Search Results

You are looking at 31 - 37 of 37 items for :

Clear All
Open access

Tanja Dolinsek, Lara Prosen, Maja Cemazar, Tjasa Potocnik and Gregor Sersa

radiosensitization of BRAF mutated melanoma cells with BRAF inhibitor PLX-4032 by clonogenic and invasion assay and was associated with enhancement of G1 cell cycle arrest. 15 Furthermore, the combination of BRAF inhibitor and irradiation was proven to be effective also in high-grade gliomas, harboring BRAF V600E mutation. Radiosensitization was observed by PLX-4720 BRAF inhibitor in vitro , whereas in BRAF non-mutated glioma cells the radiosensitizing effect was not observed. 16 The clinical studies, however, demonstrated the radiosensitization of normal tissue as well. There

Open access

Lina Savsek and Tanja Ros Opaskar

to chemotherapy and inducing cell cycle arrest. 18 Rituximab can deplete peripheral B cells while B cell precursors and mature plasma cells remain relatively unaffected, allowing for a new population of B cells to develop from lymphoid stem cells. 19 This remarkable activity allowed for its approval by the US Food and Drug Administration (FDA) in 1997 and European Medical Agency (EMA) in 1998 for treatment of CD20 positive cancers, including DLBCL, follicular lymphoma and chronic lymphocytic leukemia. 19 , 20 In addition, it is also widely used in therapy of

Open access

Tomaz Makovec

and cis- [PtCl 2 (NH 3 ) 2 ], with Pt 2+ ion that were effective in arresting the cell division. 1 Rosenberg and his group concluded that compounds capable of inhibiting E. Coli division could also be useful for treating cancer. They found that planar complex which contained Pt 2+ ion with cis configuration - later known as cisplatin - was very effective at arresting sarcoma 180 and leukaemia L1210 cells while trans isomer exhibited little antitumor activity. 1 This observation also led to the discovery of the effectiveness of this compound at regressing

Open access

Tanja Mesti, Nadia Bouchemal, Claire Banissi, Mohamed N. Triba, Carole Marbeuf-Gueye, Maja Cemazar, Laurence Le Moyec, Antoine F. Carpentier, Philippe Savarin and Janja Ocvirk

increase of 9%. GPC and PC have well-documented roles in membrane phospholipid breakdown 17 . Ex vivo MRS studies of brain tumours have identified several biomarkers of tumour growth and apoptosis, among which are increased levels of choline-containing compounds, possibly due to cell membrane disruption and altered phospholipid metabolism. 18 PC and GPC accumulation reflect early stages of growth arrest or apoptosis. 19 The analysis of cisplatin-mediated apoptosis on ovarian cancer cells, showed enhanced apoptosis that was measured by increased PC and GPC

Open access

Peter Popovic, Borut Stabuc, Rado Jansa and Manca Garbajs

. Mean time to progression (TTP) was 10.9 months ± 5.3 months (range, 5.8 – 24.8 months). Overall survival After a mean follow-up period of 27.7 months ± 10.5 months, 17 patients died. One patient died of acute respiratory infection with acute respiratory insufficiency, two of spontaneous bacterial peritonitis with sepsis, one of respiratory arrest, two of toxic encephalopaty, four of progression of HCC and the remaining of liver failure. Mean OS of the whole cohort was 33.9 months (95% CI: 28.9 – 38.9). 1-year survival was 97.1% and 2-year survival was 65

Open access

Matjaz Zwitter, Antonio Rossi, Massimo Di Maio, Maja Pohar Perme and Gilberto Lopes

), but no advantage in overall survival (OS). 15 In spite of prevailing disappointment, some researchers insisted that the negative message of the four large trials should be accepted as new knowledge rather than ignored and developed the concept of intercalated treatment. The reasoning was clear: when applied concomitantly with chemotherapy, TKIs induce G1-phase cell-cycle arrest, due to which cell-cycle dependent chemotherapeutic agents will not be effective. 16 Chemo-refractoriness of cells harboring sensitizing-EGFR mutations in the presence of gefitinib was

Open access

Taja Lozar, Klara Gersak, Maja Cemazar, Cvetka Grasic Kuhar and Tanja Jesenko

blood vessel wall and extravasation. After the arrest of CTCs in the bone marrow or distant organ, they can extravasate and remain in the target tissue in the form of disseminated tumor cell (DTC). CTCs in the circulation Tumor cells can enter the circulation through a blood or lymphatic vessel, depending on a number of factors including their accessibility, physical restrictions and active mechanisms for attracting cells to specific types of vasculature. 18 Lymphatic intravasation is also a pathway by which tumor cells can enter the blood vessels, since