14 research outputs found
Images from sentinel lymph node mapping with nearinfrared fluorescence during robot-assisted laparoscopic hysterectomy for suspicious of cervical cancer
Pelvic Sentinel Lymph Node Detection: An Increasing Role in Surgical Approaches for Early-Stage Gynecological Malignant Diseases
The mesoscale eddies and Kuroshio transport in the western North Pacific east of Taiwan from 8-year (2003–2010) model reanalysis
Multivariate analysis of histomorphological and immunohistochemical prognostic factor in endometrial carcinoma
Activated Leukocyte Cell Adhesion Molecule soluble form (sALCAM), a potential biomarker of epithelial ovarian cancer is increased in type II tumors.
Activated Leukocyte Cell Adhesion Molecule (ALCAM) is involved in cell-cell
interactions in cancer. Shedding of its ectodomain by the metalloprotease
ADAM17/TACE generates a soluble form (sALCAM). Here we show that serum
sALCAM levels were significantly higher in Epithelial Ovarian Cancer (EOC)
(P<0.005) than in controls. The performance of sALCAM as classifier, tested by
receiver operating characteristic (ROC) curve, resulted in an area under the curve
(AUC) of 0.8067. Serum sALCAM levels showed direct correlation with
Carbohydrate Antigen-125 (CA125/MUC16). Moreover, significantly higher levels
were found in type II tumors, even in stage I/II, suggesting that elevated sALCAM is
an early feature of aggressive EOC. In addition, sALCAM levels were higher in
ascites than in sera, suggesting local processing of ALCAM in the peritoneal cavity.
In immunodeficient mice, intra-peritoneally implanted with a human EOC cell line,
human sALCAM progressively increased in serum and was even higher in the ascites.
The biochemical characterization of the sALCAM in EOC sera and ascites, showed
two predominant forms of approximately 95 and 65 kDa but no EOC-specific
isoform. In addition, full-length transmembrane ALCAM but no soluble form was
detected in tumor-derived exosomes found in ascites. Finally, in vitro invasion assays
showed that inhibition of ADAM17/TACE activity decreased EOC invasive
properties, while opposite effects were mediated by a sALCAM-Fc chimera and by an
antibody interfering with ALCAM/ALCAM interactions. Altogether these data
suggest that sALCAM is a marker of EOC, which correlates with more aggressive
type II tumors, and that ADAM17/TACE activity and sALCAM itself mediate
enhanced invasiveness