Discrimination of Benign and Malignant Thyroid Nodules by Molecular Profiling

Finley, David J.; Zhu, Bin; Barden, Catherine B.; Fahey, Thomas J.

doi:10.1097/01.sla.0000137128.64978.bc

Cited by 140 publications

(110 citation statements)

References 43 publications

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“…Such a failure could be explained by the great similarity in overall gene expression profiles observed between the 2 sample groups, as demonstrated by Figures 1 and 2, which may be further indication that the 2 lesions are similar not only phenotypically but also at the level of gene expression. Our data are in disagreement with those published previously by Finley et al and by Barden et al, [11][12][13] who identified a set of genes that, by clustering algorithms, could distinguish between adenomas and follicular carcinomas. This discrepancy may be explained by the number and identity of the genes present in our arrays compared with the arrays used by other groups or by differences in mathematical and statistical approaches.…”

Section: Discussioncontrasting

confidence: 57%

“…Using oligonucleotide arrays, Finley et al identified differentially expressed genes among carcinomas, adenomas, and hyperplastic nodules; and the expression of those genes was used to cluster samples that represented different pathologies. 11,12 A similar technique was employed in the comparison of follicular carcinomas and adenomas and demonstrated different profiles after hierarchical clustering. 13 Recently, we described the identification of molecular classifiers that could distinguish between malignant and nonmalignant lesions of the gastric mucosa.…”

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confidence: 99%

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Class distinction between follicular adenomas and follicular carcinomas of the thyroid gland on the basis of their signature expression

Stolf

Santos

Simão

et al. 2006

Cancer

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Thalassemia is an inherited blood disorder that requires lifelong adherence to a complicated and burdensome medical regimen which could potentially impact emotional functioning of patients. The importance of understanding and promoting healthy emotional functioning is crucial not only to psychological well‐being, but also to physical health as it has been shown to impact adherence to medical regimens [1–4]. The current study aimed to [1] determine the prevalence of depressive and anxiety symptoms in adolescent and adult patients with thalassemia; and [2] explore possible demographic, medical, and psychosocial correlates of these symptoms in 276 patients (14–58 years old, M age = 27.83; 52% female). Overall, most patients did not report experiencing significant symptoms of anxiety and depression (33% of participants indicated experiencing symptoms of anxiety and 11% symptoms of depression). Females and older patients were more likely to experience these symptoms than males and younger patients. Symptoms of anxiety and depression were positively associated with self‐report of difficulty with adherence and negatively associated with quality of life. Given these findings, regular screening for anxiety and depression symptoms could help to identify at‐risk individuals to provide them with appropriate psychological support with the goal of improving both emotional and physical health. Am. J. Hematol., 2010. © 2010 Wiley‐Liss, Inc.

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Section: Discussioncontrasting

confidence: 57%

mentioning

confidence: 99%

Class distinction between follicular adenomas and follicular carcinomas of the thyroid gland on the basis of their signature expression

Stolf

Santos

Simão

et al. 2006

Cancer

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“…Genes regulated in a similar direction in cultured thyrocytes and autonomous adenomas, but that are regulated in the inverse way in papillary carcinomas, might reflect the differentiating action of the TSH-cAMP pathway [DIO2 (26,37), HGD (38), FHL1 (39), ITPR1 (39,40), CRABP1 (40,41), and ADM (40)], whereas common expression in the TSH-stimulated thyrocytes, autonomous adenomas, and papillary carcinomas concerns possibly proteins involved in the control or support of cell growth [EFHD2, IER2, KLF6 (10), EGR1 (10), GADD45B, and JUN]. One puzzling common property of autonomous adenomas and papillary carcinomas is the down-regulation of a number of immediate early genes [NR4A1, JUNB (10), KLF10, and ZFP36].…”

Section: Discussionmentioning

confidence: 99%

Gene expression in human thyrocytes and autonomous adenomas reveals suppression of negative feedbacks in tumorigenesis

Staveren¹,

Solís²,

Delys³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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The cAMP signaling pathway regulates growth of many cell types, including somatotrophs, thyrocytes, melanocytes, ovarian follicular granulosa cells, adrenocortical cells, and keratinocytes. Mutations of partners from the cAMP signaling cascade are involved in tumor formation. Thyroid-stimulating hormone (TSH) receptor and Gs␣ activating mutations have been detected in thyroid autonomous adenomas, Gs␣ mutations in growth hormone-secreting pituitary adenomas, and PKAR1A mutations in Carney complex, a multiple neoplasia syndrome. To gain more insight into the role of cAMP signaling in tumor formation, human primary cultures of thyrocytes were treated for different times (1.5, 3, 16, 24, and 48 h) with TSH to characterize modulations in gene expression using cDNA microarrays. This kinetic study showed a clear difference in expression, early (1.5 and 3 h) and late (16 -48 h) after the onset of TSH stimulation. This result suggests a progressive sequential process leading to a change of cell program. The gene expression profile of the long-term stimulated cultures resembled the autonomous adenomas, but not papillary carcinomas. The molecular phenotype of the adenomas thus confirms the role of long-term stimulation of the TSH-cAMP cascade in the pathology. TSH induced a striking up-regulation of different negative feedback modulators of the cAMP cascade, presumably insuring the oneshot effect of the stimulus. Some were down-or nonregulated in adenomas, suggesting a loss of negative feedback control in the tumors. These results suggest that in tumorigenesis, activation of proliferation pathways may be complemented by suppression of multiple corresponding negative feedbacks, i.e., specific tumor suppressors.cyclic AMP ͉ microarrays ͉ papillary tumors ͉ thyrotropin T ight regulation of the second messenger cAMP is of crucial importance for cells because it regulates function, differentiation, and proliferation (1). In cells in which cAMP stimulates growth, activating mutations in partners of this pathway induce uncontrolled growth. In most benign thyroid autonomous adenomas, activating mutations have been found in the thyroidstimulating hormone (TSH) receptor (TSHR) (2) and, to a lesser extent, in the Gs␣ protein, an activator of the cAMP-producing adenylyl cyclase (1, 3). These mutations result in a TSHindependent growth and lead to hyperfunction (1). In addition, activating mutations of the Gs␣ protein have been detected in growth hormone-secreting pituitary adenomas (4) and inactivating mutations in the type I-␣ regulatory subunit inhibiting protein kinase A (PKAR1A) in Carney complex, a multiple neoplasia syndrome (5).Our knowledge of the genes regulated by the cAMP-protein kinase A cascade and its uncontrolled activation is still sketchy (6). To gain more insight into the cAMP-activated signal transduction cascade in tumors, human primary cultures of thyrocytes treated for different times with the TSH growth and differentiation stimulus were used as a model. Thyrocytes in primary culture are expected to be better mod...

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“…Distinctive gene expression patterns are associated with a wide variety of morphological, biological and clinical parameters. This approach has now begun to be applied to thyroid cancer (Huang et al, 2001;Finley et al, 2004;Giordano et al, 2005;Jarzab et al, 2005;Eszlinger et al, 2006). Although some studies have included FVPTCs and minimally invasive FTCs, none has examined the challenging group of tumours of uncertain malignancy (T-UM).…”

Section: Introductionmentioning

confidence: 99%

Microarray analysis refines classification of non-medullary thyroid tumours of uncertain malignancy

et al. 2007

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Discrimination of Benign and Malignant Thyroid Nodules by Molecular Profiling

Cited by 140 publications

References 43 publications

Class distinction between follicular adenomas and follicular carcinomas of the thyroid gland on the basis of their signature expression

Class distinction between follicular adenomas and follicular carcinomas of the thyroid gland on the basis of their signature expression

Gene expression in human thyrocytes and autonomous adenomas reveals suppression of negative feedbacks in tumorigenesis

Microarray analysis refines classification of non-medullary thyroid tumours of uncertain malignancy

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