scholarly journals Single-cell dissection of a rare human prostate basal cell carcinoma

2019 ◽  
Author(s):  
Xianbin Su ◽  
Qi Long ◽  
Juanjie Bo ◽  
Yi Shi ◽  
Li-Nan Zhao ◽  
...  

AbstractAs 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 5 putative driver genes mutated are CASC5, NUTM1, PTPRC, KMT2C and TBX3. The top 3 nucleotide substitutions are C>T, T>C and C>A, similar to common prostate cancer. The distribution of the variant allele frequency values indicated these single cells are from the same tumor clone. The transcriptomes of 69 single cells were obtained, and they 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 (TF) co-variance 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.

2021 ◽  
pp. 106689692110173
Author(s):  
Vilde Pedersen ◽  
Katrine S. Petersen ◽  
Klaus Brasso ◽  
Olga Østrup ◽  
Anand C. Loya

Basal cell carcinomas of prostate (BCCP) are very rare. Most arise in the transition zone and thus are associated with lower urinary tract symptoms and rarely associated with elevated prostate-specific antigen (PSA). These features make diagnosis/early diagnosis difficult because of the routine protocols followed. Basal cell carcinomas have distinctive histopathological, immunohistochemical, and to some extent also different molecular characteristics. Basal cell carcinoma in situ (BCCIS) is a nonexistent histological lesion as per the current literature, but here is an attempt to describe it through this case. A 74-year-old man presented with hematuria and previous diagnosis of prostatic hyperplasia. Based on this history, he underwent a prostatectomy ad modum Freyer. Pathological examination surprisingly revealed a diffusely infiltrative tumor with nonacinar adenocarcinoma morphology and many glandular structures probably representing BCCIS. Tumor was diagnosed as BCCP. Patient presented with metastasis to the abdominal wall 8 months postprostatectomy. BCCP is an aggressive type of prostate cancer, which might be challenging to diagnose based on routine protocols. This results in delayed diagnosis and treatment and thus poor prognosis. Furthermore, patients with this subtype of prostate cancer need appropriately designed, and maybe a totally different follow-up regimen as PSA is of no use for BCCP patients. Finally, diagnosis of BCCIS, if agreed upon its existence needs to be studied in larger cohorts as a precursor lesion.


2007 ◽  
Vol 96 (3) ◽  
pp. 523-528 ◽  
Author(s):  
N J Rukin ◽  
M P Zeegers ◽  
S Ramachandran ◽  
C J Luscombe ◽  
S Liu ◽  
...  

2014 ◽  
Vol 54 (8) ◽  
pp. 905-915 ◽  
Author(s):  
Onder Bozdogan ◽  
Isik G. Yulug ◽  
Ibrahim Vargel ◽  
Tarik Cavusoglu ◽  
Ayse A. Karabulut ◽  
...  

2019 ◽  
Vol 1 (1) ◽  
pp. 36-38

The last decade was marked by a statistically significant increase in the incidence of skin cancers, which motivated the development of new studies to later understand the behavior of these pathologies developing new therapeutic approaches. Also, the multitude of premalignant lesions as well as the complex classification of the carcinomas required a more accurate differentiation of the differential diagnosis, and in this regard the present electron microscopic study contributes significantly. A tumor is a very complex ecosystem represented in particular by (1) genetically modified neoplastic cells and (2) tumor stroma represented by (a) various other cell types (fibroblasts, fibrocytes, mast cells, inflammatory cells, endothelial cells, myelinated or non-myelinated nerves, etc.), and (b) extracellular matrix (basal lamina, elastic fibers and collagen, but also soluble molecules) [1]. The purpose of this study was to discover new aspects of ultrastructure that occur in basal cell carcinoma cases investigated by us, related to the capacity of invasiveness of these tumors. Fresh tumor fragments were obtained with the informed consent of the patients. Here we present some peculiar aspects concerning infrastructure of tumor cells involved in invasive process, especially desmosomal and hemidesmosomal junctions, invadopodia and shedding membrane vesicles. Moreover, here we report about new described cell phenotype termed telocytes involved in cell signaling by their homo- and heterocellular contacts. Telocytes from basal cell carcinoma stroma exhibit a reduced number of heterocellular contacts, which suggests a possible perturbation of tissue homeostasis modulation. Electron microscopic investigations revealed that in invasive basal cell carcinoma intercellular junctions, namely desmosomes are severely altered and that the tumor cells generate and disseminate membrane vesicles, including exosomes inside of the peritumoral stroma. Using transmission electron microscopy to investigate invasive basal cell carcinoma, we have managed to determine the relevance of all these changes for the purpose of evaluation of the invasive capacity of tumor cells within the peritumoral stroma.


2007 ◽  
Vol 177 (4S) ◽  
pp. 75-75
Author(s):  
Nicholas J. Rukin ◽  
Maurice P. Zeegers ◽  
Sudarshan Ramachandran ◽  
Chritopher J. Luscombe ◽  
Samson Liu ◽  
...  

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