A phase II study of PS-341 (Bortezomib) in advanced or metastatic urothelial cancer. A trial of the Princess Margaret Hospital and University of Chicago phase II consortia

Gomez-Abuin, Gonzalo; Winquist, Eric; Stadler, Walter M.; Pond, Greg; Degendorfer, Pamela; Wright, John J.; Moore, Malcolm J.

doi:10.1007/s10637-006-9009-4

Cited by 33 publications

(19 citation statements)

References 13 publications

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“…61 To our knowledge, there is limited experience with targeted agents in previously treated patients with UC; the reports on a pair of phase 2 studies have been disappointing. 62,63 There were no significant responses noted among 20 patients treated with the proteosome inhibitor bortezomib, and there were only 2 PRs reported among 59 patients treated with lapatinib, an erb-B2 and EGFR dual tyrosine kinase inhibitor.…”

Section: Targeted Therapy In Ucmentioning

confidence: 99%

Advanced bladder cancer: Status of first‐line chemotherapy and the search for active agents in the second‐line setting

Gallagher

Milowsky

Bajorin

2008

Cancer

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Section: Targeted Therapy In Ucmentioning

confidence: 99%

Advanced bladder cancer: Status of first‐line chemotherapy and the search for active agents in the second‐line setting

Gallagher

Milowsky

Bajorin

2008

Cancer

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“…However, in contrast to its effectiveness in the treatment of multiple myeloma and mantle cell lymphoma, this inhibitor had an unfortunate lack of efficacy in several types of solid tumors in clinical trials (59)(60)(61)(62)(63). Interestingly, (cancer) stem cells have been reported to be associated with elevated expression of anti-apoptotic proteins such as Bcl2, which makes them more permissive for oncogenic transformation (64,65).…”

Section: Proteasome Activity As a Csc Markermentioning

confidence: 99%

Cancer stem cells don’t waste their time cleaning—low proteasome activity, a marker for cancer stem cell function

Lenos¹,

Vermeulen²

2016

Ann. Transl. Med.

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A population of stem-like cells in tumors, the so-called cancer stem cells (CSCs), are being held responsible for therapy resistance and tumor recurrence. In analogy with normal stem cells, CSCs possess the capacity of long term self-renewal and multilineage differentiation. CSCs are believed to be more resistant to various therapies compared to their differentiated offspring and therefore the cause of tumor relapse. Markers for CSCs have been identified using xenograft transplantation assays and lineage tracing in mouse models, however the specificity and validity of many of these markers is under debate. Recently, low proteasome activity has been postulated as a novel CSC marker. In several solid malignancies a small subset of low proteasomal activity cells with CSC characteristics were identified, suggesting that proteasomal activity might be a functional marker for CSCs. In this perspective, we will discuss a recent study by Munakata et al., describing a population of colorectal cancer cells with CSC properties, characterized by low proteasome activity and treatment resistance. We will put this finding in a broader view by discussing the challenges and issues inherent with CSC identification, as well as some emerging insights in the CSC concept.

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“…Despite preclinical activity and synergy with gemcitabine, it was shown to lack second-line clinical activity (70). Polo-like kinases (PlK) regulate cell-cycle progression and mitosis.…”

Section: Other Targeted Therapiesmentioning

confidence: 99%

New Directions for Biologic Targets in Urothelial Carcinoma

Richter

Sridhar

2012

Molecular Cancer Therapeutics

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Urothelial carcinoma remains an important oncologic problem with significant morbidity and mortality. This article provides an overview of the current status of treatment of urothelial carcinoma, with an update on current trials and recent American Society of Clinical Oncology abstracts. As an alternative to focusing on the metastatic setting, we take a broad look at drug development to date, as it spans from early disease to advanced disease in the context of emerging molecular data. This approach allows us to show that each stage involves key considerations based on emerging evidence regarding molecular biology, stage-specific novel endpoints, and rational patient selection that may help further trial designs in the future. Key issues, such as neoadjuvant versus adjuvant perioperative chemotherapy, approaches to salvage second-line therapy in the metastatic setting, and treatment of elderly and cisplatin-ineligible patients, are discussed. New paradigms in clinical research, including novel endpoints, upfront rational patient selection, biomarkers, and trial design, are also addressed. Mol Cancer Ther; 11(6); 1226-35. Ó2012 AACR.

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A phase II study of PS-341 (Bortezomib) in advanced or metastatic urothelial cancer. A trial of the Princess Margaret Hospital and University of Chicago phase II consortia

Abstract: Single-agent bortezomib is an ineffective treatment for progressive-cisplatin-refractory urothelial carcinoma and should not be considered for future clinical trials in this population of patients.

Cited by 33 publications

References 13 publications

Advanced bladder cancer: Status of first‐line chemotherapy and the search for active agents in the second‐line setting

Advanced bladder cancer: Status of first‐line chemotherapy and the search for active agents in the second‐line setting

Cancer stem cells don’t waste their time cleaning—low proteasome activity, a marker for cancer stem cell function

New Directions for Biologic Targets in Urothelial Carcinoma

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