Σάββατο, 23 Μαρτίου 2019

Cancer, Anatomy, Pathology

Pathology International
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ScienceDirect Publication: Acta Histochemica
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ScienceDirect Publication: Pathology - Research and Practice
Wed Mar 06, 2019 12:13
  Tankyrase1 antisense oligodeoxynucleotides suppress the proliferation, migration and invasion through Hippo/YAP pathway in human osteosarcoma cells
via ScienceDirect Publication: Pathology - Research and Practice
Publication date: Available online 5 March 2019

Source: Pathology - Research and Practice

Author(s): Yichi Zhou, Qi Jin, Wei Xiao, Chengjun Sun

Abstract
Osteosarcoma is the most common malignant tumor of bone with a high potential for metastasis and poor prognosis. This study intends to explore the effect of tankyrase1 (TANK1) in the development of osteosarcoma cells and the underlying mechanism. The osteosarcoma cell line MG-63 cells were cultured and transfected with tankyrase1 antisense oligodeoxynucleotides (TANK1-ASODN). Cell proliferation was detected with CCK-8 and immunofluorescence. Cell migration and invasion were examined by wound healing assay and Transwell assay, respectively. Reverse transcription-quantitative polymerase chain reaction was performed to detect the mRNA level of TANK1 and western blot was conducted to detect relative protein expression during the research. As a result, we demonstrated that TANK1 was upregulated in osteosarcoma. The TANK1-ASODN inhibited MG-63 cell proliferation, migration and invasion. The progress of epithelial-mesenchymal transition (EMT) was also suppressed in TANK1-ASODN transfected MG-63 cells compared to control group. Besides, the TANK1-ASODN activated and modulated the Hippo/YAP signaling which might be the pathway that TANK1 depended on. Overall, our finding supported that TANK1-ASODN slowed down the progress of osteosarcoma by suppressing cell proliferation, migration, invasion and EMT through Hippo/YAP pathway.

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The Journal of Pathology
Wed Mar 06, 2019 19:44
  Atypical ductal hyperplasia is a multipotent precursor of breast carcinoma
by Tanjina Kader, Prue Hill, Magnus Zethoven, David L. Goode, Kenneth Elder, Niko Thio, Maria Doyle, Timothy Semple, Wajiha Sufyan, David J. Byrne, Jia‐Min B. Pang, Anand Murugasu, Islam M Miligy, Andrew R Green, Emad A Rakha, Stephen B. Fox, G. Bruce Mann, Ian G. Campbell, Kylie L. Gorringe via The Journal of Pathology
Abstract
The current model for breast cancer progression proposes independent "low‐grade (LG) like" and "high‐grade (HG) like" pathways but lacks a known precursor to HG cancer. We applied low coverage whole genome sequencing to atypical ductal hyperplasia (ADH) with and without carcinoma to shed light on breast cancer progression. 14/20 isolated ADH cases harboured at least one copy number alteration (CNA), but had fewer aberrations than LG or HG ductal carcinoma in situ (DCIS). ADH carried more HG‐like CNA than LG DCIS (eg. 8q gain). Correspondingly, 64% (7/11) of ADH cases with synchronous HG carcinoma were clonally related, similar to LG carcinoma (67%, 6/9). This study represents a significant shift in our understanding of breast cancer progression, with ADH as a common precursor lesion to the independent "low‐grade like" and "high‐grade like" pathways. These data suggest that ADH can be a precursor of HG breast cancer and that LG and HG carcinomas can evolve from a similar ancestor lesion. We propose that although LG DCIS may be committed to a LG molecular pathway, ADH may remain multipotent, progressing to either LG or HG carcinoma. This multipotent nature suggests that some ADH could be more clinically significant than LG DCIS, requiring biomarkers for personalising management.

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Tue Mar 05, 2019 21:09
  List of Reviewers
via The Journal of Pathology
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Tue Mar 05, 2019 20:34
  Genomic landscape of inverted urothelial papilloma and urothelial papilloma of the bladder
by Sumit Isharwal, Wenhuo Hu, Judy Sarungbam, Ying‐bei Chen, Anuradha Gopalan, Samson W Fine, Satish K Tickoo, Sahussapont J. Sirintrapun, Sana Jadallah, Florence L. Loo, Eugene J Pietzak, Eugene K Cha, Bernard H Bochner, Michael F Berger, Gopa Iyer, David B Solit, Victor E Reuter, Hikmat Al‐Ahmadie via The Journal of Pathology
Abstract
Inverted urothelial papilloma (IUP) and urothelial papilloma (UP) are rare urothelial neoplasms that typically follow a benign clinical course. Oncogenic mutations in FGFR3, HRAS and the TERT promoter have been reported in these entities but no comprehensive molecular analysis has been performed. We sought to characterize the genomic landscape of IUP and UP using whole exome and targeted next generation sequencing. In IUP, 10 of 11 tumors harbored oncogenic hotspot mutations in HRAS and the remaining tumor had an oncogenic KRAS mutation. None of the IUP tumors harbored TERT promoter or FGFR3 mutations. In UP, 8 of 11 tumors had oncogenic KRAS mutations and 2 had oncogenic HRAS mutations. One UP tumor had oncogenic mutations in FGFR3, PIK3CA and the TERT promoter and arose in a patient with recurrent non‐invasive papillary urothelial carcinomas. In contrast to urothelial carcinoma, the APOBEC mutational signature was not present in any IUP and UP tumors and oncogenic alterations in chromatin remodeling genes were uncommon in both IUP and UP. The current study suggests that IUP and UP are driven primarily by RAS pathway activation and lack the more common genomic features of urothelial cancers.

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Tue Mar 05, 2019 19:59
  Why is Pancreatic Cancer so Deadly? The Pathologist's View
by Ralph H. Hruban, Matthias M. Gaida, Elizabeth Thompson, Seung‐Mo Hong, Michaël Nöe, Lodewijk A.A. Brosens, Martine Jongepier, G. Johan A. Offerhaus, Laura D. Wood via The Journal of Pathology
Abstract
The remarkable aggressiveness of pancreatic cancer has never been fully explained. Although clearly multifactorial, we postulate that venous invasion, a finding seen in most pancreatic cancers but not in most cancers of other organs, may be a significant, underappreciated, contributor to the aggressiveness of this disease.

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