#vimentin

Cellular Clear-out

To function properly, cells need to break down damaged proteins and keep harmful aggregates of clumped proteins under control. Clearing out this clutter is also a crucial step in the activation of neural stem cells (NSCs), when they leave their dormant state, or quiescence, and begin dividing to produce new neural cells. Pictured are NSCs (their nuclei labelled in cyan) in a young mouse’s brain; in red is vimentin, an intermediate filament protein with a crucial role, bringing proteasomes, protein complexes that destroy problem proteins, into contact with aggresomes, concentrated packets of damaged or clumped proteins. Without vimentin, NSCs struggle to recover from protein damage, accumulate more protein aggregates, and exit quiescence less easily. Contributing to both the destruction of aggregated proteins, involved in diseases like Alzheimer’s, and the activation of NSCs, a process that declines with ageing, vimentin could be an interesting target for researchers working towards regenerative therapies.

Written by Emmanuelle Briolat

Image by Christopher Morrow, Moore Lab

Department of Neuroscience, University of Wisconsin – Madison, Madison, WI, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Research published in Cell Stem Cell, February 2020

Primary angiosarcoma of the prostate (PASOP) is a very rare tumour which most clinicians have not encountered and may be unaware of. Literature of PASOP was reviewed by obtaining information from various internet data bases including: Google, Google Scholar, Educus and PUB Med. Less than 20 cases of PASOP have been reported. PASOP may present in a male child or adult with lower urinary tract symptoms, dysuria, haematuria, pain and constipation. There may be in some cases a history of prior radiotherapy for adenocarcinoma of prostate. Diagnosis is based upon histological examination of prostate biopsy specimens which tend to reveal: Proliferative vascular channels that are lined by atypical multi-layered or atypical solid endothelial cells, variable pleomorphic tumour cells ranging from spindle cells to large/plump cells; nuclei which are large and pleomorphic and which contain clumped chromatin and prominent nucleoli; mitotic figures of which some may look atypical are frequently seen. PASOPs on immunohistochemical staining tend to stain positively for CD34, Factor 8 (Factor VIII), Vimentin. PASOPs on immunohistochemical staining tend to exhibit negative staining for PSA, Keratin and S-100. Surgical resection with surgical margins that are clear of tumor has been shown to be the treatment associated with a chance of long-term survival but a number of reported cases of PASOP at the time of initial diagnosis had presented with metastatic disease or locally advanced disease and curative surgery with clear surgical margins has been impossible. Various adjuvant therapies had been reported but on the whole the prognosis has been poor. There is on the whole no consensus opinion on the best management options for all stages of the disease. PASOP is a rare aggressive disease. Clinicians should report cases of PASOP they encounter and should enter them into a multi-centre trial to find the best treatment option. Perhaps if patients who develop relapse disease who had previously undergone radiotherapy for prostate cancer undergo further biopsies of prostate may be new cases of PASOP would be diagnosed in the new biopsy specimens and this could illustrate that PASOPS are not as uncommon as used to be believed.

Author(s) Details

Anthony Kodzo-Grey Venyo [MB ChB FRCS(Ed) FRCSI FGCS Urol. LLM] Department of Urology, North Manchester General Hospital, Delaunay’s Road, Manchester, United Kingdom.

Background: Primary synovial sarcoma of the prostate gland (PSSP) is rare and most clinicians would be unfamiliar with its biological behaviour.

Aim: To review the literature on PSSP.

Methods: Various internet data bases were searched.

Literature Review: PSSP is extremely rare with less than 10 cases reported; affects both young and older men; its diagnosis may be made incidentally following histological and cytogenetics examinations of prostate biopsy or prostatectomy specimens which show: A specific chromosomal translocation t(X; 18; p11; q11); Uniform spindle and oval cells which have formed interlacing fascicles that mimic fibrosarcoma. The compact fascicles of tumour cells focally alternate with hypo- cellular myxoid tissue which mimic peripheral nerve sheath tumours. Focal pericytomatous pattern of polygonal cells arranged around dilated, thin-walled blood vessels. PSSP tumour cells on immunohistochemical staining, stain positively with: Vimentin (most of the cells), EMA (focal positivity), Bcl-2 (strong positivity), CD99 (strong positivity), E-cadherin (strong positivity), cytokeratin (focal positivity), CD 56 and TLE/TLE1. There is no consensus opinion on treatment of PSSP which is an aggressive tumour with poor outcome. However, an aggressive radical surgical treatment by radical prostatectomy or pelvic exenteration plus or minus adjuvant therapy would appear to be the best treatment option with curative intent to help improve prognosis. Some patients with PSSP may need palliative and supportive treatment through a multi-disciplinary team approach.

Conclusions: PSSP is a rare aggressive tumour with poor prognosis. All cases of PSSP should be entered into a multi-centre trial to ascertain the best treatment option that would improve the prognosis and to further assess its biological behaviour.

Author(s) Details

Mr. Anthony Kodzo-Grey Venyo MB ChB FRCS(Ed) FRCSI FGCS Urol. LLM Department of Urology, North Manchester General Hospital, Delaunays Road Manchester, United Kingdom.