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- Furusato, Bungo, et al.
(författare)
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CXCR4 and cancer
- 2010
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Ingår i: Pathology international (Print). - : Wiley. - 1320-5463 .- 1440-1827. ; 60:7, s. 497-505
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Forskningsöversikt (refereegranskat)abstract
- The chemokine receptor CXCR4 belongs to the large superfamily of G protein-coupled receptors and has been identified to play a crucial role in a number of biological processes, including the trafficking and homeostasis of immune cells such as T lymphocytes. CXCR4 has also been found to be a prognostic marker in various types of cancer, including leukemia and breast cancer, and recent evidence has highlighted the role of CXCR4 in prostate cancer. Furthermore, CXCR4 expression is upregulated in cancer metastasis, leading to enhanced signaling. These observations suggest that CXCR4 is important for the progression of cancer. The CXCR4-CXCL12 (stromal cell-derived factor 1 (SDF-1)) axis has additionally been identified to have a role in normal stem cell homing. Interestingly, cancer stem cells also express CXCR4, indicating that the CXCR4-SDF-1 axis may direct the trafficking and metastasis of these cells to organs that express high levels of SDF-1, such as the lymph nodes, lungs, liver, and bone. This review focuses on the current knowledge of CXCR4 regulation and how deregulation of this protein may contribute to the progression of cancer.
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| 2. |
- Talvitie, Heidi, et al.
(författare)
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Solitary fibrous tumor of the prostate : A report of two cases
- 2011
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Ingår i: Pathology international (Print). - Carlton South, Vic., Australia : Blackwell Scientific Publications for the Japanese Society of Pathology. - 1320-5463 .- 1440-1827. ; 61:9, s. 536-538
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Tidskriftsartikel (refereegranskat)abstract
- We here report two cases of solitary fibrous tumor (SFT) arising in the prostate. Two men, 66 and 69 years old, with urinary tract symptoms were diagnosed with SFT on transrectal needle biopsy and transurethral resection of the prostate, respectively. The tumors were removed by a low anterior resection including tumor, prostate and rectum en bloc and cystoprostatectomy, respectively. Both tumors were well-circumscribed but also showed some infiltration of the prostate glands. They were composed of storiform bundles of bland spindle cells that stained strongly for CD34 and vimentin but negative for muscle markers. Although rare, SFT should be considered as differential diagnosis of spindle cell lesions on prostate biopsies.
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| 7. |
- Epstein, JI
(författare)
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Retraction
- 2016
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Ingår i: Pathology international. - : Wiley. - 1440-1827 .- 1320-5463. ; 66:10, s. 600-602
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Tidskriftsartikel (refereegranskat)
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| 8. |
- Takahashi, Reisuke H., et al.
(författare)
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Plaque formation and the intraneuronal accumulation of β-amyloid in Alzheimer's disease
- 2017
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Ingår i: Pathology International. - : Wiley. - 1320-5463. ; 67:4, s. 185-193
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Forskningsöversikt (refereegranskat)abstract
- Amyloid plaques and neurofibrillary tangles (NFTs) in the brain are the neuropathological hallmarks of Alzheimer's disease (AD). Amyloid plaques are composed of β-amyloid peptides (Aβ), while NFTs contain hyperphosphorylated tau proteins. Patients with familial AD who have mutations in the amyloid precursor protein (APP) gene have either increased production of Aβ or generate more aggregation-prone forms of Aβ. The findings of familial AD mutations in the APP gene suggest that Aβ plays a central role in the pathophysiology of AD. Aβ42, composed of 42 amino acid residues, aggregates readily and is considered to form amyloid plaque. However, the processes of plaque formation are still not well known. It is generally thought that Aβ is secreted into the extracellular space and aggregates to form amyloid plaques. Aβ as extracellular aggregates and amyloid plaques are thought to be toxic to the surrounding neurons. The intraneuronal accumulation of Aβ has more recently been demonstrated and is reported to be involved in synaptic dysfunction, cognitive impairment, and the formation of amyloid plaques in AD. We herein provide an overview of the process of the intraneuronal accumulation of Aβ and plaque formation, and discuss its implications for the pathology, early diagnosis, and therapy of AD.
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