Le Pollina

Association between breast cancer and autoimmune thyroid disorders: no increase of lymphocytic infiltrates in breast malignant tissues

An association between thyroid autoimmunity and breast cancer (BC) has been consistently reported, but the cause of this association is still unknown. The role of lymphocytic infiltration (LI) in breast tumorigenesis is controversial and several data suggest that in BC an increase of lymphoid cell infiltrates or a dysfunctional local immune response may be detected very early during tumor development. Chronic autoimmune thyroiditis is characterized by different degrees of LI in thyroid gland and BC cells share some antigenic properties similar to those detected in thyroid tissue, such as sodium iodide symporter (NIS) and peroxidase activity. The aim of this study was to evaluate the frequency and amount of LI in malignant and in normal peritumoral breast tissues, as expression of autoimmune morphological changes, in a group of BC patients with thyroid autoimmunity. We suppose that an increased LI in breast tissues of this group of patients may help explain the association between BC and thyroid autoimmunity. The study group included 26 BC patients with thyroperoxidase antibodies positivity (TPOAb+), 14 of them (53.8%) with Hashimoto’s thyroiditis (HT), and 30 BC patients with no evidence of thyroid autoimmune disorders. Malignant and surrounding normal breast tissues were assessed for LI. The amount of LI was scored as very scanty or scanty (LI S) and moderate or marked (LI M), independently by two expert pathologists. LI S was detected in 19/26 (73.1%) BC tissues from patients with TPOAb positivity and LI M in 7 (26.9%). All BC patients with HT had LI S. LI S was detected in 25/30 (83%) and LI M in 5/30 (17%) of BC tissue from patients with no thyroid autoimmunity. The difference in the amount of LI of BC tissues in patient with or without autoimmune thyroid disorders was not significant. The LI was generally absent or very scanty in remote breast tissue in all cases. In conclusion, in breast malignancies the presence of humoral and/or clinical evidence of thyroid autoimmunity is not associated to autoimmune morphological changes of cancer and peritumoral normal tissue. The LI does not seem to have any role in tumorigenesis in patients with BC and thyroid autoimmunity. (J. Endocrinol. Invest. 29: 248–251, 2006)

Presence of endothelin-1 in the normal and pathological human thyroid

An immunohistochemical study with two rabbit polyclonal antibodies I-AR76 and CA-08-351 against Endothelin-1 (ET-1) was performed in 133 human thyroid specimens: 5 normal thyroids, 30 multinodular goiters (15 toxic and 15 nontoxic), 20 Graves’ diseases, 5 Hashimoto’s thyroiditis, 26 adenomas (6 Hürthle cell, 16 toxic and 4 nontoxic), 30 classic papillary carcinomas, 3 minimally invasive follicular carcinomas, 1 widely invasive follicular carcinoma, 3 undifferentiated carcinomas and 10 medullary carcinoma. All normal thyroids, non toxic multinodular goiters and non toxic adenomas, 4 (66%) Hürthle cell adenomas, 3 (15%) Graves’ diseases, 1 (33%) case of minimally invasive follicular carcinoma showed rare follicular cells with weak cytoplasmic immunoreactivity. Many immunoreactive follicular cells, with or without oxyphilic changes, were observed in all specimens of Hashimoto’s disease, while the lymphocytic infiltrate was always negative. Twenty-seven (90%) classic papillary carcinomas were positive. Immunoreactivity was intra-cytoplasmic, weak in 14 cases and intense in 13. The cells of toxic adenoma and toxic multinodular goiter were negative, whereas the acellular stroma was intensely positive in both cases. Medullary and undifferentiated carcinomas were negative. These results show ET-1 immunoreactivity in normal and pathological human thyroids. In particular, the high content of this peptide in the thyroid papillary carcinoma suggests that ET-1, whose mitogenic role has recently been emphasized, could be involved in the growth of this tumor.