Use of irinotecan for treatment of small cell carcinoma of the prostate

Tung, Wei Lin; Wang, Yuwei; Gout, Peter W.; LIu, Dean-Mo; Gleave, Martin; Wang, Yuzhuo

doi:10.1002/pros.21283

Cited by 26 publications

(19 citation statements)

References 30 publications

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“…In a phase III trial, the combination of 5-fluouracil, leucovorin, oxaliplatin, and irinotecan resulted in better responses, progression-free survival, and overall survival when compared with the standard single drug therapy with gemcitabine for metastatic pancreatic ductal adenocarcinoma [97]. In small-cell prostatic carcinoma, irinotecan promoted an increase in autophagy of treated tumors as indicated by an increase in LC3B expression [98, 99]. Nevertheless, authors of this research state that the role of autophagy is complex.…”

Section: The Reverse Warburg Effect In Cancer: Pharmacological Modmentioning

confidence: 99%

“…In general, as mentioned before, a considerable amount of caution should be exercised for the interpretation of the consequences of cancer chemotherapy on autophagy. Other chemotherapeutic agents like the glycoside oleandrin, some platinum compounds, the multikinase inhibitor sorafenib, and some histone-deacetylase inhibitors have demonstrated effects on the autophagy rate in pancreatic carcinoma cell lines [98, 99]. As proposed, autophagy may be involved in carcinogenesis, tumor progression, and dissemination and may be associated at least in part with the actions of some chemotherapy for pancreatic ductal adenocarcinoma as well.…”

Section: The Reverse Warburg Effect In Cancer: Pharmacological Modmentioning

confidence: 99%

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Autophagy, Warburg, and Warburg Reverse Effects in Human Cancer

González

Álvarez

Ropolo

et al. 2014

BioMed Research International

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Autophagy is a highly regulated-cell pathway for degrading long-lived proteins as well as for clearing cytoplasmic organelles. Autophagy is a key contributor to cellular homeostasis and metabolism. Warburg hypothesized that cancer growth is frequently associated with a deviation of a set of energy generation mechanisms to a nonoxidative breakdown of glucose. This cellular phenomenon seems to rely on a respiratory impairment, linked to mitochondrial dysfunction. This mitochondrial dysfunction results in a switch to anaerobic glycolysis. It has been recently suggested that epithelial cancer cells may induce the Warburg effect in neighboring stromal fibroblasts in which autophagy was activated. These series of observations drove to the proposal of a putative reverse Warburg effect of pathophysiological relevance for, at least, some tumor phenotypes. In this review we introduce the autophagy process and its regulation and its selective pathways and role in cancer cell metabolism. We define and describe the Warburg effect and the newly suggested “reverse” hypothesis. We also discuss the potential value of modulating autophagy with several pharmacological agents able to modify the Warburg effect. The association of the Warburg effect in cancer and stromal cells to tumor-related autophagy may be of relevance for further development of experimental therapeutics as well as for cancer prevention.

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Section: The Reverse Warburg Effect In Cancer: Pharmacological Modmentioning

confidence: 99%

Section: The Reverse Warburg Effect In Cancer: Pharmacological Modmentioning

confidence: 99%

Autophagy, Warburg, and Warburg Reverse Effects in Human Cancer

González

Álvarez

Ropolo

et al. 2014

BioMed Research International

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“…To overcome this hurdle, we have developed transplantable, metastatic and nonmetastatic patient-derived prostate cancer tissue xenograft lines in NOD-SCID (nonobese diabetic/severe combined immunodeficient) mice. The subrenal capsule grafting technique used to develop such cancer tissue lines tends to retain important properties of the original cancers, including histopathology, chromosomal aberrations and gene expression profiles, resulting in xenograft lines that closely resemble the original cancers 789. Recently, we have developed paired metastatic (LTL-313H) and nonmetastatic (LTL-313B) prostate cancer sublines from one patient's specimen, that are suitable for investigating the molecular basis of metastasis 10…”

Section: Introductionmentioning

confidence: 99%

Prostate cancer metastasis-driving genes: hurdles and potential approaches in their identification

2014

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Metastatic prostate cancer is currently incurable. Metastasis is thought to result from changes in the expression of specific metastasis-driving genes in nonmetastatic prostate cancer tissue, leading to a cascade of activated downstream genes that set the metastatic process in motion. Such genes could potentially serve as effective therapeutic targets for improved management of the disease. They could be identified by comparative analysis of gene expression profiles of patient-derived metastatic and nonmetastatic prostate cancer tissues to pinpoint genes showing altered expression, followed by determining whether silencing of such genes can lead to inhibition of metastatic properties. Various hurdles encountered in this approach are discussed, including (i) the need for clinically relevant, nonmetastatic and metastatic prostate cancer tissues such as xenografts of patients’ prostate cancers developed via subrenal capsule grafting technology and (ii) limitations in the currently available methodology for identification of master regulatory genes.

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“…Use of LTL352, a transplantable tissue line developed from a patient's NEPC specimen, has indicated that irinotecan, a topoisomerase I inhibitor, is potentially useful for therapy of refractory NEPC, in particular in combination with cisplatin 60. Recently the LTL352 model was also used to determine the efficacy of a new aurora kinase inhibitor, PHA-739358, in NEPC 61.…”

Section: Applications Of Next Generation Prostate Cancer Xenograft Momentioning

confidence: 99%

Next generation patient-derived prostate cancer xenograft models

et al. 2014

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There is a critical need for more effective therapeutic approaches for prostate cancer. Research in this area, however, has been seriously hampered by a lack of clinically relevant, experimental in vivo models of the disease. This review particularly focuses on the development of prostate cancer xenograft models based on subrenal capsule grafting of patients’ tumor tissue into nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. This technique allows successful development of transplantable, patient-derived cancer tissue xenograft lines not only from aggressive metastatic, but also from localized prostate cancer tissues. The xenografts have been found to retain key biological properties of the original malignancies, including histopathological and molecular characteristics, tumor heterogeneity, response to androgen ablation and metastatic ability. As such, they are highly clinically relevant and provide valuable tools for studies of prostate cancer progression at cellular and molecular levels, drug screening for personalized cancer therapy and preclinical drug efficacy testing; especially when a panel of models is used to cover a broader spectrum of the disease. These xenograft models could therefore be viewed as next-generation models of prostate cancer.

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Use of irinotecan for treatment of small cell carcinoma of the prostate

Abstract: Tumor tissue lines established via subrenal capsule xenografting provide models with clinical relevance and the present study suggests that irinotecan could be useful for therapy of refractory prostatic SCC, in particular in combination with cisplatin.

Cited by 26 publications

References 30 publications

Autophagy, Warburg, and Warburg Reverse Effects in Human Cancer

Autophagy, Warburg, and Warburg Reverse Effects in Human Cancer

Prostate cancer metastasis-driving genes: hurdles and potential approaches in their identification

Next generation patient-derived prostate cancer xenograft models

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