BMI and pausal status in 300 subjects affected by breast cancer and 300 control cases.

<p>Mantel – Haenszel χ² p<0.05.</p

Comparison of peak intensities average (μA) between Breast cancer patients with high BMI and low BMI.

<p>Only significant peaks (P-value<0.01) are reported.</p><p> <b>Legend:</b></p>*<p> = From IMAC 30 Dataset.</p>**<p> = From CM 10 Dataset.</p

Clinicopathological features in a case study of 300 patients affected by breast cancer and 300 control with negative mammography result.

*<p>: χ² test.</p

Release of ALCAM is sensitive to ADAM17/TACE silencing.

<p>(A) Analysis of lysates from TPC-1 and A2774 cells, resolved on 4–12% SDS-PAGE and immunoblotted with anti-ADAM17/TACE antibodies. Arrows indicate inactive (130 kDa) and active (80 kDa) forms of ADAM17/TACE enzyme. Normalization of results was obtained with immunoblotting analysis of beta-actin. (B) Expression of ADAM17/TACE protein by TPC-1 cells transfected with an ADAM17/TACE-specific small interfering RNA (siRNA) (OTP17), or with non-targeting siRNA (NT) as detected by western blot. The amount of protein was calculated by comparative densitometric scanning with beta-actin. (C) ELISA detection of ALCAM release by TPC-1 cells after transfection with siRNA specifically inhibiting ADAM-17/TACE (OTP17, black column) or with non-targeting siRNA (NT, white column). (D) Conditioned medium (CM) from TPC-1 cells, cultured with pervanadate (PV) (60 min), epidermal growth factor (EGF) (24 h), or medium alone (ctr, 24 h) in the presence (black columns) or in absence (white columns) of CGS27023A (CGS) was assessed by ELISA for ALCAM. Columns, means of three experiments (cells cultured in presence of 10, 1, or 0.1 µM CGS); bars, SD. *, P<0.05. Grey bar: in absence of CGS, but in presence of orthovanadate (OV).</p

Comparison of peak intensities average (μA) between high BMI breast cancer patients and healthy subjects.

<p>Only significant peaks (P-value<0.01) are reported.</p><p> <b>Legend:</b></p>*<p> = From IMAC 30 Dataset.</p>**<p> = From CM 10 Dataset.</p

Logistic multivariate model with breast cancer as dependent variable.

<p>Logistic multivariate model with breast cancer as dependent variable.</p

Changes in ALCAM expression induced by ionomycin or phorbol myristate acetate (PMA).

<p>Total lysates (Lys) and conditioned medium (CM) from TPC-1 cells, treated or not with 1 µM ionomycin (iono) or 50 ng/mL PMA for 2 h, were resolved by 3–8% SDS-PAGE and immunoblotted with ALCAM antibody. Both treatments led to an increase of secreted ALCAM isoforms; especially PMA induced a gain of 60-kDa isoform expression. Arrow indicates the membrane-localized ALCAM isoform in lysate, and arrowheads indicate shed-ALCAM isoforms in CM, respectively. Beta-actin was used as a loading control.</p

Immunohistochemical reactivity of thyroid tumors.

<p>ALCAM, activated leukocyte cell adhesion molecule; PTC, papillary thyroid carcinoma;</p><p>MTC, medullary thyroid carcinoma.</p><p>CD56 and TTF-1 were negative in three out of four PTC cases. MTCs showed comparable positive immunostaining results for CD56 but were completely negative for TTF-1.</p

CGS decreases TPC-1 cell motility.

<p>Cells were seeded onto cell culture plates, as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0017141#s4" target="_blank">materials and methods</a>. TPC-1 cells were exposed to CGS treatment or vehicle. At cell confluence, a scratch was performed using a 10 µl tip and the wound measured. After a 15 h treatment, the plate area remaining free of cells was measured. The cell-free area accounted for 44.5% of the image when the scratch was applied, P<0.05 versus DMSO control.</p

Clinical-pathological breast cancer characteristics and BMI, χ² test was used to calculate p-value.

<p>Clinical-pathological breast cancer characteristics and BMI, χ² test was used to calculate p-value.</p