A Phase II Study of Troglitazone, an Activator of the PPAR?? Receptor, in Patients with Chemotherapy-Resistant Metastatic Colorectal Cancer

Kulke, Matthew H.; Demetri, George D.; Sharpless, Norman E.; Ryan, David P.; Shivdasani, Ramesh A.; Clark, Justice; Spiegelman, Bruce M.; Kim, Haesook; Mayer, Robert J.; Fuchs, Charles S.

doi:10.1097/00130404-200209000-00010

Cited by 150 publications

(115 citation statements)

References 17 publications

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“…122 The efficacy of troglitazone was also evaluated in 25 patients with metastatic colorectal carcinoma but all patients had progressive disease. 123 In breast cancer, two human trials have been conducted. In one study, no objective response to troglitazone after 8 weeks of treatment was observed in 22 women with refractory breast cancer.…”

Section: Safety Issues and Pparγ Agonists In Clinical Developmentmentioning

confidence: 99%

Peroxisome proliferator-activated receptor γ in bladder cancer: A promising therapeutic target

Mansure¹,

Nassim²,

Kassouf³

2009

Cancer Biology & Therapy

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Section: Safety Issues and Pparγ Agonists In Clinical Developmentmentioning

confidence: 99%

Peroxisome proliferator-activated receptor γ in bladder cancer: A promising therapeutic target

Mansure¹,

Nassim²,

Kassouf³

2009

Cancer Biology & Therapy

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“…For example, by inducing terminal differentiation in neoplasms, cancer researchers hope to stop abnormal proliferation. Tumor suppressing drugs that were created using this mechanistic understanding are currently in human clinical trials (Kulke et al 2002).…”

Section: Cancer and Embryogenesismentioning

confidence: 99%

Perspective: Embedded Molecular Switches, Anticancer Selection, and Effects on Ontogenetic Rates: A Hypothesis of Developmental Constraint on Morphogenesis and Evolution

Kavanagh

2003

Evolution

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Abstract. The switch between the cell cycle and the progress of differentiation in developmental pathways is prevalent throughout the eukaryotes in all major cell lineages. Disruptions to the molecular signals regulating the switch between proliferative and differentiating states are severe, often resulting in cancer formation (uncontrolled proliferation) or major developmental disorders. Uncontrolled proliferation and developmental disorders are potentially lethal defects in the developing animal. Therefore, natural selection would likely favor a tightly controlled regulatory mechanism to help prevent these fundamental defects. Although selection is usually thought of as a consequence of environmental or ecological influences, in this case the selective force to maintain this molecular switch is internal, manifested as a potentially lethal developmental defect. The morphogenetic consequences of this prevalent, deeply embedded, and tightly controlled mechanistic switch are currently unexplored, however experimental and correlative evidence from several sources suggest that there are important consequences on the control of growth rates and developmental rates in organs and in the whole animal. These observations lead one to consider the possibility of a developmental constraint on ontogenetic rates and morphological evolution maintained by natural selection against cancer and other embryonic lethal defects.

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“…[30][31][32] Consequently, the efficacy of PPAR-g ligands on a variety of nonlipogenic malignancies was tested but, unfortunately, yielded little improvement in outcome. 33,34 Thus, enthusiasm for the use of PPAR-g ligands as differentiation-promoting therapy has somewhat waned. 30 Nevertheless, our study suggests that the vast majority of dedifferentiated liposarcoma retain detectable levels of PPAR-g protein, and re-evaluation of this selected group of sarcomas with therapy targeting PPAR-g may be worthwhile.…”

Section: Discussionmentioning

confidence: 99%

Immunostaining for peroxisome proliferator gamma distinguishes dedifferentiated liposarcoma from other retroperitoneal sarcomas

et al. 2008

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A Phase II Study of Troglitazone, an Activator of the PPAR?? Receptor, in Patients with Chemotherapy-Resistant Metastatic Colorectal Cancer

Abstract: Troglitazone is not an active agent for the treatment of metastatic colorectal cancer.

Cited by 150 publications

References 17 publications

Peroxisome proliferator-activated receptor γ in bladder cancer: A promising therapeutic target

Peroxisome proliferator-activated receptor γ in bladder cancer: A promising therapeutic target

Perspective: Embedded Molecular Switches, Anticancer Selection, and Effects on Ontogenetic Rates: A Hypothesis of Developmental Constraint on Morphogenesis and Evolution

Immunostaining for peroxisome proliferator gamma distinguishes dedifferentiated liposarcoma from other retroperitoneal sarcomas

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