scholarly journals A 3D topographical model of parenchymal infiltration and perivascular invasion in glioblastoma

2018 ◽  
Vol 2 (3) ◽  
pp. 031903 ◽  
Author(s):  
Kayla J. Wolf ◽  
Stacey Lee ◽  
Sanjay Kumar
2019 ◽  
Vol 98 (5-8) ◽  
pp. 151046 ◽  
Author(s):  
Roxana Solga ◽  
Juliane Behrens ◽  
Anja Ziemann ◽  
Adrien Riou ◽  
Carolin Berwanger ◽  
...  

2016 ◽  
Author(s):  
Benjamin Krusche ◽  
Cristina Ottone ◽  
Melanie P Clements ◽  
Ewan R Johnstone ◽  
Katrin Goetsch ◽  
...  

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Go Asano ◽  
Katsuyuki Miyabe ◽  
Hiroyuki Kato ◽  
Michihiro Yoshida ◽  
Takeshi Sawada ◽  
...  

AbstractWe aimed to assess some of the potential genetic pathways for cancer development from non-malignant intraductal papillary mucinous neoplasm (IPMN) by evaluating genetic mutations and methylation. In total, 46 dissected regions in 33 IPMN cases were analyzed and compared between malignant-potential and benign cases, or between malignant-potential and benign tissue dissected regions including low-grade IPMN dissected regions accompanied by malignant-potential regions. Several gene mutations, gene methylations, and proteins were assessed by pyrosequencing and immunohistochemical analysis. RASSF1A methylation was more frequent in malignant-potential dissected regions (p = 0.0329). LINE-1 methylation was inversely correlated with GNAS mutation (r =  − 0.3739, p = 0.0105). In cases with malignant-potential dissected regions, GNAS mutation was associated with less frequent perivascular invasion (p = 0.0128), perineural invasion (p = 0.0377), and lymph node metastasis (p = 0.0377) but significantly longer overall survival, compared to malignant-potential cases without GNAS mutation (p = 0.0419). The presence of concordant KRAS and GNAS mutations in the malignant-potential and benign dissected regions were more frequent among branch-duct IPMN cases than among the other types (p = 0.0319). Methylation of RASSF1A, CDKN2A, and LINE-1 and GNAS mutation may be relevant to cancer development, IPMN subtypes, and cancer prognosis.


2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 1049-1049
Author(s):  
Elisabetta Munzone ◽  
Edoardo Botteri ◽  
Vincenzo Bagnardi ◽  
Angela Sciandivasci ◽  
Gaetano Aurilio ◽  
...  

1049 Background: TNBC represent a heterogeneous disease in terms of biology, prognosis, and treatment response. We propose a prognostic model to identify homogeneous subgroups of patients and tailor risk-adapted adjuvant therapies indications. Methods: We analyzed 1,049 pts operated in our institute from 1997 to 2007 for early TNBC. Pts who received neoadjuvant chemotherapy (CT), with T4 tumors or previous history of cancer were excluded. Death from BC was the primary endpoint of the study. We calculated an individual predicted risk using a multivariable Cox regression model, with age, tumor size, number of positive lymph nodes and Ki-67 analyzed as continuous covariates, and tumor grade and perivascular invasion as categorical covariates. Results: Median age was 52 years, 562 (53.4%) and 670 (65.1%) pts had a pT1 and pN0 TNBC, respectively. Median Ki-67 was 48%. Adjuvant CT regimens were distributed as follows: classical CMF 388 (37.0%), anthracycline containing regimens 455 (43.4%), taxanes 12 (1.1%), other regimens 66 (6.3%) and no CT 128 (12.2%). After a median follow-up of 6 years, 131 deaths from BC were observed (5-year cumulative incidence 11.9%). At multivariable analysis, age, tumor size, number of positive lymph nodes, Ki-67, tumor grade and perivascular invasion were associated with the risk of death and were included in the prognostic model. Its predictive accuracy was good (C-index 0.73). We subsequently identified three homogeneous prognostic subgroups - low, medium and high-risk - according to the tertiles values of the predicted risk. The outcomes are shown in the table. Conclusions: We could identify homogeneous prognostic subgroups of TNBC pts according to clinical-pathological features. This prognostic model suggests that the use of CT in TN low-risk pts might be questionable. We are currently externally validating this model on a different series of pts. [Table: see text]


2014 ◽  
Vol 32 (15_suppl) ◽  
pp. 2057-2057
Author(s):  
Gregory Joseph Baker ◽  
Viveka Nand Yadav ◽  
Sebastien Motsch ◽  
Carl Johannes Koschmann ◽  
Anda-Alexandra Calinescu ◽  
...  

Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 18 ◽  
Author(s):  
Simone Pacioni ◽  
Quintino Giorgio D’Alessandris ◽  
Mariachiara Buccarelli ◽  
Alessandra Boe ◽  
Maurizio Martini ◽  
...  

The question whether perivascular glioma cells invading the brain far from the tumor bulk may disrupt the blood–brain barrier (BBB) represents a crucial issue because under this condition tumor cells would be no more protected from the reach of chemotherapeutic drugs. A recent in vivo study that used human xenolines, demonstrated that single glioma cells migrating away from the tumor bulk are sufficient to breach the BBB. Here, we used brain xenografts of patient-derived glioma stem-like cells (GSCs) to show by immunostaining that in spite of massive perivascular invasion, BBB integrity was preserved in the majority of vessels located outside the tumor bulk. Interestingly, the tumor cells that invaded the brain for the longest distances traveled along vessels with retained BBB integrity. In surgical specimens of malignant glioma, the area of brain invasion showed several vessels with preserved BBB that were surrounded by tumor cells. On transmission electron microscopy, the cell inter-junctions and basal lamina of the brain endothelium were preserved even in conditions in which the tumor cells lay adjacently to blood vessels. In conclusion, BBB integrity associates with extensive perivascular invasion of glioma cells.


2012 ◽  
Vol 54 (8) ◽  
pp. 1162-1165 ◽  
Author(s):  
Nicolas Dupin ◽  
Hervé Lecuyer ◽  
Agnès Carlotti ◽  
Claire Poyart ◽  
Mathieu Coureuil ◽  
...  

Oncotarget ◽  
2016 ◽  
Vol 7 (50) ◽  
pp. 83701-83719 ◽  
Author(s):  
Viveka Nand Yadav ◽  
Daniel Zamler ◽  
Gregory J. Baker ◽  
Padma Kadiyala ◽  
Anat Erdreich-Epstein ◽  
...  

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