scholarly journals Theranostic Role of 32P-ATP as Radiopharmaceutical for the Induction of Massive Cell Death within Avascular Tumor Core

Theranostics ◽  
2017 ◽  
Vol 7 (18) ◽  
pp. 4399-4409 ◽  
Author(s):  
Mirco Galiè ◽  
Federico Boschi ◽  
Ilaria Scambi ◽  
Flavia Merigo ◽  
Pasquina Marzola ◽  
...  
Author(s):  
Natalia V. Dorogova ◽  
Yuliya A. Galimova ◽  
Elena Us. Bolobolova ◽  
Elina M. Baricheva ◽  
Svetlana A. Fedorova

Apmis ◽  
2008 ◽  
Vol 116 (5) ◽  
pp. 417-417
Author(s):  
Marie S. Ostenfeld ◽  
Jesper B. Bramsen ◽  
Jørgen Kjems ◽  
Torben Ørntoft ◽  
Lars Dyrskjøt

BMC Cancer ◽  
2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Ancély F. dos Santos ◽  
Letícia F. Terra ◽  
Rosangela A. M. Wailemann ◽  
Talita C. Oliveira ◽  
Vinícius de Morais Gomes ◽  
...  

Apmis ◽  
2008 ◽  
Vol 116 (5) ◽  
pp. 417-417
Author(s):  
Marie S. Ostenfeld ◽  
Jesper B. Bramsen ◽  
Jørgen Kjems ◽  
Torben Ørntoft ◽  
Lars Dyrskjøt

2021 ◽  
Vol 11 ◽  
Author(s):  
Benedikt Linder ◽  
Abigail Schiesl ◽  
Martin Voss ◽  
Franz Rödel ◽  
Stephanie Hehlgans ◽  
...  

PurposeDexamethasone (Dex) is the most common corticosteroid to treat edema in glioblastoma (GBM) patients. Recent studies identified the addition of Dex to radiation therapy (RT) to be associated with poor survival. Independently, Tumor Treating Fields (TTFields) provides a novel anti-cancer modality for patients with primary and recurrent GBM. Whether Dex influences the efficacy of TTFields, however, remains elusive.MethodsHuman GBM cell lines MZ54 and U251 were treated with RT or TTFields in combination with Dex and the effects on cell counts and cell death were determined via flow cytometry. We further performed a retrospective analysis of GBM patients with TTFields treatment +/- concomitant Dex and analysed its impact on progression-free (PFS) and overall survival (OS).ResultsThe addition of Dex significantly reduced the efficacy of RT in U251, but not in MZ54 cells. TTFields (200 kHz/250 kHz) induced massive cell death in both cell lines. Concomitant treatment of TTFields and Dex did not reduce the overall efficacy of TTFields. Further, in our retrospective clinical analysis, we found that the addition of Dex to TTFields therapy did not influence PFS nor OS.ConclusionOur translational investigation indicates that the efficacy of TTFields therapy in patients with GBM and GBM cell lines is not affected by the addition of Dex.


2017 ◽  
Vol 214 (6) ◽  
pp. 1655-1662 ◽  
Author(s):  
Gui-Wei He ◽  
Claudia Günther ◽  
Veronika Thonn ◽  
Yu-Qiang Yu ◽  
Eva Martini ◽  
...  

Cancer cells often acquire capabilities to evade cell death induced by current chemotherapeutic treatment approaches. Caspase-8, a central initiator of death receptor–mediated apoptosis, for example, is frequently inactivated in human cancers via multiple mechanisms such as mutation. Here, we show an approach to overcome cell death resistance in caspase-8–deficient colorectal cancer (CRC) by induction of necroptosis. In both a hereditary and a xenograft mouse model of caspase-8–deficient CRC, second mitochondria-derived activator of caspase (SMAC) mimetic treatment induced massive cell death and led to regression of tumors. We further demonstrate that receptor-interacting protein kinase 3 (RIP3), which is highly expressed in mouse models of CRC and in a subset of human CRC cell lines, is the deciding factor of cancer cell susceptibility to SMAC mimetic–induced necroptosis. Thus, our data implicate that it may be worthwhile to selectively evaluate the efficacy of SMAC mimetic treatment in CRC patients with caspase-8 deficiency in clinical trials for the development of more effective personalized therapy.


Oncotarget ◽  
2015 ◽  
Vol 7 (1) ◽  
pp. 433-445 ◽  
Author(s):  
Setareh Safavi ◽  
Sofia Järnum ◽  
Christoffer Vannas ◽  
Sameer Udhane ◽  
Emma Jonasson ◽  
...  

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