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1. Table S1 from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome

Author

Silwal-Pandit, Laxmi, primary, Stålberg, Stina M., primary, Johansson, Henrik J., primary, Mermelekas, Georgios, primary, Lothe, Inger Marie B., primary, Skrede, Martina L., primary, Dalsgaard, Astrid Marie, primary, Nebdal, Daniel J. H., primary, Helland, Åslaug, primary, Lingjærde, Ole Christian, primary, Labori, Knut Jørgen, primary, Skålhegg, Bjørn S., primary, Lehtiö, Janne, primary, and Kure, Elin H., primary

Published
2023
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2. Data from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome

Author

Silwal-Pandit, Laxmi, primary, Stålberg, Stina M., primary, Johansson, Henrik J., primary, Mermelekas, Georgios, primary, Lothe, Inger Marie B., primary, Skrede, Martina L., primary, Dalsgaard, Astrid Marie, primary, Nebdal, Daniel J. H., primary, Helland, Åslaug, primary, Lingjærde, Ole Christian, primary, Labori, Knut Jørgen, primary, Skålhegg, Bjørn S., primary, Lehtiö, Janne, primary, and Kure, Elin H., primary

Published
2023
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3. Table S5-S9 from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome

Author

Silwal-Pandit, Laxmi, primary, Stålberg, Stina M., primary, Johansson, Henrik J., primary, Mermelekas, Georgios, primary, Lothe, Inger Marie B., primary, Skrede, Martina L., primary, Dalsgaard, Astrid Marie, primary, Nebdal, Daniel J. H., primary, Helland, Åslaug, primary, Lingjærde, Ole Christian, primary, Labori, Knut Jørgen, primary, Skålhegg, Bjørn S., primary, Lehtiö, Janne, primary, and Kure, Elin H., primary

Published
2023
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4. Table S10A and S10B from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome

Author

Silwal-Pandit, Laxmi, primary, Stålberg, Stina M., primary, Johansson, Henrik J., primary, Mermelekas, Georgios, primary, Lothe, Inger Marie B., primary, Skrede, Martina L., primary, Dalsgaard, Astrid Marie, primary, Nebdal, Daniel J. H., primary, Helland, Åslaug, primary, Lingjærde, Ole Christian, primary, Labori, Knut Jørgen, primary, Skålhegg, Bjørn S., primary, Lehtiö, Janne, primary, and Kure, Elin H., primary

Published
2023
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5. Figures FS1-FS15 from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome

Author

Silwal-Pandit, Laxmi, primary, Stålberg, Stina M., primary, Johansson, Henrik J., primary, Mermelekas, Georgios, primary, Lothe, Inger Marie B., primary, Skrede, Martina L., primary, Dalsgaard, Astrid Marie, primary, Nebdal, Daniel J. H., primary, Helland, Åslaug, primary, Lingjærde, Ole Christian, primary, Labori, Knut Jørgen, primary, Skålhegg, Bjørn S., primary, Lehtiö, Janne, primary, and Kure, Elin H., primary

Published
2023
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6. Supplementary Methods SM1 from Proteome Analysis of Pancreatic Tumors Implicates Extracellular Matrix in Patient Outcome

Author

Silwal-Pandit, Laxmi, primary, Stålberg, Stina M., primary, Johansson, Henrik J., primary, Mermelekas, Georgios, primary, Lothe, Inger Marie B., primary, Skrede, Martina L., primary, Dalsgaard, Astrid Marie, primary, Nebdal, Daniel J. H., primary, Helland, Åslaug, primary, Lingjærde, Ole Christian, primary, Labori, Knut Jørgen, primary, Skålhegg, Bjørn S., primary, Lehtiö, Janne, primary, and Kure, Elin H., primary

Published
2023
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7. Supplementary Figure S3. The figure shows CNA profile of three IPMN samples. from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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8. Supplementary Figure S5. Frequency plot of the CNAs of periampullary adenocarcinomas based on site of origin. from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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9. Supplementary Table S1: Frequencies of gains and losses for selected genes in both OUH and TCGA cohorts. from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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10. Supplementary Figure S1. Heatmap shows the cytobands amplified and deleted in OUH and TCGA cohort. from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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11. Supplementary Figure S2. CNA profile of the two xenografts cell lines and their original tumors. from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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12. Data from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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13. Supplementary Table S3: Table shows the pathway deregulated in OUH and TCGA cohort. from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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14. Supplementary Figure S4. Correlation between genome instability index (GII) and ploidy. from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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15. Supplementary file: Legends of supplementary material from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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16. Supplementary Table S2: Table shows the correlation score (r) between allele frequency and gene expression from The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., primary, Bowitz Lothe, Inger Marie, primary, Labori, Knut Jørgen, primary, Dentro, Stefan C., primary, Buanes, Trond, primary, Skrede, Martina L., primary, Dalsgaard, Astrid M., primary, Munthe, Else, primary, Myklebost, Ola, primary, Lingjærde, Ole Christian, primary, Børresen-Dale, Anne-Lise, primary, Ikdahl, Tone, primary, Van Loo, Peter, primary, Nord, Silje, primary, and Kure, Elin H., primary

Published
2023
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17. Proteome analysis of pancreatic tumors implicates extracellular matrix in patient outcome

Author

Silwal-Pandit, Laxmi, primary, Stålberg, Stina M., additional, Johansson, Henrik Johan, additional, Mermelekas, Georgios, additional, Lothe, Inger Marie B., additional, Skrede, Martina L, additional, Dalsgaard, Astrid Marie, additional, Nebdal, Daniel J. H., additional, Helland, Åslaug, additional, Lingjærde, Ole Christian, additional, Labori, Knut Jørgen, additional, Skalhegg, Bjorn S, additional, Lehtio, Janne, additional, and Kure, Elin H, additional

Published
2022
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23. The cellular proteome of pancreatic ductal adenocarcinoma

Author

Silwal-Pandit, Laxmi, primary, Johansson, Henrik, additional, Stålberg, Stina M., additional, Mermelekas, Georgios, additional, Bowitz Lothe, Inger-Marie, additional, Skrede, Martina L., additional, Dalsgaard, Astrid M., additional, Helland, Åslaug, additional, Skålhegg, Bjørn S., additional, Labori, Knut Jørgen, additional, Lingjærde, Ole Christian, additional, Lehtiö, Janne, additional, and Kure, Elin, additional

Published
2019
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24. The fatty acid binding protein 7 (FABP7) is involved in proliferation and invasion of melanoma cells

Author

Trøen Gunhild, Rosnes Anne, Skrede Martina, Jørgensen Kjersti, Slipicevic Ana, Davidson Ben, and Flørenes Vivi

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background The molecular mechanisms underlying melanoma tumor development and progression are still not completely understood. One of the new candidates that emerged from a recent gene expression profiling study is fatty acid-binding protein 7 (FABP7), involved in lipid metabolism, gene regulation, cell growth and differentiation. Methods We studied the functional role of FABP7 in human melanoma cell lines and using immunohistochemistry analyzed its expression pattern and clinical role in 11 nevi, 149 primary melanomas and 68 metastases. Results FABP7 mRNA and protein level is down-regulated following treatment of melanoma cell lines with a PKC activator (PMA) or MEK1 inhibitor (PD98059). Down-regulation of FABP7 using siRNA decreased cell proliferation and invasion but did not affect apoptosis. In clinical specimens, FABP7 was expressed in 91% of nevi, 71% of primary melanomas and 70% of metastases, with a cytoplasmic and/or nuclear localization. FABP7 expression was associated with tumor thickness in superficial spreading melanoma (P = 0.021). In addition, we observed a trend for an association between FABP7 expression and Ki-67 score (P = 0.070) and shorter relapse-free survival (P = 0.069) in this group of patients. Conclusion Our data suggest that FABP7 can be regulated by PKC and the MAPK/ERK1/2 pathway through independent mechanisms in melanoma cell lines. Furthermore, FABP7 is involved in cell proliferation and invasion in vitro, and may be associated with tumor progression in melanoma.

Published
2008
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25. Variation in gene expression patterns in effusions and primary tumors from serous ovarian cancer patients

Author

Tropè Claes G, Givant-Horwitz Vered, Goldberg Iris, Berner Aasmund, Risberg Björn, Flørenes Vivi, Reich Reuven, Skrede Martina, Davidson Ben, Schaner Marci E, Kristensen Gunnar B, Nesland Jahn M, and Børresen-Dale Anne-Lise

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background While numerous studies have characterized primary ovarian tumors, little information is available regarding expression patterns of metastatic sites of this cancer. To define sets of genes that distinguish primary and metastatic ovarian tumors, we used cDNA microarrays to characterize global gene expression patterns in 38 effusions (28 peritoneal, 10 pleural) and 8 corresponding primary ovarian tumors, and searched for associations between expression patterns and clinical parameters. Results We observed multidimensional variation in expression patterns among the cancers. Coordinate variation in expression of genes from two chromosomal regions, 8q and 19q, was seen in subsets of the cancers indicating possible amplifications in these regions. A set of 112 unique genes of known function was differentially expressed between primary tumors and effusions using supervised analysis. Relatively few differences were seen between effusions isolated from the pleural and peritoneal cavities or between effusions from patients diagnosed with stage III and stage IV cancers. A set of 84 unique genes was identified that distinguished high from lower grade ovarian cancers. The results were corroborated using immunocytochemistry, mRNA in situ hybridization, and immunoblotting. Conclusion The extensive variation in expression patterns observed underscores the molecular heterogeneity of ovarian cancer, but suggests a similar molecular profile for ovarian carcinoma cells in serosal cavities.

Published
2005
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26. The Genomic Landscape of Pancreatic and Periampullary Adenocarcinoma

Author

Sandhu, Vandana, primary, Wedge, David C., additional, Bowitz Lothe, Inger Marie, additional, Labori, Knut Jørgen, additional, Dentro, Stefan C., additional, Buanes, Trond, additional, Skrede, Martina L., additional, Dalsgaard, Astrid M., additional, Munthe, Else, additional, Myklebost, Ola, additional, Lingjærde, Ole Christian, additional, Børresen-Dale, Anne-Lise, additional, Ikdahl, Tone, additional, Van Loo, Peter, additional, Nord, Silje, additional, and Kure, Elin H., additional

Published
2016
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27. Molecular signatures of mRNAs and miRNAs as prognostic biomarkers in pancreatobiliary and intestinal types of periampullary adenocarcinomas

Author

Sandhu, Vandana, primary, Bowitz Lothe, Inger Marie, additional, Labori, Knut Jørgen, additional, Lingjærde, Ole Christian, additional, Buanes, Trond, additional, Dalsgaard, Astrid M., additional, Skrede, Martina, additional, Hamfjord, Julian, additional, Haaland, Terese, additional, Eide, Tor J., additional, Børresen-Dale, Anne-Lise, additional, Ikdahl, Tone, additional, and Kure, Elin H., additional

Published
2015
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33. Variation in gene expression patterns in effusions and primary tumors from serous ovarian cancer patients

Author

Schaner, Marci E, primary, Davidson, Ben, additional, Skrede, Martina, additional, Reich, Reuven, additional, Flørenes, Vivi Ann, additional, Risberg, Björn, additional, Berner, Aasmund, additional, Goldberg, Iris, additional, Givant-Horwitz, Vered, additional, Tropè, Claes G, additional, Kristensen, Gunnar B, additional, Nesland, Jahn M, additional, and Børresen-Dale, Anne-Lise, additional

Published
2005
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36. Constant denaturant gel electrophoresis (CDGE) in BRCA1 mutation screening

Author

Andersen, Tone Ikdahl, primary, Eiken, Hans Geir, additional, Couch, Fergus, additional, Kaada, Grete, additional, Skrede, Martina, additional, Johnsen, Hilde, additional, Aloysius, Thomas A., additional, Tveit, Kjell M., additional, Tranebjærg, Lisbeth, additional, Dørum, Anne, additional, Møller, Pål, additional, Weber, Barbara L., additional, and Børresen‐Dale, Anne‐Lise, additional

Published
1998
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37. Constant denaturant gel electrophoresis (CDGE) inBRCA1 mutation screening

Author

Andersen, Tone Ikdahl, primary, Eiken, Hans Geir, additional, Couch, Fergus, additional, Kaada, Grete, additional, Skrede, Martina, additional, Johnsen, Hilde, additional, Aloysius, Thomas A., additional, Tveit, Kjell M., additional, Tranebjærg, Lisbeth, additional, Dørum, Anne, additional, Møller, Pål, additional, Weber, Barbara L., additional, and Børresen-Dale, Anne-Lise, additional

Published
1998
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38. Screening forESR mutations in breast and ovarian cancer patients

Author

Andersen, Tone Ikdahl, primary, Wooster, Richard, additional, Laake, Kirsten, additional, Collins, Nadine, additional, Warren, William, additional, Skrede, Martina, additional, Eeles, Rose, additional, Tveit, Kjell M., additional, Johnston, Stephen R. D., additional, Dowsett, Mitchell, additional, Olsen, Anne O., additional, Møller, Pål, additional, Stratton, Mike R., additional, and Børresen-Dale, Anne-Lise, additional

Published
1997
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39. Screening for ESR mutations in breast and ovarian cancer patients

Author

Andersen, Tone Ikdahl, primary, Wooster, Richard, additional, Laake, Kirsten, additional, Collins, Nadine, additional, Warren, William, additional, Skrede, Martina, additional, Eeles, Rose, additional, Tveit, Kjell M., additional, Johnston, Stephen R.D., additional, Dowsett, Mitchell, additional, Olsen, Anne O., additional, Møller, Pål, additional, Stratton, Mike R., additional, and Børresen‐Dale, Anne‐Lise, additional

Published
1997
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41. Wobble-enhanced ARMS Method for Detection of KRASand BRAFMutations

Author

Hamfjord, Julian, Stangeland, Astrid M., Skrede, Martina L., Tveit, Kjell M., Ikdahl, Tone, and Kure, Elin H.

Abstract

Monoclonal antibodies targeting the epidermal growth factor receptor have expanded the range of treatment options for patients with metastatic colorectal cancer. However, somatic mutations in the KRASand BRAFgenes have proven to be molecular predictors of resistance to treatment with anti-epidermal growth factor receptor therapy in these patients. Thus, we have developed a sensitive mutation assay, wobble-enhanced amplification refractory mutation system, for detecting the 8 most commonly reported mutations of clinical importance in the KRASand BRAFgenes; KRASg.34G>C (p.G12R), g.34G>A (p.G12S), g.34G>T (p.G12C), g.35G>A (p.G12D), g.35G>C (p.G12A), g.35G>T (p.G12V), g.38G>A (p.G13D), and BRAFg.1799T>A (p.V600E). A total of 28 candidate setups were designed based on bioinformatics and primerprobe design. Eight candidate setups were thus selected using a synthetic oligonucleotide model. The setups were further validated through several experiments using formalin-fixed paraffin-embedded tissue and cell lines. The results confirm that the wobble-enhanced amplification refractory mutation system method is quick, cost effective, and sensitive. The method is optimized to handle a typical template input of 1 to 20 ng DNA per polymerase chain reaction and can be implemented in any laboratory with ease with a real-time polymerase chain reaction instrument capable of handling TaqMan techonology. The steps used to develop this method can be implemented to design assays for other mutations located in KRAS, BRAF, or other candidate genes.

Published
2011
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42. Expression and activation of the nerve growth factor receptor TrkA in serous ovarian carcinoma.

Author

Davidson B, Reich R, Lazarovici P, Nesland JM, Skrede M, Risberg B, Tropé CG, and Flørenes VA

Subjects
Adult, Aged, Aged, 80 and over, Cyclin-Dependent Kinase Inhibitor p21, Cyclins analysis, Cystadenocarcinoma, Serous mortality, Female, Fibroblast Growth Factor 2 genetics, Humans, Middle Aged, Nerve Growth Factor analysis, Ovarian Neoplasms mortality, Peptide Fragments analysis, Poly(ADP-ribose) Polymerases analysis, RNA, Messenger analysis, Receptor, trkA physiology, Tumor Suppressor Protein p53 analysis, Vascular Endothelial Growth Factor A genetics, Cystadenocarcinoma, Serous chemistry, Ovarian Neoplasms chemistry, Receptor, trkA analysis
Abstract

Purpose: The purpose is to analyze the possible correlation between expression and activation of the high-affinity nerve growth factor (NGF) receptor TrkA, cell cycle protein expression, and disease outcome in serous ovarian carcinoma. In addition, we wished to study the possible link between expression of NGF, a novel angiogenic factor and its receptor TrkA, and the expression of factors involved in angiogenesis in effusions and solid tumors., Experimental Design: Sections from 80 malignant effusions and 65 corresponding solid tumors were evaluated for protein expression of NGF, TrkA, and phospho-TrkA (p-TrkA). Effusions were additionally studied for expression of p53, p21(WAF1/CIP1), Ki-67, and the M(r) 85,000-cleaved fragment of poly(ADP-ribose) polymerase (p85-PARP) using immunohistochemistry (IHC). Thirty-two effusions were studied for TrkA, p-TrkA, p53, and p21(WAF1/CIP1) expression using immunoblotting. mRNA expression of basic fibroblast growth factor (bFGF), interleukin 8, and vascular endothelial growth factor (VEGF) was studied in 63 effusions and all solid tumors using in situ hybridization. Protein expression of bFGF, interleukin 8, and VEGF was additionally studied in 30 effusions using IHC., Results: NGF, TrkA, and p-TrkA were expressed in carcinoma cells in effusions in 60 of 80 (75%), 64 of 80 (80%), and 15 of 80 (19%) specimens, respectively. In solid tumors, p-TrkA expression was more frequent (52 of 65 tumors; 80%) and was accompanied by p-TrkA expression in endothelial cells. NGF colocalized with bFGF protein (P = 0.016) and mRNA (P = 0.032) in effusions, and with VEGF (P < 0.001) and bFGF (P = 0.008) in solid tumors. In survival analysis, expression of p85-PARP (P = 0.017) and cytoplasmic TrkA (P < 0.001) in effusions predicted better outcome, whereas membrane expression of p-TrkA in solid tumors correlated with poor survival (P = 0.004). Diffuse expression of p53 and Ki-67 was often seen using IHC, whereas p21(WAF1/CIP1) and p85-PARP expression was infrequent and focal. None of these correlated with NGF or TrkA expression or activity., Conclusions: Coexpression of NGF with molecules involved in angiogenesis and p-TrkA expression in endothelial cells suggest that the proangiogenic role attributed to NGF in vitro and in vivo may be relevant in clinical cancer. Expression of p85-PARP as a marker of apoptosis and cytoplasmic expression of TrkA (probably representing nonglycosylated receptor) predict better outcome, whereas p-TrkA activation correlates with poor outcome in advanced stage serous ovarian carcinoma.

Published
2003

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