Correlation between 99m Tc-pertechnetate uptakes and expressions of human sodium iodide symporter gene in breast tumor tissues

Moon, Dae Hyuk; Lee, Sung‐Jin; Park, Ki Young; Park, Kun Ku; Ahn, Se Hyun; Pai, Moon Sun; Chang, Hyo Won; Lee, Hee Kyung; Ahn, Il-Min

doi:10.1016/s0969-8051(01)00243-8

Cited by 77 publications

(31 citation statements)

References 12 publications

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“…However, the 211123_at NIS probe set did not detect significant differences in NIS mRNA levels despite that not all breast tumors have been reported to express NIS mRNA [5,9,31]. As shown in Figure 1A, log 2 NIS mRNA levels detected among normal, non-lactating breast tissues (mean 5.1 ± 0.42, light gray line ) were comparable to breast tumor NIS mRNA levels (ER+, 5.4 ± 0.38, dark gray line , and ER-, 5.2 ± 0.51, black line ).…”

Section: Resultsmentioning

confidence: 99%

“…NIS mRNA level deviated by less than 12% of the mean regardless of the NIS probe set/microarray platform utilized, suggesting that NIS variability among breast cancers cannot be reliably detected by several Affymetrix platforms. Moon et al [5] previously reported that nearly all breast tumors examined (N = 24/25) had detectable NIS mRNA by RT-PCR and the extent of variation in NIS mRNA levels among tumors was about 10-fold (median 0.6 ± 0.27, range 0.10-1.27 arbitrary units).…”

Section: Resultsmentioning

confidence: 99%

“…It has been reported that 34-96% of breast tumors express NIS mRNA [5,9,30]. However, Moon et al [5] was the only study to quantify NIS mRNA levels among breast tumors by competitive RT-PCR followed by densitometry of ethidium bromide staining. Interestingly, Moon et al [5] reported that nearly all breast tumors had NIS mRNA levels comparable to that of peri-tumoral normal breast tissues.…”

Section: Discussionmentioning

confidence: 99%

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Microarray analysis of genes associated with cell surface NIS protein levels in breast cancer

et al. 2011

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BackgroundNa+/I- symporter (NIS)-mediated iodide uptake allows radioiodine therapy for thyroid cancer. NIS is also expressed in breast tumors, raising potential for radionuclide therapy of breast cancer. However, NIS expression in most breast cancers is low and may not be sufficient for radionuclide therapy. We aimed to identify biomarkers associated with NIS expression such that mechanisms underlying NIS modulation in human breast tumors may be elucidated.MethodsPublished oligonucleotide microarray data within the National Center for Biotechnology Information Gene Expression Omnibus database were analyzed to identify gene expression tightly correlated with NIS mRNA level among human breast tumors. NIS immunostaining was performed in a tissue microarray composed of 28 human breast tumors which had corresponding oligonucleotide microarray data available for each tumor such that gene expression associated with cell surface NIS protein level could be identified.Results and DiscussionNIS mRNA levels do not vary among breast tumors or when compared to normal breast tissues when detected by Affymetrix oligonucleotide microarray platforms. Cell surface NIS protein levels are much more variable than their corresponding NIS mRNA levels. Despite a limited number of breast tumors examined, our analysis identified cysteinyl-tRNA synthetase as a biomarker that is highly associated with cell surface NIS protein levels in the ER-positive breast cancer subtype.ConclusionsFurther investigation on genes associated with cell surface NIS protein levels within each breast cancer molecular subtype may lead to novel targets for selectively increasing NIS expression/function in a subset of breast cancers patients.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Microarray analysis of genes associated with cell surface NIS protein levels in breast cancer

et al. 2011

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“…Despite NIS expression being identified within breast cancers, only high levels of NIS mRNA expression correlated to measurable NIS functionality, with 17% of NIS-positive tumours being capable of 99m Tc-pertechnetate uptake (Moon et al 2001). The low percentage of tumours capable of radioiodide uptake was confirmed in a later study with only two out of eight of NIS-positive tumours (25%) displaying detectable 123 I K uptake (Wapnir et al 2004).…”

Section: Nis In Breast Cancermentioning

confidence: 88%

Iodide transport and breast cancer

Poole¹,

McCabe²

2015

Journal of Endocrinology

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Breast cancer is the second most common cancer worldwide and the leading cause of cancer death in women, with incidence rates that continue to rise. The heterogeneity of the disease makes breast cancer exceptionally difficult to treat, particularly for those patients with triple-negative disease. To address the therapeutic complexity of these tumours, new strategies for diagnosis and treatment are urgently required. The ability of lactating and malignant breast cells to uptake and transport iodide has led to the hypothesis that radioiodide therapy could be a potentially viable treatment for many breast cancer patients. Understanding how iodide is transported, and the factors regulating the expression and function of the proteins responsible for iodide transport, is critical for translating this hypothesis into reality. This review covers the three known iodide transporters -the sodium iodide symporter, pendrin and the sodium-coupled monocarboxylate transporter -and their role in iodide transport in breast cells, along with efforts to manipulate them to increase the potential for radioiodide therapy as a treatment for breast cancer.

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“…131 I − treatment is well tolerated, with only a few minor side effects [27, 28]. Therefore, it would be highly desirable to extend this therapeutic approach to NIS-expressing breast cancers [10, 11, 29]. It should be emphasized that the covalent incorporation of I − into thyroglobulin (i.e., I − organification), which occurs in the normal thyroid, is not required for NIS-mediated radioiodide therapy to be effective.…”

Section: Discussionmentioning

confidence: 99%

Regression of experimental NIS-expressing breast cancer brain metastases in response to radioiodide/gemcitabine dual therapy

Renier

Reyna-Neyra

et al. 2016

Oncotarget

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Treating breast cancer brain metastases (BCBMs) is challenging. Na+/I− symporter (NIS) expression in BCBMs would permit their selective targeting with radioiodide (131I−). We show impressive enhancement of tumor response by combining131I− with gemcitabine (GEM), a cytotoxic radiosensitizer. Nude mice mammary fat-pad (MFP) tumors and BCBMs were generated with braintropic MDA-MB-231Br cells transduced with bicistronically-linked NIS and firefly luciferase cDNAs. Response was monitored in vivo via bioluminescent imaging and NIS tumor expression.131I−/GEM therapy inhibited MFP tumor growth more effectively than either agent alone. BCBMs were treated with: high or low-dose GEM (58 or 14.5 mg/Kg×4); 131I− (1mCi or 2×0.5 mCi 7 days apart); and 131I−/GEM therapy. By post-injection day (PID) 25, 82-86% of controls and 78-83% of 131I−-treated BCBM grew, whereas 17% low-dose and 36% high-dose GEM regressed. The latter tumors were smaller than the controls with comparable NIS expression (~20% of cells). High and low-dose 131I−/GEM combinations caused 89% and 57% tumor regression, respectively. High-dose GEM/131I− delayed tumor growth: tumors increased 5-fold in size by PID45 (controls by PID18). Although fewer than 25% of cells expressed NIS, GEM/131I− caused dramatic tumor regression in NIS-transduced BCBMs. This effect was synergistic, and supports the hypothesis that GEM radiosensitizes cells to 131I−.

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Correlation between 99m Tc-pertechnetate uptakes and expressions of human sodium iodide symporter gene in breast tumor tissues

Cited by 77 publications

References 12 publications

Microarray analysis of genes associated with cell surface NIS protein levels in breast cancer

Microarray analysis of genes associated with cell surface NIS protein levels in breast cancer

Iodide transport and breast cancer

Regression of experimental NIS-expressing breast cancer brain metastases in response to radioiodide/gemcitabine dual therapy

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