A phase II trial of rosiglitazone in patients with thyroglobulin-positive and radioiodine-negative differentiated thyroid cancer

Kebebew, Electron; Peng, Miao; Reiff, Emily; Treseler, Patrick A.; Woeber, Kenneth A.; Clark, Orlo H.; Greenspan, Francis S.; Lindsay, Sheila; Duh, Quan‐Yang; Morita, Eugene

doi:10.1016/j.surg.2006.07.038

Cited by 103 publications

(73 citation statements)

References 17 publications

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“…Others have recently reported that rosiglitazone could synergisti- cally enhance the antitumor effect of certain anticancer drugs, 16 and promising results have been reported in clinical trials. 29,30 As rosiglitazone is a widely used antidiabetic drug, it would be more clinically relevant to explore the anticancer effect of this agent.…”

Section: Discussionmentioning

confidence: 99%

Loss of XIAP sensitizes rosiglitazone‐induced growth inhibition of colon cancer in vivo

Dai

Qiao

Chan

et al. 2008

Intl Journal of Cancer

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Ligands for peroxisome proliferator-activated receptor gamma (PPARc) possess anticancer properties. However, the efficacy of PPARc ligands varies in different cancers. In colon cancer, the role of PPARc and its ligands is controversial. We recently showed that downregulation of X-linked inhibitor of apoptosis protein (XIAP) could sensitize colon cancer cells to troglitazone, and 15-deoxy-D12,14-prostaglandin J2 (15-PGJ2) induced cell killing. In our study, we aimed to examine whether rosiglitazone, another more clinically relevant PPARc ligand, has any synergistic anticancer effect with XIAP downregulation in colon cancer. Human colon cancer cell lines HCT116-XIAP 1/1 cells and HCT116-XIAP 2/2 cells were treated with various concentrations of rosiglitazone. The effects of rosiglitazone on cell proliferation, apoptosis and growth of xenograft colon cancers were studied. Rosiglitazone barely suppressed the growth and only very weakly induced apoptosis in HCT116 cells in vitro. Loss of XIAP did not sensitize HCT116 cells to rosiglitazone-induced growth inhibition or apoptosis. In vivo studies revealed that rosiglitazone strongly suppressed the growth of xenograft colon cancer, especially tumors derived from HCT116-XIAP 2/2 cells. The rosiglitazone-treated tumor had reduced expression of ki-67 and lowered mitotic rate. Downregulation of XIAP was associated with an impaired activation of PPARc by its ligand. Rosiglitazone induced marked upregulation of PTEN in HCT116-XIAP 2/2 cells, as well as in xenograft tumors derived from HCT116-XIAP 2/2 cells. We concluded that rosiglitazone significantly suppresses the growth of xenograft colon cancer, and downregulation of XIAP sensitizes the xenograft tumors to rosiglitazone-induced tumor suppression in vivo via upregulation of PTEN.

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Section: Discussionmentioning

confidence: 99%

Loss of XIAP sensitizes rosiglitazone‐induced growth inhibition of colon cancer in vivo

Dai

Qiao

Chan

et al. 2008

Intl Journal of Cancer

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“…In an initial pilot study, Philips et al tried rosiglitazone in five patients who showed negative iodine whole body scans with high serum Tg, and only one of them showed a faint increase in iodine uptake [44]. On the contrary, Kebebew et al reported a more positive result: 4/10 patients showed a significant increase in iodine uptake after rosiglitazone treatment [45]. However, the same group reported somewhat disappointing results several years later.…”

Section: Pparγ Agonistsmentioning

confidence: 99%

“…So far, rosiglitazone is the only drug that has been tried in thyroid cancer patients [45][46][47][48][49]. However, as troglitazone was reported to be more effective than any other thiazolinedione in a cell study [43], appropriate drug selection will be an issue.…”

Section: Pparγ Agonistsmentioning

confidence: 99%

Alternative Medical Treatment for Radioiodine-Refractory Thyroid Cancers

Paeng

Kang

Park

et al. 2011

Nucl Med Mol Imaging

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Thyroid cancer is one of the most rapidly increasing cancers in many countries. Although most thyroid cancers are differentiated cancers and easily treated with radioiodine (RI), a portion of differentiated and undifferentiated cancers is refractory not only to RI therapy, but also to radiotherapy and chemotherapy. Thus, various alternative therapies have been tested in RI-refractory thyroid cancers. These alternative therapies include two major categories: redifferentiation therapy and recent molecular target therapy. Several clinical trials have investigated these therapies. They demonstrated potential effects of the therapies, although the results have been somewhat limited so far. Thus, the future strategy for undifferentiated thyroid cancers will involve individualized, lesion-specific, and combined therapy. In this review, the basic mechanism of each redifferentiation and molecular target therapy is discussed, and results of recent clinical trials using these therapeutic agents are summarized.

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“…Uptake of RAI improved in four of 10 patients in one study [120] and in six of 23 patients in the other [121]. In both studies, tissue was tested for PPAR-␥ expression; however, the results correlating PPAR-␥ expression and response to rosiglitazone are conflicting [120,121]. Further trials are being conducted on the effect of rosiglitazone in patients with locally advanced or metastatic DTC [51].…”

Section: Therapies To Restore Rai Aviditymentioning

confidence: 99%

Standard and Emerging Therapies for Metastatic Differentiated Thyroid Cancer

et al. 2010

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After completing this course, the reader will be able to:1. Describe the role and limitations of traditional treatments for metastatic differentiated thyroid cancer.2. Discuss the molecular basis of and clinical evidence for novel and emerging treatments for metastatic differentiated thyroid cancer.3. Identify suitable candidates for clinical trials among your patients with radioactive iodine refractory, metastatic differentiated thyroid cancer and enroll them.This article is available for continuing medical education credit at CME.TheOncologist.com. CME CME ABSTRACTDifferentiated thyroid cancer accounts for >90% of cases of thyroid cancer, with most patients having an excellent prognosis. Distant metastases occur in 10%-15% of patients, decreasing the overall 10-year survival rate in this group to 40%. Radioactive iodine has been the mainstay of treatment for distant metastases, with good results when lesions retain the ability to take up iodine. For patients with metastatic disease resistant to radioactive iodine, treatment options are few and survival is poor. Chemotherapy and external beam radiotherapy have been used in these patients, but with disappointing results. In recent years, our understanding of the molecular pathways involved in thyroid cancer has increased and a number of molecular targets have been identified. These targets include the protooncogenes BRAF and RET, known to be common mutations in thyroid cancer; vascular endothelial growth factor receptor and platelet-derived growth factor receptor, associated with angiogenesis; and the sodiumiodide symporter, with the aim of restoring its The Oncologist CME Program is located online at http://cme.theoncologist.com/.To take the CME activity related to this article, you must be a registered user. EndocrinologyThe

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A phase II trial of rosiglitazone in patients with thyroglobulin-positive and radioiodine-negative differentiated thyroid cancer

Cited by 103 publications

References 17 publications

Loss of XIAP sensitizes rosiglitazone‐induced growth inhibition of colon cancer in vivo

Loss of XIAP sensitizes rosiglitazone‐induced growth inhibition of colon cancer in vivo

Alternative Medical Treatment for Radioiodine-Refractory Thyroid Cancers

Standard and Emerging Therapies for Metastatic Differentiated Thyroid Cancer

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