scholarly journals A Case of AIDS-Related Malignant Lymphoma Cells Infiltrating Into an Anal Lesion

2014 ◽  
Vol 67 (4) ◽  
pp. 263-267
Author(s):  
Hiromitsu Matsuda ◽  
Ryuichi Mibu ◽  
Takayuki Toyonaga ◽  
Yukio Sonoda ◽  
Hidetoshi Kiyonaga ◽  
...  
1984 ◽  
Vol 72 (6) ◽  
pp. 368-371 ◽  
Author(s):  
D. Huhn ◽  
G. Wochinger ◽  
M. Darsow

2019 ◽  
Author(s):  
Yue-Li Sun Sun ◽  
Wen-Qi Jiang ◽  
Qiu-Yun L uo ◽  
Da-Jun Yang ◽  
Yu-Chen Cai ◽  
...  

2019 ◽  
Author(s):  
Yue-Li Sun ◽  
Wen-Qi Jiang ◽  
Qiu-Yun Luo ◽  
Da-Jun Yang ◽  
Yu-Chen Cai ◽  
...  

Abstract Background: Bcl-2 family members play an important role in the development of malignant lymphoma and can induce drug resistance in anticancer treatment. The development of small molecules targeting Bcl-2 family protein can be new strategy for malignant lymphoma treatment. In this study, we investigate the antitumor effect and the cellular mechanism of a novel Bcl-2/Bcl-xL dual inhibitor BM-1197 in DCBCL and Burkitt lymphoma cells. Methods: CCK-8 assay was used to detect cell viability. Apoptosis was determined by Hoechst 33258 staining and flow cytometry. The activity of caspase-3/caspase-9 was determined using the caspase-3/ caspase-9 activity kit. Western blotting analysis was performed to evaluate the change of protein expression. The functional analysis was evalueated via immunoprecipitation and siRNA interference. Human malignant lymphoma xenograft models in nude mice were established for in vivo efficacy detection. Results: We find that BM-1197 exerts potent growth-inhibitory activity against lymphoma cells which harbor Bcl-2 and Bcl-xL high expression in vitro and has synergistic effect with chemotherapeutic drugs. Mechanistically, we see that the intrinsic apoptosis pathway is activated upon BM-1197 treatment. BM-1197 affects the protein interaction of Bak/Bcl-xl, Bim/Bcl-2, Bim/Bcl-xl, PUMA/Bcl-2 and induced conformational change in the Bax protein.which results in activation of Bax and release cytochrome c, and activated caspase -9, -3, -7 and finally induce cell apoptosis. Furthermore, our data demonstrates that BM-1197 exhibits strong anti-tumor effects against established human malignant lymphoma xenograft models. Conclusions: Our study demonstrated BM-1197 exerts potent antitumor effects both in vitro and in vivo, and provides promising preclinical data for further development of BM-1197 in malignant lymphoma.


Neurosurgery ◽  
1989 ◽  
Vol 25 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Shobu Shibata

Abstract With the aim of finding characteristics pointing to the primary site, computed tomography examination from 9 patients with primary brain malignant lymphoma (non-Hodgkin's lymphoma originating in the central nervous system, NHL-CNS) (5 single, 4 multiple lesions) were analyzed. The tumors were usually situated in the basal ganglia, corpus callosum, or cerebellum and were always in contact with either the ependyma of the ventricles or the subarachnoid space. Tumors with widespread infiltration of white matter surrounding the ventricles were characteristic of NHL-CNS. Microscopic examination of 3 autopsy cases revealed infiltration of the subependymal layer of the lateral ventricles and the third and fourth ventricles by lymphoma cells. The entire extent of the choroid plexus was invaded by tumor cells. There were multiple foci of similar cells invading the periventricular white matter. The subarachnoid space was filled with lymphoma cells. In many areas the Virchow-Robin spaces and pial-glial membranes were disrupted, and invasion of the underlying gray matter by tumor cells was seen. The ultrastructure of the blood vessels of NHL-CNS was compared with those in glial, nonglial, and metastatic brain tumors. The essential feature in NHL-CNS was fenestrated vessels. They resembled the blood vessels found in nonglial and metastatic brain tumors, but were distinctly different from those seen in glial tumors with nonfenestrated vessels. Although the following scheme in proposed with reservations, it could account for the sites of origin of NHL-CNS: lymphocytes located in the choroid plexus stroma or the subarachnoid space are activated, caused to proliferate, and finally become neoplastic. Then these cells migrate through the underlying parenchyma along the Virchow-Robin spaces and multiply until they present themselves as primary brain tumors.


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