La Petite presse : journal quotidien... / [rédacteur en chef : Balathier Bragelonne]

29 décembre 18841884/12/29 (A18,N6810)

MOESM2 of Tumor size, stage and grade alterations of urinary peptidome in RCC

Additional file 2: Table S2.   A) Peptides with a statistically significant (p < 0.05) urinary abundance (m/z area) according to the pT. B) Peptides with a statistical significant (p < 0.05) urinary abundance (m/z area) compared to CTRLs and at different pT (1 = pT1a; 2 = pT1b; 3 = pT2a and 4 = pT > 2b). Up/down refer to the over/under representation of the peptide in ccRCC patients compared to control subject

MOESM5 of Tumor size, stage and grade alterations of urinary peptidome in RCC

Additional file 5: Table S5.   Identification of MALDI signals varied according to tumour size, pT or grade. LM = linear mode, RM = reflector mode, PTM = possible hypothetical modification predicted by Mascot

The Contrasting Role of p16^Ink4A Patterns of Expression in Neuroendocrine and Non-Neuroendocrine Lung Tumors: A Comprehensive Analysis with Clinicopathologic and Molecular Correlations

<div><p>Lung cancer encompasses a constellation of malignancies with no validated prognostic markers. p16^Ink4A expression has been reported in different subtypes of lung cancers; however, its prognostic value is controversial. Here, we sought to investigate the clinical significance of p16^Ink4A immunoexpression according to specific staining patterns and its operational implications. A total of 502 tumors, including 277 adenocarcinomas, 84 squamous cell carcinomas, 22 large cell carcinomas, 47 typical carcinoids, 12 atypical carcinoids, 28 large cell neuroendocrine carcinomas, and 32 small cell carcinomas were reviewed and subjected to immunohistochemical analysis for p16^Ink4A and Ki67. The spectrum of p16^Ink4A expression was annotated for each case as negative, sporadic, focal, or diffuse. Expression at immunohistochemical level showed intra-tumor homogeneity, regardless tumor histotype. Enrichments in cells expressing p16^Ink4A were observed from lower- to higher-grade neuroendocrine malignancies, whereas a decrease was seen in poorly and undifferentiated non-neuroendocrine carcinomas. Tumor proliferation indices were higher in neuroendocrine tumors expressing p16^Ink4A while non-neuroendocrine malignancies immunoreactive for p16^Ink4A showed a decrease in Ki67-positive cells. Quantitative statistical analyses including each histotype and the p16^Ink4A status confirmed the independent prognostic role of p16^Ink4A expression, being a high-risk indicator in neuroendocrine tumors and a marker of good prognosis in non-neuroendocrine lung malignancies. In this study, we provide circumstantial evidence to suggest that the routinary assessment of p16^Ink4A expression using a three-tiered scoring algorithm, even in a small biopsy, may constitute a reliable, reproducible, and cost-effective substrate for a more accurate risk stratification of each individual patient.</p></div

Representative micrographs of p16^Ink4A expression patterns in primary lung tumors.

<p>For each case, the first core on the left side represents the matched non-neoplastic lung tissue, whereas the following four cores depict different topographic areas of the tumor, including tumor invasive front (original magnification, 5x). The histologic detail of the immunohistochemical analysis for each case can be appreciated in the insets (original magnification, 20x). A. Small cell carcinoma displaying diffuse p16^Ink4A immunostain; B. Moderately differentiated (G2) adenocarcinoma showing focal p16^Ink4A expression; C. Typical carcinoid with sporadic p16^Ink4A expression pattern; D. Poorly differentiated (G3) squamous cell carcinoma negative for p16^Ink4A.</p

Representation of the differential Ki67 values between p16^Ink4A-negative and p16^Ink4A-positive lung tumors.

<p>The highest differences in Ki67 indices according to p16^Ink4A expression can be observed in the poorly differentiated malignancies (<i>i</i>.<i>e</i>. small cell carcinomas and large cell carcinomas), with opposite fashions between neuroendocrine and non-neuroendocrine tumors.</p

Sox2 is a miR-34b target in prostate cancer.

<p><b>A)</b> Sox2 expression was analyzed by immunoblotting in BPH-1 or DU145 cells after transfection with miR-34b mimics or control sequence for 72 h. Untr., untreated sample. p-miR-34b or a-miR-34b, precursor or antagonist miR-34b; p-Ctrl or a-Ctrl, non-targeting controls for precursor or antagonist molecules. <b>B</b>) Sox2 immunoreactivity was analyzed in a prostate TMAs, which included normal tissues, pre-neoplastic (PIN) and tumor (PCa) lesions from 192 patients, and in benign prostatic hyperplasia (BPH) samples. Sox2 is highly expressed in basal cell layer from non-neoplastic tissues and in epithelial cells in cancer tissue. <b>C, D</b>) Sox2 elevated expression characterizes PCa tissues from PIN or BPH lesions and distinguishes PCa patients with biochemical relapse. The number of PIN, PCa or BPH cases (C) or of PCa patients who underwent or not biochemical relapse during clinical follow-up (serological PSA>0.2; D) according to nuclear Sox2 staining scores is illustrated. p = 0.02 or p = 0.0006, respectively by Chi-square test.</p

miRNA expression in TRAMP-derived tissues.

<p><b>A)</b> Global miRNA profiling of prostate cancer (PCa) or prostatic intraepithelial neoplasia (PIN) lesions isolated from TRAMP mice. <b>B</b>) Scatterplot diagram of miRNAs with differential expression of at least 20 folds between PIN and PCa tissues of TRAMP mice. Of the identified 121 deregulated miRNAs (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0130060#pone.0130060.s007" target="_blank">S1 Table</a>) 61 had human orthologs. <b>C, D</b>) Comparison of significant miRNA signatures between prostate cell lines and TRAMP lesions. Only four miRNAs were in common between the two experimental systems. Expression analysis followed by unsupervised hierarchical clustering <b>D</b>) of miR-224, -34b-3p, -138 and miR-34c-5p reveals that androgen-independent prostate cancer cells are more similar to TRAMP tissues than to androgen-dependent or non-tumorigenic prostate human cells.</p

Genome-wide screening of copy number alterations and LOH events in renal cell carcinomas and integration with gene expression profile-0

<p><b>Copyright information:</b></p><p>Taken from "Genome-wide screening of copy number alterations and LOH events in renal cell carcinomas and integration with gene expression profile"</p><p>http://www.molecular-cancer.com/content/7/1/6</p><p>Molecular Cancer 2008;7():6-6.</p><p>Published online 14 Jan 2008</p><p>PMCID:PMC2253555.</p><p></p>d blue blocks). Each tumor sample was compared to its matched normal blood sample, and regions of DNA copy number gain (red lines) and copy number loss (green lines) were plotted along each chromosome. Datasets from only GeneChip50K Hind arrays were used

Analysis of p16^Ink4A overexpression in neuroendocrine lung tumors reveals an increase in the proportion of positive neoplastic cells within each tumor histotype moving from lower to higher grade malignancies.

<p>Each bar represents a histotype, as indicated on the left; the specific patterns of p16^Ink4A immunoexpression are color-coded on the basis of the legend on the right. TC: typical carcinoid; AC: atypical carcinoid; LCNEC: large cell neuroendocrine carcinoma; SCLC: small cell carcinoma.</p