Modified administration schedule of Adriamycin in solid tumors

Kolarić, K; Maricić, Z; Nola, P; Krusić, J

doi:10.1007/bf00305363

Cited by 12 publications

(4 citation statements)

References 2 publications

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“…In the literature, adria- mycin treatment was reported to have a 31% and 37% partial response rate. 16,17 These inadequate response rates led the researchers to find out new methods to reestablish RAI uptake in tumor cells. RA was one of the first agents to be tried in the reinduction of RAI uptake owing to its redifferentiation effect.…”

Section: Discussionmentioning

confidence: 99%

The Comparative Effects of Gene Modulators on Thyroid-Specific Genes and Radioiodine Uptake

Tuncel

Aydin

Yaman

et al. 2007

Cancer Biotherapy and Radiopharmaceuticals

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The aim of this study was to comparatively investigate the effects of 5-azacytidine-C (5-Aza), trichostatin-A (TSA), and all-trans retinoic acid (ATRA) on the mRNA expressions of the sodium and iodine (Na/I) symporter (NIS), thyroglobulin (Tg), thyroid peroxidase (TPO), and the thyroid-stimulating hormone receptor (TSH-R), as well as radioiodine (RAI) uptake in cancer (B-CPAP) and normal (Nthy-ori 3-1) thyroid cell lines. Cell lines were treated with 10 ng/mL of TSA, 5 microM of 5-AZA, and 1 microM of ATRA, according to the MTT (methyl-thiazol-tetrazolium) test results. Additionally, recombinant thyroid-stimulating hormone (rTSH) was also applied, with a selected dose of 100 ng/mL. Following the treatment, NIS, Tg, TPO, and TSH-R mRNA levels were detected by real-time-polymerase chain reaction (RT-PCR) and RAI uptakes were measured by using a well counter as counts/cell number. 5-Aza increased TSH-R mRNA expression in both of the cell lines and decreased TPO, NIS, and Tg mRNA levels in the cancer cell line. In the normal thyroid cell line, 5-AZA increased TPO mRNA levels by 2-fold and made no differences in NIS and Tg mRNA levels. TSA treatment repressed NIS and Tg mRNA levels and made no change on other thyroid-specific genes that were investigated in the cancer cell line. In the normal thyroid cell line, TSA increased TSH-R mRNA levels in 72 hours and created no important difference in the other genes. ATRA repressed the TSH-R mRNA levels in the normal thyroid cell line and increased the TPO and Tg mRNA levels slightly in both the cell lines. Furthermore, in short-term treatment, ATRA repressed the NIS gene expression slightly, but in the long term, this repression turned to basal levels. 5-Aza, TSA, and ATRA did not make any changes in RAI uptake in the cancer cell line, but rTSH increased RAI uptake significantly. In the normal thyroid cell line, TSA and ATRA decreased RAI uptake (to 1/10 and 1/2, respectively), but 5-Aza and rTSH increased RAI uptake significantly (2- and 4-fold, respectively). In our study, we showed an increase in TSH-R gene expression and radioiodine uptake with 5-Aza. Further in vitro and in vivo studies are needed to support our findings and the potential clinical use of this agent.

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Section: Discussionmentioning

confidence: 99%

The Comparative Effects of Gene Modulators on Thyroid-Specific Genes and Radioiodine Uptake

Tuncel

Aydin

Yaman

et al. 2007

Cancer Biotherapy and Radiopharmaceuticals

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“…In the literature, adriamycin treatment was reported to have a 31% and 37% partial response rate. 16,17 These inadequate response rates led the researchers to seek out new methods to reestablish RAI uptake in tumor cells. RA was one of the first agents to be tried in the reinduction of RAI uptake owing to its redifferentiation effect.…”

Section: Discussionmentioning

confidence: 99%

The Comparative Effects of Gene Modulators on Thyroid-Specific Genes and Radioiodine Uptake

Tuncel

Aydin

Yaman

et al. 2007

Cancer Biotherapy and Radiopharmaceuticals

View full text Add to dashboard Cite

The aim of this study was to comparatively investigate the effects of 5-azacytidine-C (5-Aza), trichostatin-A (TSA), and all-trans retinoic acid (ATRA) on mRNA expressions of Na/I symporter (NIS), thyroglobulin (Tg), thyroid peroxidase (TPO), and thyroid stimulating hormone receptor (TSH-R), and radioiodine (RAI) uptake in cancer (B-CPAP) and normal (Nthy-ori 3-1) thyroid cell lines. Cell lines were treated with 10 ng/mL of TSA, 5 microM of 5-Aza, and 1 microM of ATRA, according to the MTT (methyl-thiazol-tetrazolium) test results. Additionally, recombinant thyroid stimulating hormone (rTSH) was also applied, with a selected dose of 100 ng/mL. Following the treatment, NIS, Tg, TPO, and TSH-R mRNA levels were detected by real-time-polymerase chain reaction (RT-PCR) and RAI uptakes were measured by using a well counter as the counts/cell number. 5-Aza increased TSH-R mRNA expression in both of the cell lines and decreased TPO, NIS, and Tg mRNA levels in the cancer cell line. In the normal thyroid cell line, 5-Aza increased TPO mRNA levels 2-fold and made no differences in NIS and Tg mRNA levels. TSA treatment repressed NIS and Tg mRNA levels, and made no differences on other thyroid specific genes investigated in the cancer cell line. In the normal thyroid cell line, TSA increased TSH-R mRNA levels in 72 hours and created no important differences in other genes. ATRA repressed the TSH-R mRNA levels in the normal thyroid cell line and increased the TPO and Tg mRNA levels slightly in both cell lines. Furthermore, in short-term treatment, ATRA repressed NIS gene expression slightly, but in the long term, this repression turned to basal levels. 5-Aza, TSA, and ATRA did not make any differences in RAI uptake in the cancer cell line, but rTSH increased RAI uptake significantly. In the normal thyroid cell line, TSA and ATRA decreased RAI uptake (to 1/10 and 1/2, respectively), but 5-Aza and rTSH increased RAI uptake significantly (2- and 4-fold, respectively). We have shown an increase in TSH-R gene expression and radioiodine uptake with 5-Aza. Further in vitro and in vivo studies are needed to support our findings and the potential clinical use of this agent.

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“…Conventional parenteral cytotoxic chemotherapy has been unsuccessful in controlling these tumors. Clinical trials with various combinations of doxorubicin, bleomycin, and a platinum-based agent have yielded unsatisfactory results, with response rates of 314% [Droz et al 1990;Kolaric et al 1977;Scherubl et al 1990;Williams et al 1986]. Similarly disappointing, the adverse event (AE) profile of these drugs is dose limiting, with patients experiencing significant neutropenia, nausea/vomiting, diarrhea, anorexia, even congestive heart failure [Argiris et al 2008].…”

Section: Introductionmentioning

confidence: 99%

Review: Thyroid cancer: emerging role for targeted therapies

Sipos

Shah

2009

Ther Adv Med Oncol

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The histology and clinical behavior of thyroid cancer are highly diverse. Although most are indolent tumors with a very favorable outcome with the current standard of care therapy, a small subset of tumors may be among the most lethal malignancies known to man. While surgery and radioactive iodine are the standard of care for differentiated thyroid cancers (DTC) and are effective in curing a majority of such patients, those with iodineresistant cancers pose a great challenge for clinicians, as these patients have limited treatment options and poor prognoses. Medullary thyroid carcinoma (MTC) has no effective systemic therapy despite the genetic and signaling defects that have been well characterized for the last two decades. Anaplastic thyroid cancer (ATC) is one of the most aggressive solid tumors that remains fatal despite conventional multimodality therapy. Increased understanding of the pathogenesis of papillary thyroid carcinoma, the most common type of DTC, as well as ATC, has led to the development of targeted therapies aimed at signaling pathways and angiogenesis that are critical to the development and/or progression of such tumors. Development of tyrosine kinase inhibitors targeting known pathogenetic defects in MTC has led to testing of such agents in the clinic. Numerous clinical trials have been conducted over the last 5 years to examine the effects of these targeted molecular therapies on the outcomes of patients with iodine-refractory DTC, MTC and ATC. Conduction of such trials in the last few years represents a major breakthrough in the field of thyroid cancer. Several trials testing targeted therapies offer promise for setting new standards for the future of patients with progressive thyroid cancer. The purpose of this paper is to outline the recent advances in understanding of the pathogenesis of thyroid cancer and to summarize the results of the clinical trials with these targeted therapies.

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Modified administration schedule of Adriamycin in solid tumors

Cited by 12 publications

References 2 publications

The Comparative Effects of Gene Modulators on Thyroid-Specific Genes and Radioiodine Uptake

The Comparative Effects of Gene Modulators on Thyroid-Specific Genes and Radioiodine Uptake

The Comparative Effects of Gene Modulators on Thyroid-Specific Genes and Radioiodine Uptake

Review: Thyroid cancer: emerging role for targeted therapies

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