TY - JOUR
T1 - Increased Incidence of Well-Differentiated Thyroid Cancer Associated with Hashimoto Thyroiditis and the Role of the PI3k/Akt Pathway
AU - Larson, Shawn D.
AU - Jackson, Lindsey N.
AU - Riall, Taylor S.
AU - Uchida, Tatsuo
AU - Thomas, Robert P.
AU - Qiu, Suimin
AU - Evers, B. Mark
N1 - Funding Information:
Supported by grants R01CA104748, R01DK48498, P01DK35608, and T32DK07639 from the National Institutes of Health and a Jeane B Kempner Scholar award (to SDL).
PY - 2007/5
Y1 - 2007/5
N2 - Background: The link between inflammation and cancer is well-established, but the link between Hashimoto thyroiditis (HT) and thyroid cancer remains controversial. The purpose of our study was to determine the incidence of patients with thyroid cancer and associated HT at our institution, to correlate our patient population demographics with the Surveillance, Epidemiology and End Results (SEER) database, and to assess the expression of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in patients with HT. Study Design: Demographic and histologic data were collected from patients undergoing thyroid resection at the University of Texas Medical Branch from 1987 to 2002 and compared with the SEER database. Immunohistochemistry for phosphorylated Akt (a marker of PI3K activity), Akt isoforms and PTEN (an inhibitor of PI3K) was performed on paraffin-embedded blocks of resected thyroid tissue. Results: Our patient population demographics and thyroid cancer incidence by histologic type were similar to patients in the SEER database. Ninety-eight (37.7%) resected specimens had pathologic changes consistent with HT; 43 (43.8%) had an associated well-differentiated thyroid cancer. Increased phosphorylated Akt, Akt1, and Akt2 expression was noted in regions of HT and thyroid cancer compared with regions of normal surrounding thyroid tissue. Conclusions: Patients with HT were three times more likely to have thyroid cancer, suggesting a strong link between chronic inflammation and cancer development. PI3K/Akt expression was increased in both HT and well-differentiated thyroid cancer, suggesting a possible molecular mechanism for thyroid carcinogenesis.
AB - Background: The link between inflammation and cancer is well-established, but the link between Hashimoto thyroiditis (HT) and thyroid cancer remains controversial. The purpose of our study was to determine the incidence of patients with thyroid cancer and associated HT at our institution, to correlate our patient population demographics with the Surveillance, Epidemiology and End Results (SEER) database, and to assess the expression of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in patients with HT. Study Design: Demographic and histologic data were collected from patients undergoing thyroid resection at the University of Texas Medical Branch from 1987 to 2002 and compared with the SEER database. Immunohistochemistry for phosphorylated Akt (a marker of PI3K activity), Akt isoforms and PTEN (an inhibitor of PI3K) was performed on paraffin-embedded blocks of resected thyroid tissue. Results: Our patient population demographics and thyroid cancer incidence by histologic type were similar to patients in the SEER database. Ninety-eight (37.7%) resected specimens had pathologic changes consistent with HT; 43 (43.8%) had an associated well-differentiated thyroid cancer. Increased phosphorylated Akt, Akt1, and Akt2 expression was noted in regions of HT and thyroid cancer compared with regions of normal surrounding thyroid tissue. Conclusions: Patients with HT were three times more likely to have thyroid cancer, suggesting a strong link between chronic inflammation and cancer development. PI3K/Akt expression was increased in both HT and well-differentiated thyroid cancer, suggesting a possible molecular mechanism for thyroid carcinogenesis.
UR - http://www.scopus.com/inward/record.url?scp=34247534062&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34247534062&partnerID=8YFLogxK
U2 - 10.1016/j.jamcollsurg.2006.12.037
DO - 10.1016/j.jamcollsurg.2006.12.037
M3 - Article
C2 - 17481480
AN - SCOPUS:34247534062
SN - 1072-7515
VL - 204
SP - 764
EP - 773
JO - Journal of the American College of Surgeons
JF - Journal of the American College of Surgeons
IS - 5
ER -