Presence and possible role of vascular endothelial growth factor in thyroid cell growth and function

Jf, Wang; Milosveski, V; C, Schramek; Fong, G. H.; Becks, G P; Hill, D. J.

doi:10.1677/joe.0.1570005

Cited by 90 publications

(54 citation statements)

References 26 publications

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“…It is suggested that sunitinib and sorafenib decrease thyroid function by interfering with VEGF function or impairing thyroid blood flow (2,24). In several reports, however, including the present analysis, bevacizumab did not appear to be associated with altered thyroid homeostasis (25,26). Based on this finding, the neutralization of VEGF would therefore have no significant effect on thyroid function.…”

Section: Discussioncontrasting

confidence: 45%

Hypothyroidism in patients with colorectal carcinoma treated with fluoropyrimidines

et al. 2013

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Abstract. Targeted therapy with tyrosine kinase inhibitors, including vascular endothelial growth factor receptors, has been demonstrated to induce hypothyroidism and thyroid dysfunction. Cancer patients with thyroid dysfunction may be underdiagnosed and undertreated. Thyroid function in colorectal cancer patients receiving fluoropyrimidine-based chemotherapy with or without bevacizumab was evaluated at baseline and monthly. In the present study, 3 of 27 (11.1%) patients who received fluoropyrimidine-based chemotherapy developed a thyroid-stimulating hormone (TSH) level >10 µU/ml, and 13 (48.1%) developed an elevation above the upper limit of the normal range. No difference in TSH elevation was noted between the bevacizumab and chemotherapy-alone group (50 vs. 45%; P=1.00, respectively). Three (11.1%) patients developed a TSH level >10 µU/ml and 2 with hypothyroidism were treated with thyroid hormone replacement therapy. We demonstrated that bevacizumab does not affect thyroid function but fluoropyrimidines may induce thyroid dysfunction in patients with colorectal cancer. Further investigation is required to clarify the mechanism of fluoropyrimidine-induced thyroid dysfunction.

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Section: Discussioncontrasting

confidence: 45%

Hypothyroidism in patients with colorectal carcinoma treated with fluoropyrimidines

et al. 2013

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“…In both cases, it followed a single phase increase that became significant at day 4 of treatment (4.0-and 2.9-fold increase, for Flk1/ VEGFR2 and flt-1/VEGFR1, respectively) and reached a peak at day 12 as previously reported. 29,30 FGF2 protein expression followed the two vascular remodeling phases as well. FGF2 was detected at low levels from day 0 to day 2 of treatment ( Figure 5A), a strong increase occurred at day 3, followed by a subsequent drop at days 4 and 6.…”

Section: Iodine Deficiency Induces Biphasic Changes In the Expressionmentioning

confidence: 96%

Iodine Deficiency Induces a Thyroid Stimulating Hormone-Independent Early Phase of Microvascular Reshaping in the Thyroid

Gérard

Poncin

Caetano

et al. 2008

The American Journal of Pathology

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Expansion of the thyroid microvasculature is the earliest event during goiter formation, always occurring before thyrocyte proliferation; however, the precise mechanisms governing this physiological angiogenesis are not well understood. Using reverse transcriptase-polymerase chain reaction and immunohistochemistry to measure gene expression and laser Doppler to measure blood flow in an animal model of goitrogenesis, we show that thyroid angiogenesis occurred into two successive phases. The first phase lasted a week and involved vascular activation; this process was thyroid-stimulating hormone (TSH)-independent and was directly triggered by expression of vascular endothelial growth factor (VEGF) by thyrocytes as soon as the intracellular iodine content decreased. This early reaction was followed by an increase in thyroid blood flow and endothelial cell proliferation, both of which were mediated by VEGF and inhibited by VEGF-blocking antibodies. The second, angiogenic, phase was TSH-dependent and was activated as TSH levels increased. This phase involved substantial up-regulation of the major proangiogenic factors VEGF-A, fibroblast growth factor-2, angiopoietin 1, and NG2 as well as their receptors Flk-1/VEGFR2, Flt-1/ VEGFR1, and Tie-2. In conclusion, goiter-associated angiogenesis promotes thyroid adaptation to iodine deficiency. Specifically, as soon as the iodine supply is limited, thyrocytes produce proangiogenic signals that elicit early TSH-independent microvascular activation; if iodine deficiency persists, TSH plasma levels increase, triggering the second angiogenic phase that supports thyrocyte proliferation.

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“…26 the role of veGF in thyroid signaling is uncertain. 40,41 unlike treatment with antiangiogenic tKis, bevacizumab is not associated with altered thyroid homeostasis. 42,43 other factors, such as platelet derived growth factor α and c Kit, have roles in thyroid homeostasis, but so far no data have been published.…”

Section: Reviewsmentioning

confidence: 98%

Hypothyroidism related to tyrosine kinase inhibitors: an emerging toxic effect of targeted therapy

et al. 2009

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Presence and possible role of vascular endothelial growth factor in thyroid cell growth and function

Abstract: Angiogenesis is an important component in the

Cited by 90 publications

References 26 publications

Hypothyroidism in patients with colorectal carcinoma treated with fluoropyrimidines

Hypothyroidism in patients with colorectal carcinoma treated with fluoropyrimidines

Iodine Deficiency Induces a Thyroid Stimulating Hormone-Independent Early Phase of Microvascular Reshaping in the Thyroid

Hypothyroidism related to tyrosine kinase inhibitors: an emerging toxic effect of targeted therapy

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