Clusterin expression was associated with large tumor size (P = 0.04), estrogen and progesterone receptor negative status (P = 0.02 and P = 0.001, respectively) and with the progression from primary carcinoma to metastatic carcinoma in lymph nodes (80% metastatic nodes had positive expression) (P = 0.004).
PRAME levels in müllerian carcinoma were unrelated to survival; however, PRAME protein expression was up-regulated in solid metastases compared with primary carcinoma and effusions (P < .001).
All patients that expressed EGFR transcripts in the peripheral blood were found to express the EGFR protein in the corresponding primary carcinoma, as assessed by immunohistochemistry.
Clusterin expression was associated with large tumor size (P = 0.04), estrogen and progesterone receptor negative status (P = 0.02 and P = 0.001, respectively) and with the progression from primary carcinoma to metastatic carcinoma in lymph nodes (80% metastatic nodes had positive expression) (P = 0.004).
Genetic heterogeneity of BRAF was studied by comparing the mutation status in different samples of tumor as follows: (a) 2 separate areas (each >1.5 cm in diameter) within the primary tumor, (b) a more than 1.5 cm area of primary carcinoma and a second 5 mm area simulating a fine needle aspiration sample from a different portion of the primary tumor, (c) primary carcinoma and its lymph node metastasis at thyroidectomy, (d) primary carcinoma and the recurrent metastasis, and (e) differentiated and anaplastic areas in the primary carcinoma.
GH was maintained in the concurrent lymph node metastases with some variations; however, two cases with clusters of HER2 amplified cells in the primary carcinoma showed HER2 amplification in the nodal metastasis.
Identical FRA16D deletions in two cell lines (one derived from the primary carcinoma and the other from a secondary metastasis) demonstrate that FRA16D DNA instability can be an early, transient event.
In a patient with esophageal squamous cell carcinoma, we sequenced all the p53 cDNA translated regions (exon 2-10) of primary carcinoma, and confirmed one p53 nonsense mutation in exon 10.
In contrast, the functional assay permitted us to detect p53 mutations in 66% of patients with stage T1 tumors (72% of case of high grade 3) and in all cases with primary carcinoma in situ and in 4 cases of stage T2 tumors.
Interestingly, among the matrix metalloproteinase family, only MMP7 was identified as a differentially overexpressed gene in both the primary carcinoma and the metastatic cells in comparison with the normal cells.
No normal thyroid tissues or primary tumors from which the cell lines were derived demonstrated exon 8 mutations, using this technique. p53 immunocytochemistry demonstrated a progression of p53 immunopositivity between synchronous and metachronous neoplasms, paralleling the neoplastic progression from a benign adenoma to primary carcinoma, regional, and distant metastasis and ultimately, the cell lines, where intense immunopositivity is noted.
Nuclear USP22 expression significantly increased from normal mucosa through adenoma to primary carcinoma (P < 0.0001) and from primary carcinoma to liver metastasis (P = 0.021).