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Articles by D. B Evans
Total Records ( 3 ) for D. B Evans
  E. J Silberfein , R Bao , A Lopez , E. G Grubbs , J. E Lee , D. B Evans and N. D. Perrier
 

Objectives  To evaluate and categorize the locations of missed parathyroid glands found during reoperative parathyroidectomy and to determine any factors associated with these locations.

Design  Retrospective cohort study.

Setting  Tertiary referral center.

Patients  Fifty-four patients who underwent reoperative parathyroidectomy for persistent or recurrent hyperparathyroidism from January 1, 2005, through January 1, 2009.

Main Outcome Measures  Location of missed parathyroid glands and their association with continuous variables were analyzed using a Kruskal-Wallis test, and associations between gland location and categorical variables were evaluated using the Fisher exact test.

Results  Among 54 patients, 50 abnormal parathyroid glands were identified, resected, and classified as follows: 5 (10%) were type A (adherent to the posterior thyroid capsule); 11 (22%), type B (behind the thyroid in the tracheoesophageal groove); 7 (14%), type C (close to the clavicle in the prevertebral space); 3 (6%), type D (directly over the recurrent laryngeal nerve); 9 (18%), type E (easy to identify; near the inferior thyroid pole); 13 (26%), type F (fallen into the thymus); and 2 (4%), type G (gauche, within the thyroid gland). No demographic, biochemical, or pathological factors were significantly associated with gland location. Among the 43 patients followed up for 6 months, 40 (93%) had documented cures.

Conclusions  Missed glands after parathyroidectomy for hyperparathyroidism can be found in standard locations in most cases. A standardized nomenclature system based on the regional anatomy and the embryology of the parathyroid glands can guide a systematic exploration for parathyroid adenomas that are not easily identified and facilitate communication about gland locations.

  S Banerjee , M Zvelebil , P Furet , U Mueller Vieira , D. B Evans , M Dowsett and L. A. Martin
 

Endocrine therapy is well established for the treatment of breast cancer, and antiangiogenic agents are showing considerable promise. Targeting the vascular endothelial growth factor (VEGF) and estrogen receptor (ER) signaling pathways concomitantly may provide enhanced therapeutic benefit in ER-positive breast cancer. Therefore, the effects of the VEGF receptor (VEGFR) tyrosine kinase inhibitor PTK787/ZK222584 (PTK/ZK) were investigated using human breast cancer cell lines engineered to express aromatase. As expected in this system, estrogen (E2) or androstenedione induced a proliferative response and increased ER-mediated transcription in ER-positive cell lines expressing aromatase. However, surprisingly, in the presence of androstenedione, PTK/ZK suppressed both the androstenedione-stimulated proliferation and ER-mediated transcription. PTK/ZK alone and in the presence of E2 had no observable effect on proliferation or ER-mediated transcription. These effects result from PTK/ZK having previously unrecognized antiaromatase activity and PTK/ZK being a competitive aromatase inhibitor. Computer-assisted molecular modeling showed that PTK/ZK could potentially bind directly to aromatase. The demonstration that PTK/ZK inhibits aromatase and VEGFR indicates that agents cross-inhibiting two important classes of targets in breast cancer could be developed. [Cancer Res 2009;69(11):4716–23]

 
 
 
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