La neutrophil gelatinase-associated lipocalin, ou LCN 2, facteur d’agressivité dans le carcinome rénal à cellules claires (CRCC)

Perrin, Christophe; Patard, Jean-Jaques; Jouan, Florence; Collet, Nicolas; Théoleyre, Sandrine; Edeline, Julien; Zerrouki, S.; Laguerre, Brigitte; Bellaud-Roturaud, M.-A.; Rioux‐Leclercq, Nathalie; Vigneau, Cécile

doi:10.1016/j.purol.2011.06.005

Cited by 13 publications

(7 citation statements)

References 18 publications

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“…El-Mesallamy et al , observed higher levels of lipocalin 2 in pre-operative cases compared to post-operative cases [47]. Similarly, clinico-pathological analyses of Lipocalin 2 in the present study showed higher levels of lipocalin 2 during pre-operative and pre-chemotherapy patient group.…”

Section: Discussionsupporting

confidence: 79%

MUC4-Mediated Regulation of Acute Phase Protein Lipocalin 2 through HER2/AKT/NF-κB Signaling in Pancreatic Cancer

Kaur

Sharma

Krishn

et al. 2014

Clinical Cancer Research

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Purpose MUC4 shows aberrant expression in early pancreatic lesions and a high specificity for pancreatic cancer (PC). It thus has a high potential to be a sensitive and specific biomarker. Unfortunately, its low serum level limits its diagnostic/prognostic potential. We here report that a multi-faceted acute phase protein lipocalin 2, regulated by MUC4, could be a potential diagnostic/prognostic marker for pancreatic cancer. Experimental Designs and Results Overexpression/knockdown, luciferase reporter and molecular inhibition studies revealed that MUC4 regulates lipocalin 2 by stabilizing HER2 and stimulating AKT, which results in the activation of NF-κB. Immunohistochemical analyses of lipocalin 2 and MUC4 showed a significant positive correlation between MUC4 and lipocalin 2 in primary, metastatic tissues (Spearman correlation coefficient 0.71, p-value=0.002) from rapid autopsy tissue sample from PC patients as well as in serum and tissue samples from spontaneous KRASG12D mouse PC model (Spearman correlation coefficient 0.98, p-value <0.05). Lipocalin 2 levels increased progressively with disease advancement (344.2 ±22.8 ng/ml for 10 week to 3067.2±572.6 for 50 week; p<0.0001). In human PC cases, significantly elevated levels of lipocalin 2 were observed in PC patients (148±13.18 ng/ml) in comparison to controls (73.27±4.9 ng/ml, p-value=0.014). Analyses of pre- and post-chemotherapy patients showed higher lipocalin 2 levels in pre-chemotherapy patients (121.7 ng/ml, 95% C.I. 98.1–150.9) in comparison to the post-chemotherapy (92.6 ng/ml, 95% C.I. 76.7–111.6, p-value=0.06) group. Conclusions The present study delineates the association and the downstream mechanisms of MUC4-regulated elevation of lipocalin-2 (via HER2/AKT/NF-κB) and its clinical significance for prognosis of pancreatic cancer.

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Section: Discussionsupporting

confidence: 79%

MUC4-Mediated Regulation of Acute Phase Protein Lipocalin 2 through HER2/AKT/NF-κB Signaling in Pancreatic Cancer

Kaur

Sharma

Krishn

et al. 2014

Clinical Cancer Research

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“…By immunohistochemistry, Perrin et al showed that NGAL was expressed by neutrophils infiltrating ccRCC and that the density of NGAL-expressing neutrophils was associated with poor outcomes (18). Furthermore, they reported that high NGAL concentrations in serum were also associated with shorter progression-free survival (18). In patients treated with sunitinib, Porta et al demonstrated that serum levels of NGAL were significant predictors of progression-free survival (19).…”

Section: Discussionmentioning

confidence: 99%

“…Tumor cells excrete elevated levels of NGAL resulting in an increase of the local concentration of MMP-9, which is capable of affecting various aspects of tumor progression. High concentrations of MMP-9/NGAL complex in serum have been associated with a shorter progression-free survival and poor overall survival (18). The results outlined in the present study indicate that the mean values of serum NGAL and MMP-9/NGAL complex are higher in ccRCC patients compared with oncocytoma patients.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of neutrophil gelatinase-associated lipocalin (NGAL), matrix metalloproteinase-9 (MMP-9) and their complex MMP-9/NGAL in sera and urine of patients with kidney tumors

Carlo

2013

Oncology Letters

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Recent evidence suggests that neutrophil gelatinase-associated lipocalin (NGAL) is required for the development and/or progression of benign and malignant disease, and is overexpressed in several types of tumor. Matrix metalloproteinase-9 (MMP-9), by degrading components of the extracellular matrix and thus promoting the release of growth factors, is important in tumor growth and tumorigenicity. NGAL protects MMP-9 from proteolytic degradation and enhances its enzymatic activities by binding and forming the MMP-9/NGAL complex. Therefore, NGAL, MMP-9 and their complex MMP-9/NGAL have been proposed as soluble biomarkers for numerous malignancies. In the present study, we measured the concentration of these molecules in sera and urine of patients with kidney disease using ELISA. Of these patients, 16 had clear cell renal cell carcinoma (ccRCC) and 4 had oncocytoma. Sera and urine samples of 53 healthy patients were used as controls. In sera, MMP-9 was enhanced in ccRCC patients compared with oncocytoma patients. In urine, the most abundant molecule was NGAL and its mean value was higher in cancer patients. However, there was a broad overlap of the data and we did not identify any correlation with disease type, stage or grade. Therefore, these molecules may not be useful as biomarkers for predicting kidney carcinoma.

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“…NGAL is a 25 kD protein produced by innate immunity cells, as well as tumor cells, and forms complexes with MMP-9 to protect it from degradation—thus enhancing tumor growth 57 . NGAL levels were measured in 85 patients prior to the initiation of Sunitinib treatment by immunohistochemistry 57 .…”

Section: Treatments For Advanced Renal Cell Carcinomamentioning

confidence: 99%

“…NGAL levels were measured in 85 patients prior to the initiation of Sunitinib treatment by immunohistochemistry 57 . Patients were classified as favorable (n=46) and intermediate (n=3) according to MSKCC criteria.…”

Section: Treatments For Advanced Renal Cell Carcinomamentioning

confidence: 99%

Molecular Marker for Predicting Treatment Response in Advanced Renal Cell Carcinoma: Does the Promise Fulfill Clinical Need?

2013

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Renal cell carcinoma (RCC) is largely diagnosed incidentally on imaging taken for unrelated reasons. The management of localized lesions is primarily extirpative with excellent results. Treatment of advanced RCC has evolved over recent years with the use of targeted therapies such as tyrosine kinase inhibitors, mammalian target of rapamycin inhibitors, and antibody-mediated therapies. The treatment response to these targeted therapies is highly variable, with no clear clinical method of identifying patients who will benefit from or not tolerate therapy. The field of molecular markers has evolved significantly in the last decade, with a multitude of markers identified that predict treatment response and drug toxicity. The following review critically evaluates those molecular markers that have been assessed for their utility in predicting treatment response in patients with advanced/metastatic renal cell carcinoma (mRCC). Identifying the ideal treatment for these patients will improve responses to therapy, minimize morbidity, and save significant healthcare dollars.

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La neutrophil gelatinase-associated lipocalin, ou LCN 2, facteur d’agressivité dans le carcinome rénal à cellules claires (CRCC)

Cited by 13 publications

References 18 publications

MUC4-Mediated Regulation of Acute Phase Protein Lipocalin 2 through HER2/AKT/NF-κB Signaling in Pancreatic Cancer

MUC4-Mediated Regulation of Acute Phase Protein Lipocalin 2 through HER2/AKT/NF-κB Signaling in Pancreatic Cancer

Evaluation of neutrophil gelatinase-associated lipocalin (NGAL), matrix metalloproteinase-9 (MMP-9) and their complex MMP-9/NGAL in sera and urine of patients with kidney tumors

Molecular Marker for Predicting Treatment Response in Advanced Renal Cell Carcinoma: Does the Promise Fulfill Clinical Need?

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