Amanda Kirane
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Amanda Kirane has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Roderich E. Schwarz
Division of Surgical Oncology, Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, Texas, United States of America
2 shared publications - Gene E Ewing
Department of Pathology, UT Southwestern Medical Center, Dallas, TX, USA
1 shared publication - Jason E. Toombs
UT Southwestern Medical Center
1 shared publication - Jean J Bao
Department of Surgery, Division of Surgical Oncology, UT Southwestern Medical Center, Dallas, TX, USA
1 shared publication - John C. Mansour
Department of Surgery, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center (UTSW), Dallas, Texas
1 shared publication - Margaret A. Schwarz
Department of Pediatrics
1 shared publication
Latest Publications
- Open Access
- 20 April 2012
- Published by Springer Nature in World Journal of Surgical Oncology
- Vol. 10 (1) , 59
Intraduodenal sarcoma recurrence of retroperitoneal origin: an unusual cause for a duodenal obstruction
Soft tissue sarcomas are uncommon tumors, and intraduodenal soft tissue sarcoma manifestation is even more rare. Only three cases of intraduodenal sarcomas have been reported in the literature thus far. Here, we report a case of an intraduodenal recurrence of a retroperitoneal sarcoma causing bowel obstruction. This unusual recurrence pattern likely relates to the patient’s previous resection and radiation treatment, and highlights the benefits, limitations and follow-up strategies after multimodality treatment.
- 20 April 2012
- Published by Springer Nature in World Journal of Surgical Oncology
- Vol. 10 (1) , 59
Open AccessIntraduodenal sarcoma recurrence of retroperitoneal origin: an unusual cause for a duodenal obstruction
Soft tissue sarcomas are uncommon tumors, and intraduodenal soft tissue sarcoma manifestation is even more rare. Only three cases of intraduodenal sarcomas have been reported in the literature thus far. Here, we report a case of an intraduodenal recurrence of a retroperitoneal sarcoma causing bowel obstruction. This unusual recurrence pattern likely relates to the patient’s previous resection and radiation treatment, and highlights the benefits, limitations and follow-up strategies after multimodality treatment.
- Open Access
- 12 January 2011
- Published by Springer Nature in BMC Cancer
- Vol. 11 (1) , 15
Smac mimetic-derived augmentation of chemotherapeutic response in experimental pancreatic cancer
Background: Pancreatic ductal adenocarcinoma (PDAC) is highly resistant to conventional chemotherapy, in part due to the overexpression of inhibitors of apoptosis proteins (IAPs). Smac is an endogenous IAP-antagonist, which renders synthetic Smac mimetics attractive anticancer agents. We evaluated the benefits of combining a Smac mimetic, JP1201 (JP), with conventional chemotherapy agents used for PDAC management. Methods: Cell viability assays and protein expression analysis were performed using WST-1 reagent and Western blotting, respectively. Apoptosis was detected by annexin V/propidium iodide staining. In vivo tumor growth and survival studies were performed in murine PDAC xenografts. Results: JP and gemcitabine (Gem) inhibited PDAC cell proliferation with additive effects in combination. The percentage of early apoptotic cells in controls, JP, Gem and JP + Gem was 17%, 26%, 26% and 38%, respectively. JP-induced apoptosis was accompanied by PARP-1 cleavage. Similar additive anti-proliferative effects were seen for combinations of JP with doxorubicin (Dox) and docetaxel (DT). The JP + Gem combination caused a 30% decrease in tumor size in vivo compared to controls. Median animal survival was improved significantly in mice treated with JP + Gem (38 d) compared to controls (22 d), JP (28 d) or Gem (32 d) (p = 0.01). Animal survival was also improved with JP + DT treatment (32 d) compared to controls (16 d), JP (21 d) or DT alone (27 d). Conclusions: These results warrant further exploration of strategies that promote chemotherapy-induced apoptosis of tumors and highlight the potential of Smac mimetics in clinical PDAC therapy.
- 12 January 2011
- Published by Springer Nature in BMC Cancer
- Vol. 11 (1) , 15
Open AccessSmac mimetic-derived augmentation of chemotherapeutic response in experimental pancreatic cancer
Background: Pancreatic ductal adenocarcinoma (PDAC) is highly resistant to conventional chemotherapy, in part due to the overexpression of inhibitors of apoptosis proteins (IAPs). Smac is an endogenous IAP-antagonist, which renders synthetic Smac mimetics attractive anticancer agents. We evaluated the benefits of combining a Smac mimetic, JP1201 (JP), with conventional chemotherapy agents used for PDAC management. Methods: Cell viability assays and protein expression analysis were performed using WST-1 reagent and Western blotting, respectively. Apoptosis was detected by annexin V/propidium iodide staining. In vivo tumor growth and survival studies were performed in murine PDAC xenografts. Results: JP and gemcitabine (Gem) inhibited PDAC cell proliferation with additive effects in combination. The percentage of early apoptotic cells in controls, JP, Gem and JP + Gem was 17%, 26%, 26% and 38%, respectively. JP-induced apoptosis was accompanied by PARP-1 cleavage. Similar additive anti-proliferative effects were seen for combinations of JP with doxorubicin (Dox) and docetaxel (DT). The JP + Gem combination caused a 30% decrease in tumor size in vivo compared to controls. Median animal survival was improved significantly in mice treated with JP + Gem (38 d) compared to controls (22 d), JP (28 d) or Gem (32 d) (p = 0.01). Animal survival was also improved with JP + DT treatment (32 d) compared to controls (16 d), JP (21 d) or DT alone (27 d). Conclusions: These results warrant further exploration of strategies that promote chemotherapy-induced apoptosis of tumors and highlight the potential of Smac mimetics in clinical PDAC therapy.