Thyroid hormones in fibrocystic breast disease

Martínez, Luis; Castilla, José Antonio; Gil, Teresa; Sánchez-Molina, Jorge; Alarcón, José; Marcos, Cristina Fernández; Herruzo, A

doi:10.1530/eje.0.1320673

Cited by 9 publications

(6 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, AREG seems to play an intermediary role in maturing the mammary gland and in stimulating the initiation of mammary oncogenesis. Martinez et al [29] treated MCF-7 cells with 10 −9 M E 2 , 10 −9 M E 2 with 10 −6 M TAM (E 2 + TAM), TAM alone, and vehicle control for 24 hours. They observed that adding TAM to the treatment with E 2 decreased AREG mRNA expression by 38%, suggesting that E 2 stimulates AREG expression via ER.…”

Section: Discussionmentioning

confidence: 99%

Estrogen-Responsive Genes Overlap with Triiodothyronine-Responsive Genes in a Breast Carcinoma Cell Line

Figueiredo

Cestari

Conde

et al. 2014

The Scientific World Journal

View full text Add to dashboard Cite

It has been well established that estrogen plays an important role in the progression and treatment of breast cancer. However, the role of triiodothyronine (T3) remains controversial. We have previously shown its capacity to stimulate the development of positive estrogen receptor breast carcinoma, induce the expression of genes (PR, TGF-alpha) normally stimulated by estradiol (E2), and suppress genes (TGF-beta) normally inhibited by E2. Since T3 regulates growth hormones, metabolism, and differentiation, it is important to verify its action on other genes normally induced by E2. Therefore, we used DNA microarrays to compare gene expression patterns in MCF-7 breast adenocarcinoma cells treated with E2 and T3. Several genes were modulated by both E2 and T3 in MCF-7 cells (Student's t-test, P < 0.05). Specifically, we found eight genes that were differentially expressed after treatment with both E2 and T3, including amphiregulin, fibulin 1, claudin 6, pericentriolar material 1, premature ovarian failure 1B, factor for adipocyte differentiation-104, sterile alpha motif domain containing 9, and likely ortholog of rat vacuole membrane protein 1 (fold change > 2.0, pFDR < 0.05). We confirmed our microarray results by real-time PCR. Our findings reveal that certain genes in MCF-7 cells can be regulated by both E2 and T3.

show abstract

Section: Discussionmentioning

confidence: 99%

Estrogen-Responsive Genes Overlap with Triiodothyronine-Responsive Genes in a Breast Carcinoma Cell Line

Figueiredo

Cestari

Conde

et al. 2014

The Scientific World Journal

View full text Add to dashboard Cite

show abstract

“…TR are also present in human breast cancer cell lines (Burke and McGuire, 1978;Zhou-Li et al, 1992), but con¯icting reports describe both mitogenic and antimitogenic e ects of T3 (Nogueira and Brentani, 1996;MartõÂ nez et al, 2000). A role of T3 in the physiology of ®brocystic breast disease has been suggested (MartõÂ nez et al, 1995). Although there is little evidence that overt thyroid disease causes breast cancer, hypothyroidism has been proposed to favor the development of breast cancer by sensitizing breast tissue to the growth promoting action of estrogen, prolactin, and carcinogens (Smyth et al, 1996;Smyth, 1997).…”

Section: Discussionmentioning

confidence: 99%

Expression of thyroid hormone receptor/erbA genes is altered in human breast cancer

et al. 2002

View full text Add to dashboard Cite

The relation between thyroid status and diseases and cancer is unclear. No detailed analysis of thyroid hormone receptor (TR) expression in human breast cancer has been reported. We have analysed the expression and mutational status of the TRa1, encoded by the c-erbA proto-oncogene, TRb1 and TRb2 isoforms in 70 sporadic breast cancers. Alterations in the RNA level of TRb1, TRa1, or both were found in a number of patients. No expression of TRb2 RNA was detected. Western blotting analysis con®rmed the di erences in expression at the protein level in those cases where su cient tumor sample was available. Additionally, tumor-speci®c truncated TRb1 RNA was found in six patients. Strikingly, three transcripts shared the same breakpoint. Only one tumor carried the corresponding deletion at the genomic DNA level, suggesting that the remaining abnormal TRb1 transcripts are aberrant splicing products. Though no signi®cant correlation was found between TRb1 alteration and any clinical parameter, it showed a tendency to associate with early age of onset (550 years). Our results reveal speci®c alterations in the expression of TRb and TRa genes in a subset of breast cancer patients, suggesting that deregulation of thyroid hormone target genes may be involved in the generation of this neoplasia.

show abstract

“…Almost every form of thyroid disease including hyperthyroidism has been identified in association with breast cancer (9-11). Moreover, hyperthyroidism accounts for 2% of all patients presenting adult gynecomastia (12) and it has also been suggested that free triiodothyronine (T 3 ) plays an important role in the physiology of fibrocystic breast disease (13). Consistent with the proposal that thyroid hormones act on the breast, TR have been described in breast cancer (14).…”

Section: Introductionmentioning

confidence: 91%

Profile of thyroid hormones in breast cancer patients

Saraiva

Figueiredo

Padovani

et al. 2005

Braz J Med Biol Res

View full text Add to dashboard Cite

Estrogen involvement in breast cancer has been established; however, the association between breast cancer and thyroid diseases is controversial. Estrogen-like effects of thyroid hormone on breast cancer cell growth in culture have been reported. The objective of the present study was to determine the profile of thyroid hormones in breast cancer patients. Serum aliquots from 26 patients with breast cancer ranging in age from 30 to 85 years and age-matched normal controls (N = 22) were analyzed for free triiodothyronine (T 3 F), free thyroxine (T 4 F), thyroid-stimulating hormone (TSH), antiperoxidase antibody (TPO), and estradiol (E 2 ). Estrogen receptor ß (ERß) was determined in tumor tissues by immunohistochemistry. Thyroid disease incidence was higher in patients than in controls (58 vs 18%, P < 0.05). Subclinical hyperthyroidism was the most frequent disorder in patients (31%); hypothyroidism (8%) and positive anti-TPO antibodies (19%) were also found. Subclinical hypothyroidism was the only dysfunction (18%) found in controls. Hyperthyroidism was associated with postmenopausal patients, as shown by significantly higher mean T 3 and T 4 values and lower TSH levels in this group of breast cancer patients than in controls. The majority of positive ERß tumors were clustered in the postmenopausal patients and all cases presenting subclinical hyperthyroidism in this subgroup concomitantly exhibited Erß-positive tumors. Subclinical hyperthyroidism was present in only one of 6 premenopausal patients. We show here that postmenopausal breast cancer patients have a significantly increased thyroid hormone/ E 2 ratio (P < 0.05), suggesting a possible tumor growth-promoting effect caused by this misbalance.

show abstract

Thyroid hormones in fibrocystic breast disease

Cited by 9 publications

References 14 publications

Estrogen-Responsive Genes Overlap with Triiodothyronine-Responsive Genes in a Breast Carcinoma Cell Line

Estrogen-Responsive Genes Overlap with Triiodothyronine-Responsive Genes in a Breast Carcinoma Cell Line

Expression of thyroid hormone receptor/erbA genes is altered in human breast cancer

Profile of thyroid hormones in breast cancer patients

Contact Info

Product

Resources

About