma of the prostate in a 40-year-old patient.Case presentationOur patient initially presented an obstructive lower urinary tract symptoms with a normal initial level of prostate specific antigen (PSA) test (3.5 ng/m). The transurethral resection of the prostate (TURP) was in favor of a prostatic basal cell carcinoma with its specific anatomopathological and immunohistochemical characteristics. The prostatic MRI and thoraco-abdominal CT realized after the TURP revealed a tumoral lesion of the prostatic peripheral zone with extra-capsular extension combined with right seminal vesicle invasion and a suggestion of posterior bladder wall adherence. No evidence of visceral or nodal metastases at this point. Considering the tumor being locally advanced, a concurrent chemoradiotherapy with intensity modulated technique was indicated after a multidisciplinary meeting with a 70 Gy total target dose delivered in 35 fractions and weekly Cisplatin. A year and a half after, he developed a cerebellous metastases revealed by intracranial hypertension with no other visceral lesion and complete local remission with the disappearance of the lower urinary tract symptoms and the pain and the appearance of a prostatic atrophy. The PSA level was still on the upper limit of normal. He underwent metastasectomy, and the anatomopathological study was in favor of a cerebellous metastasis of the known BCC. The patient presented postoperatively paraparesis of lower limbs with balance problems for which he was placed in palliative care with indication of postoperative radiation therapy in case of improvement of his general condition. He did not recover and deceased three months later.ConclusionsThe prostatic basal cell carcinoma is a rare aggressive entity often non-evoked at the clinical or radiological stages because of its unspecific appearance. The diagnostic of these tumors is based on histological examination and a large immunohistochemistry panel. Given its scarity, very few data is available for locally advanced non-metastatic stages treated by radiation therapy. We assess here a good local response with concurrent chemoradiation therapy.

A method for reliable detection of genomic point mutations based on single-cell target-sequencing

The analysis of genomic point mutations is one of the research strategies to explore the clonal evolution of tumor cells. At present, clonal evolution of tumor cells is mainly determined by bulk sampling and sequencing of different sections of the tumor. Since this approach analyzes a mixture of different cell types, it may not accurately represent the clonal evolution of specific tumor cell populations and likely miss low frequency mutations, especially when the sequencing depths are not sufficient. To address this issue, we have developed a strategy to analyze genomic point mutations from prostate basal cell carcinoma (BCC) tissues at single-cell resolution. Firstly, we optimized the single-cell whole genome amplification procedure with HepG2 cells. Then the single cells from BCC tissue were captured by a microfluidic chip of Fluidigm and processed for whole-genome amplification. Both SCUBE3 and MST1L genomic mutations were obtained by whole exome sequencing. Finally, we examined the genomic mutations through single-cell targeted amplification and Sanger sequencing. The established method successfully reconfirmed the mutations of SCUBE3 and MST1L in BCC at single cell level. The strategy established in this study could provide a useful tool for determining the clonal evolution of tumor cells based on genomic mutations at single-cell resolution.

Hormone -Refractory Prostatic Adenocarcinoma Mimicking Basal Cell Carcinoma: A Case Report

Abstract Prostate cancer is an androgen-driven malignancy. Patients with late-stage prostate cancer often receive androgen-deprivation therapy to suppress the disease progression. Under the selection pressure, some prostate cancers transform to androgen-independent cancers. Treatment-induced small cell neuroendocrine carcinoma is one of the examples. In the last decade, patients with disseminated prostate cancer frequently received second-generation androgen-deprivation agents, such as abiraterone, enzalutamide, and apalutamide. Those more potent drugs have led to an emergence of a novel type of androgen-independent carcinoma named “double-negative” prostate cancer, which is immunohistochemically negative for both neuroendocrine markers and androgen targets. In this report, we present a typical case of “double-negative” end-stage prostate cancer that morphologically resembled basal cell carcinoma of prostate, basaloid large nest type.

Mutational and transcriptomic landscapes of a rare human prostate basal cell carcinoma.

As a rare subtype of prostate carcinoma, basal cell carcinoma (BCC) has not been studied extensively and thus lacks systematic molecular characterization. Here, we applied single-cell genomic amplification and RNA-Seq to a specimen of human prostate BCC (CK34βE12+ /P63+ /PAP- /PSA- ). The mutational landscape was obtained via whole exome sequencing of the amplification mixture of 49 single cells, and the transcriptomes of 69 single cells were also obtained. The five putative driver genes mutated in BCC are CASC5, NUTM1, PTPRC, KMT2C, and TBX3, and the top three nucleotide substitutions are C>T, T>C, and C>A, similar to common prostate cancer. The distribution of the variant allele frequency values indicated that these single cells are from the same tumor clone. The 69 single cells were clustered into tumor, stromal, and immune cells based on their global transcriptomic profiles. The tumor cells specifically express basal cell markers like KRT5, KRT14, and KRT23 and epithelial markers EPCAM, CDH1, and CD24. The transcription factor covariance network analysis showed that the BCC tumor cells have distinct regulatory networks. By comparison with current prostate cancer datasets, we found that some of the bulk samples exhibit basal cell signatures. Interestingly, at single-cell resolution the gene expression patterns of prostate BCC tumor cells show uniqueness compared with that of common prostate cancer-derived circulating tumor cells. This study, for the first time, discloses the comprehensive mutational and transcriptomic landscapes of prostate BCC, which lays a foundation for the understanding of its tumorigenesis mechanism and provides new insights into prostate cancers in general.

MYB-NFIB gene fusion in prostatic basal cell carcinoma: clinicopathologic correlates and comparison with basal cell adenoma and florid basal cell hyperplasia

Prostatic basal cell carcinoma is a malignant neoplasm composed of basaloid cells forming infiltrative nests and tubules, which may potentially be misdiagnosed as benign basal cell proliferations (i.e., florid basal cell hyperplasia or basal cell adenoma) and also closely resembles adenoid cystic carcinoma of the salivary gland. MYB-NFIB gene rearrangement occurs in 30–86% of salivary gland adenoid cystic carcinomas. We sought to further characterize MYB gene rearrangement in prostatic basal cell carcinoma and correlate MYB-NFIB fusion status with other clinicopathologic characteristics. To this end, FISH analysis for MYB-NFIB gene fusion using fusion probes was performed on formalin-fixed, paraffin-embedded tissue sections from prostatic basal cell carcinoma (n = 30), florid basal cell hyperplasia (n = 18), and basal cell adenoma (n = 4). Fourteen of 30 (47%) cases of basal cell carcinoma were positive for MYB-NFIB gene fusion FISH, and no cases of benign basal cell proliferations were positive (p < 0.05). FISH-positive patients (mean age = 63 years, range: 35–81) tended to be younger than FISH-negative patients (mean age = 70 years, range: 55–93). Most FISH-positive cases demonstrated adenoid cystic carcinoma-like morphology (57%), and most FISH-negative cases demonstrated nonadenoid cystic carcinoma-like morphology (93%); one case (FISH-positive) demonstrated areas with both adenoid cystic carcinoma-like and nonadenoid cystic carcinoma-like morphology. FISH-positive cases more frequently demonstrated perineural invasion (50% vs. 14%, p < 0.05) compared to FISH-negative cases. Conversely, tall basal cells (i.e., neoplastic cells at least two times taller than wide) were more frequent in FISH-negative cases than FISH-positive cases (93% vs. 36%, p < 0.05). Approximately, 50% of prostatic basal cell carcinoma harbor MYB-NFIB gene fusion. The majority of these cases were characterized by adenoid cystic carcinoma-like morphology, perineural invasion, and lack tall basal cells. Florid basal cell hyperplasia and basal cell adenoma are negative for MYB-NFIB gene fusion.

A subset of prostatic basal cell carcinomas harbor the MYB rearrangement of adenoid cystic carcinoma.

Adenoid cystic carcinoma (ACC) is a basaloid tumor consisting of myoepithelial and ductal cells typically arranged in a cribriform pattern. Adenoid cystic carcinoma is generally regarded as a form of salivary gland carcinoma, but it can arise from sites unassociated with salivary tissue. A rare form of prostate carcinoma exhibits ACC-like features; it is no longer regarded as a true ACC but rather as prostatic basal cell carcinoma (PBCC) and within the spectrum of basaloid prostatic proliferations. True ACCs often harbor MYB translocations resulting in the MYB-NFIB fusion protein. MYB analysis could clarify the true nature of prostatic carcinomas that exhibit ACC features and thus help refine the classification of prostatic basaloid proliferations. Twelve PBCCs were identified from the pathology consultation files of Johns Hopkins Hospital. The histopathologic features were reviewed, and break-apart fluorescence in situ hybridization for MYB was performed. All 12 cases exhibited prominent basaloid histology. Four were purely solid, 7 exhibited a cribriform pattern reminiscent of salivary ACC, and 1 had a mixed pattern. The MYB rearrangement was detected in 2 (29%) of 7 ACC-like carcinomas but in none (0%) of the 5 PBCCs with a prominent solid pattern. True ACCs can arise in the prostate as is evidenced by the presence of the characteristic MYB rearrangement. When dealing with malignant basaloid proliferations in the prostate, recommendations to consolidate ACCs with other tumor types may need to be reassessed, particularly in light of the rapidly advancing field of biologic therapy where the identification of tumor-specific genetic alterations presents novel therapeutic targets.

Basal cell carcinoma of the prostate: clinicopathologic analysis of three cases and a review of the literature

BackgroundAlthough conventional adenocarcinoma accounts for the majority of prostatic carcinomas, it is important to recognize rare variants, like basal cell carcinoma (BCC), which has distinctive histopathological and biological features.Case reportWe analyzed three cases of prostatic BCC and all of them complained of acute urinary retention and digital rectal examination disclosed a stony hard prostate. However, all of them presented with low prostate-specific antigen. The diagnosis relied on transrectal ultrasound-guided needle biopsies or transurethral resection of the prostate (TURP). The microscopic findings suggested basaloid cells with large pleomorphic nuclei and scant cytoplasm, showing peripheral palisading and forming solid nests, and immunohistochemical markers like 34βE12, p63 and Ki67 staining, were positive. After active treatment, two of the patients are alive with tumor and one died five months after discharge from our hospital.

Prostatic Basal Cell Carcinoma: A Case Report and Review of the Literature

Prostatic Basal Cell Carcinoma: A Case Report and Review of the Literature

Basal cell carcinoma of prostate: clinicopathologic analysis of two cases

Basal cell carcinoma of prostate: clinicopathologic analysis of two cases

Basal cell carcinoma of the prostate: Report of a case and review of the published reports

Prostatic basal cell carcinoma (BCC), a distinctive variant of adenocarcinoma, is rare. We report a patient with pure basaloid BCC showing an extraprostatic extension and lymph node metastases. A 67-year-old man with urinary outlet obstruction was referred to our hospital. Digital rectal examination disclosed a stony hard prostate. Serum prostate-specific antigen and prostatic acid phosphatase were within the normal range. Transrectal needle biopsy of the prostate was followed by transurethral resection as symptomatic treatment. The lesion was diagnosed histopathologically as BCC. Despite antiandrogen therapy distant metastases developed, and the patient died 5 months postoperatively. We discuss the histological and immunohistochemical findings in this case.