A prospective feasibility trial to determine the significance of the sentinel node gradient in breast cancer: a predictor of nodal metastasis location.

BACKGROUND: Sentinel lymph node (SN) biopsy is standard for breast cancer staging, but SN dye gradients and their significance have never been characterized. If predictive of SN metastasis location, their use for focused pathology examination might improve intraoperative imprint cytology sensitivity. METHODS: This prospective trial enrolled clinically lymph node-negative patients with invasive breast cancer not undergoing neoadjuvant chemotherapy. Surgeons marked SN gradients at their bluest end. Nodal halves were examined separately by imprint cytology, and the marked SN half was correlated to metastasis location. Demographic, pathologic, and prognostic features were recorded. RESULTS: Mean patient age and tumor size for the 102 patients was 59.6 years and 2.2 cm, respectively. Of 169 SNs, 159 (94.1%) had dye gradients, which varied by tumor quadrant, but not by histology, diagnosis method, grade, or stage. Among 41 marked SNs with metastases, 92.7% were present in the halves marked by the surgeon. Fourteen were confined to 1 nodal half, with 11 on the marked side and 3 on the unmarked side (P = .029). Metastases were smaller when confined to 1 versus both SN halves (0.14 vs 0.75 cm; P = .005), and smaller (0.87 vs 0.13 cm; P < .0001) when missed intraoperatively. CONCLUSIONS: Dye gradients occur in most SNs and predict metastasis location. The smallest metastases are hardest to detect intraoperatively and are usually confined to the marked SN half. This suggests that marking an SN's bluest half warrants further study to explore whether its correlation to metastasis location may be exploited to focus pathologic examination and decrease the reoperative axillary dissection rate.

Recurring translocation (10;17) and deletion (14q) in clear cell sarcoma of the kidney.

CONTEXT: Clear cell sarcoma of the kidney (CCSK) is a prognostically unfavorable renal neoplasm of childhood. Previous cytogenetic studies of CCSK have reported balanced translocations t(10;17)(q22;p13) and t(10;17)(q11;p12). Although the tumor suppressor gene p53 is located at the chromosome 17p13 breakpoint, p53 abnormalities are rarely present in these tumors. OBJECTIVE: To identify cytogenetic abnormalities in CCSK and correlate these findings with other clinicopathologic parameters. DESIGN: A retrospective review of CCSK patients from 1990 to 2005 was conducted at our medical center. We performed clinical and histologic review, p53 immunohistochemical and classic cytogenetics (or ploidy analysis), and p53 fluorescence in situ hybridization analyses. RESULTS: Five male patients (age range, 6 months to 4 years) were identified with cytogenetic abnormalities. Of 3 cytogenetically informative cases, one revealed a clonal balanced translocation t(10;17)(q22;p13) and an interstitial deletion of chromosome 14, del(14)(q24.1q31.1), and the other 2 patients had normal karyotypes. Fluorescence in situ hybridization for p53 in the t(10;17) case revealed no deletion. Immunohistochemical evaluation of p53 demonstrated lack of nuclear protein accumulation in all cases. CONCLUSIONS: Together with the published literature, our results indicate that translocation (10;17) and interstitial deletions of chromosome 14q are recurring cytogenetic lesions in CCSK. To date, 3 cases of CCSK or "sarcomatoid Wilms tumors" have been reported to exhibit t(10;17). One previously reported case of CCSK contained deletion 14q. Results of p53 immunohistochemistry and/or p53 fluorescence in situ hybridization in this report suggest lack of mutations or deletions of this tumor suppressor in these CCSK cases. The t(10;17) breakpoint and deletion of chromosome 14q24 suggest that other genes are involved in tumor pathogenesis.