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1. Germline variation at 8q24 and prostate cancer risk in men of European ancestry.

Author

Carter B.D., Kerns S., Ostrer H., Zhang H.-W., Cao G., Lin J., Li M., Feng N., Li J., He W., Guo X., Sun Z., Wang G., Guo J., Southey M.C., FitzGerald L.M., Marsden G., Gomez-Caamano A., Carballo A., Peleteiro P., Calvo P., Szulkin R., Llorca J., Dierssen-Sotos T., Gomez-Acebo I., Lin H.-Y., Ostrander E.A., Bisbjerg R., Klarskov P., Roder M.A., Iversen P., Holleczek B., Stegmaier C., Schnoeller T., Bohnert P., John E.M., Ost P., Teo S.-H., Gamulin M., Kulis T., Kastelan Z., Slavov C., Popov E., Van den Broeck T., Joniau S., Larkin S., Castelao J.E., Martinez M.E., van Schaik R.H.N., Xu J., Lindstrom S., Riboli E., Berry C., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Freedman M., Cenee S., Sanchez M., Wiklund F., Chanock S.J., Easton D.F., Eeles R.A., Kote-Jarai Z., Conti D.V., Haiman C.A., Hutchinson A., Ling J., Papargiris M., Matejcic M., Saunders E.J., Dadaev T., Brook M.N., Wang K., Sheng X., Olama A.A.A., Schumacher F.R., Ingles S.A., Govindasami K., Benlloch S., Berndt S.I., Albanes D., Koutros S., Muir K., Stevens V.L., Gapstur S.M., Tangen C.M., Batra J., Clements J., Gronberg H., Pashayan N., Schleutker J., Wolk A., West C., Mucci L., Kraft P., Cancel-Tassin G., Sorensen K.D., Maehle L., Grindedal E.M., Strom S.S., Neal D.E., Hamdy F.C., Donovan J.L., Travis R.C., Hamilton R.J., Rosenstein B., Lu Y.-J., Giles G.G., Kibel A.S., Vega A., Bensen J.T., Kogevinas M., Penney K.L., Park J.Y., Stanford J.L., Cybulski C., Nordestgaard B.G., Brenner H., Maier C., Kim J., Teixeira M.R., Neuhausen S.L., De Ruyck K., Razack A., Newcomb L.F., Lessel D., Kaneva R., Usmani N., Claessens F., Townsend P.A., Dominguez M.G., Roobol M.J., Menegaux F., Khaw K.-T., Cannon-Albright L.A., Pandha H., Thibodeau S.N., Schaid D.J., Henderson B.E., Stern M.C., Thwaites A., Guy M., Whitmore I., Morgan A., Fisher C., Hazel S., Livni N., Cook M., Fachal L., Weinstein S., Beane Freeman L.E., Hoover R.N., Machiela M.J., Lophatananon A., Goodman P., Moya L., Srinivasan S., Kedda M.-A., Yeadon T., Eckert A., Eklund M., Cavalli-Bjoerkman C., Dunning A.M., Sipeky C., Hakansson N., Elliott R., Ranu H., Giovannucci E., Turman C., Hunter D.J., Cussenot O., Orntoft T.F., Lane A., Lewis S.J., Davis M., Key T.J., Brown P., Kulkarni G.S., Zlotta A.R., Fleshner N.E., Finelli A., Mao X., Marzec J., MacInnis R.J., Milne R., Hopper J.L., Aguado M., Bustamante M., Castano-Vinyals G., Gracia-Lavedan E., Cecchini L., Stampfer M., Ma J., Sellers T.A., Geybels M.S., Park H., Zachariah B., Kolb S., Wokolorczyk D., Jan Lubinski, Kluzniak W., Nielsen S.F., Weisher M., Cuk K., Vogel W., Luedeke M., Logothetis C.J., Paulo P., Cardoso M., Maia S., Silva M.P., Steele L., Ding Y.C., De Meerleer G., De Langhe S., Thierens H., Lim J., Tan M.H., Ong A.T., Lin D.W., Kachakova D., Mitkova A., Mitev V., Parliament M., Jenster G., Bangma C., Schroder F.H., Truong T., Koudou Y.A., Michael A., Kierzek A., Karlsson A., Broms M., Wu H., Aukim-Hastie C., Tillmans L., Riska S., McDonnell S.K., Dearnaley D., Spurdle A., Gardiner R., Hayes V., Butler L., Taylor R., Saunders P., Kujala P., Talala K., Taari K., Bentzen S., Hicks B., Vogt A., Cox A., George A., Toi A., Evans A., van der Kwast T.H., Imai T., Saito S., Zhao S.-C., Ren G., Zhang Y., Yu Y., Wu Y., Wu J., Zhou B., Pedersen J., Lobato-Busto R., Ruiz-Dominguez J.M., Mengual L., Alcaraz A., Pow-Sang J., Herkommer K., Vlahova A., Dikov T., Christova S., Carracedo A., Tretarre B., Rebillard X., Mulot C., Jan Adolfsson, Stattin P., Johansson J.-E., Martin R.M., Thompson I.M., Chambers S., Aitken J., Horvath L., Haynes A.-M., Tilley W., Risbridger G., Aly M., Nordstrom T., Pharoah P., Tammela T.L.J., Murtola T., Auvinen A., Burnet N., Barnett G., Andriole G., Klim A., Drake B.F., Borre M., Carter B.D., Kerns S., Ostrer H., Zhang H.-W., Cao G., Lin J., Li M., Feng N., Li J., He W., Guo X., Sun Z., Wang G., Guo J., Southey M.C., FitzGerald L.M., Marsden G., Gomez-Caamano A., Carballo A., Peleteiro P., Calvo P., Szulkin R., Llorca J., Dierssen-Sotos T., Gomez-Acebo I., Lin H.-Y., Ostrander E.A., Bisbjerg R., Klarskov P., Roder M.A., Iversen P., Holleczek B., Stegmaier C., Schnoeller T., Bohnert P., John E.M., Ost P., Teo S.-H., Gamulin M., Kulis T., Kastelan Z., Slavov C., Popov E., Van den Broeck T., Joniau S., Larkin S., Castelao J.E., Martinez M.E., van Schaik R.H.N., Xu J., Lindstrom S., Riboli E., Berry C., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Freedman M., Cenee S., Sanchez M., Wiklund F., Chanock S.J., Easton D.F., Eeles R.A., Kote-Jarai Z., Conti D.V., Haiman C.A., Hutchinson A., Ling J., Papargiris M., Matejcic M., Saunders E.J., Dadaev T., Brook M.N., Wang K., Sheng X., Olama A.A.A., Schumacher F.R., Ingles S.A., Govindasami K., Benlloch S., Berndt S.I., Albanes D., Koutros S., Muir K., Stevens V.L., Gapstur S.M., Tangen C.M., Batra J., Clements J., Gronberg H., Pashayan N., Schleutker J., Wolk A., West C., Mucci L., Kraft P., Cancel-Tassin G., Sorensen K.D., Maehle L., Grindedal E.M., Strom S.S., Neal D.E., Hamdy F.C., Donovan J.L., Travis R.C., Hamilton R.J., Rosenstein B., Lu Y.-J., Giles G.G., Kibel A.S., Vega A., Bensen J.T., Kogevinas M., Penney K.L., Park J.Y., Stanford J.L., Cybulski C., Nordestgaard B.G., Brenner H., Maier C., Kim J., Teixeira M.R., Neuhausen S.L., De Ruyck K., Razack A., Newcomb L.F., Lessel D., Kaneva R., Usmani N., Claessens F., Townsend P.A., Dominguez M.G., Roobol M.J., Menegaux F., Khaw K.-T., Cannon-Albright L.A., Pandha H., Thibodeau S.N., Schaid D.J., Henderson B.E., Stern M.C., Thwaites A., Guy M., Whitmore I., Morgan A., Fisher C., Hazel S., Livni N., Cook M., Fachal L., Weinstein S., Beane Freeman L.E., Hoover R.N., Machiela M.J., Lophatananon A., Goodman P., Moya L., Srinivasan S., Kedda M.-A., Yeadon T., Eckert A., Eklund M., Cavalli-Bjoerkman C., Dunning A.M., Sipeky C., Hakansson N., Elliott R., Ranu H., Giovannucci E., Turman C., Hunter D.J., Cussenot O., Orntoft T.F., Lane A., Lewis S.J., Davis M., Key T.J., Brown P., Kulkarni G.S., Zlotta A.R., Fleshner N.E., Finelli A., Mao X., Marzec J., MacInnis R.J., Milne R., Hopper J.L., Aguado M., Bustamante M., Castano-Vinyals G., Gracia-Lavedan E., Cecchini L., Stampfer M., Ma J., Sellers T.A., Geybels M.S., Park H., Zachariah B., Kolb S., Wokolorczyk D., Jan Lubinski, Kluzniak W., Nielsen S.F., Weisher M., Cuk K., Vogel W., Luedeke M., Logothetis C.J., Paulo P., Cardoso M., Maia S., Silva M.P., Steele L., Ding Y.C., De Meerleer G., De Langhe S., Thierens H., Lim J., Tan M.H., Ong A.T., Lin D.W., Kachakova D., Mitkova A., Mitev V., Parliament M., Jenster G., Bangma C., Schroder F.H., Truong T., Koudou Y.A., Michael A., Kierzek A., Karlsson A., Broms M., Wu H., Aukim-Hastie C., Tillmans L., Riska S., McDonnell S.K., Dearnaley D., Spurdle A., Gardiner R., Hayes V., Butler L., Taylor R., Saunders P., Kujala P., Talala K., Taari K., Bentzen S., Hicks B., Vogt A., Cox A., George A., Toi A., Evans A., van der Kwast T.H., Imai T., Saito S., Zhao S.-C., Ren G., Zhang Y., Yu Y., Wu Y., Wu J., Zhou B., Pedersen J., Lobato-Busto R., Ruiz-Dominguez J.M., Mengual L., Alcaraz A., Pow-Sang J., Herkommer K., Vlahova A., Dikov T., Christova S., Carracedo A., Tretarre B., Rebillard X., Mulot C., Jan Adolfsson, Stattin P., Johansson J.-E., Martin R.M., Thompson I.M., Chambers S., Aitken J., Horvath L., Haynes A.-M., Tilley W., Risbridger G., Aly M., Nordstrom T., Pharoah P., Tammela T.L.J., Murtola T., Auvinen A., Burnet N., Barnett G., Andriole G., Klim A., Drake B.F., and Borre M.

Abstract

Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 x 10-15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62-4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification.Copyright © 2018, The Author(s).

Published
2019

2. Erratum to: Germline variation at 8q24 and prostate cancer risk in men of European ancestry (Nature Communications, (2018), 9, 1, (4616), 10.1038/s41467-018-06863-1).

Author

Wang G., Lessel D., Kaneva R., Usmani N., Kastelan Z., Slavov C., Popov E., Van den Broeck T., Joniau S., Larkin S., Castelao J.E., Martinez M.E., van Schaik R.H.N., Xu J., Lindstrom S., Riboli E., Berry C., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Freedman M., Cenee S., Sanchez M., Wiklund F., Chanock S.J., Easton D.F., Eeles R.A., Kote-Jarai Z., Conti D.V., Haiman C.A., Hutchinson A., Ling J., Papargiris M., Matejcic M., Saunders E.J., Dadaev T., Brook M.N., Wang K., Sheng X., Olama A.A.A., Schumacher F.R., Ingles S.A., Govindasami K., Benlloch S., Berndt S.I., Albanes D., Koutros S., Muir K., Stevens V.L., Gapstur S.M., Tangen C.M., Batra J., Clements J., Gronberg H., Pashayan N., Schleutker J., Wolk A., West C., Mucci L., Kraft P., Cancel-Tassin G., Sorensen K.D., Maehle L., Grindedal E.M., Strom S.S., Neal D.E., Hamdy F.C., Donovan J.L., Travis R.C., Hamilton R.J., Rosenstein B., Lu Y.-J., Giles G.G., Kibel A.S., Vega A., Bensen J.T., Kogevinas M., Penney K.L., Park J.Y., Stanford J.L., Cybulski C., Nordestgaard B.G., Brenner H., Maier C., Kim J., Teixeira M.R., Neuhausen S.L., De Ruyck K., Razack A., Newcomb L.F., Claessens F., Townsend P.A., Gago-Dominguez M., Roobol M.J., Menegaux F., Khaw K.-T., Cannon-Albright L.A., Pandha H., Thibodeau S.N., Schaid D.J., Henderson B.E., Stern M.C., Thwaites A., Guy M., Whitmore I., Morgan A., Fisher C., Hazel S., Livni N., Cook M., Fachal L., Weinstein S., Beane Freeman L.E., Hoover R.N., Machiela M.J., Lophatananon A., Carter B.D., Goodman P., Moya L., Srinivasan S., Kedda M.-A., Yeadon T., Eckert A., Eklund M., Cavalli-Bjoerkman C., Dunning A.M., Sipeky C., Hakansson N., Elliott R., Ranu H., Giovannucci E., Turman C., Hunter D.J., Cussenot O., Orntoft T.F., Lane A., Lewis S.J., Davis M., Key T.J., Brown P., Kulkarni G.S., Zlotta A.R., Fleshner N.E., Finelli A., Mao X., Marzec J., MacInnis R.J., Milne R., Hopper J.L., Aguado M., Bustamante M., Castano-Vinyals G., Gracia-Lavedan E., Cecchini L., Stampfer M., Ma J., Sellers T.A., Geybels M.S., Park H., Zachariah B., Kolb S., Wokolorczyk D., Lubinski J., Kluzniak W., Nielsen S.F., Weisher M., Cuk K., Vogel W., Luedeke M., Logothetis C.J., Paulo P., Cardoso M., Maia S., Silva M.P., Steele L., Ding Y.C., De Meerleer G., De Langhe S., Thierens H., Lim J., Tan M.H., Ong A.T., Lin D.W., Kachakova D., Mitkova A., Mitev V., Parliament M., Jenster G., Bangma C., Schroder F.H., Truong T., Koudou Y.A., Michael A., Kierzek A., Karlsson A., Broms M., Wu H., Aukim-Hastie C., Tillmans L., Riska S., McDonnell S.K., Dearnaley D., Spurdle A., Gardiner R., Hayes V., Butler L., Taylor R., Saunders P., Kujala P., Talala K., Taari K., Bentzen S., Hicks B., Vogt A., Cox A., George A., Toi A., Evans A., van der Kwast T.H., Imai T., Saito S., Zhao S.-C., Ren G., Zhang Y., Yu Y., Wu Y., Wu J., Zhou B., Pedersen J., Lobato-Busto R., Ruiz-Dominguez J.M., Mengual L., Alcaraz A., Pow-Sang J., Herkommer K., Vlahova A., Dikov T., Christova S., Carracedo A., Tretarre B., Rebillard X., Mulot C., Adolfsson J., Stattin P., Johansson J.-E., Martin R.M., Thompson I.M., Chambers S., Aitken J., Horvath L., Haynes A.-M., Tilley W., Risbridger G., Aly M., Nordstrom T., Pharoah P., Tammela T.L.J., Murtola T., Auvinen A., Burnet N., Barnett G., Andriole G., Klim A., Drake B.F., Borre M., Kerns S., Ostrer H., Zhang H.-W., Cao G., Lin J., Li M., Feng N., Li J., He W., Guo X., Sun Z., Guo J., Southey M.C., FitzGerald L.M., Marsden G., Gomez-Caamano A., Carballo A., Peleteiro P., Calvo P., Szulkin R., Llorca J., Dierssen-Sotos T., Gomez-Acebo I., Lin H.-Y., Ostrander E.A., Bisbjerg R., Klarskov P., Roder M.A., Iversen P., Holleczek B., Stegmaier C., Schnoeller T., Bohnert P., John E.M., Ost P., Teo S.-H., Gamulin M., Kulis T., Wang G., Lessel D., Kaneva R., Usmani N., Kastelan Z., Slavov C., Popov E., Van den Broeck T., Joniau S., Larkin S., Castelao J.E., Martinez M.E., van Schaik R.H.N., Xu J., Lindstrom S., Riboli E., Berry C., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Freedman M., Cenee S., Sanchez M., Wiklund F., Chanock S.J., Easton D.F., Eeles R.A., Kote-Jarai Z., Conti D.V., Haiman C.A., Hutchinson A., Ling J., Papargiris M., Matejcic M., Saunders E.J., Dadaev T., Brook M.N., Wang K., Sheng X., Olama A.A.A., Schumacher F.R., Ingles S.A., Govindasami K., Benlloch S., Berndt S.I., Albanes D., Koutros S., Muir K., Stevens V.L., Gapstur S.M., Tangen C.M., Batra J., Clements J., Gronberg H., Pashayan N., Schleutker J., Wolk A., West C., Mucci L., Kraft P., Cancel-Tassin G., Sorensen K.D., Maehle L., Grindedal E.M., Strom S.S., Neal D.E., Hamdy F.C., Donovan J.L., Travis R.C., Hamilton R.J., Rosenstein B., Lu Y.-J., Giles G.G., Kibel A.S., Vega A., Bensen J.T., Kogevinas M., Penney K.L., Park J.Y., Stanford J.L., Cybulski C., Nordestgaard B.G., Brenner H., Maier C., Kim J., Teixeira M.R., Neuhausen S.L., De Ruyck K., Razack A., Newcomb L.F., Claessens F., Townsend P.A., Gago-Dominguez M., Roobol M.J., Menegaux F., Khaw K.-T., Cannon-Albright L.A., Pandha H., Thibodeau S.N., Schaid D.J., Henderson B.E., Stern M.C., Thwaites A., Guy M., Whitmore I., Morgan A., Fisher C., Hazel S., Livni N., Cook M., Fachal L., Weinstein S., Beane Freeman L.E., Hoover R.N., Machiela M.J., Lophatananon A., Carter B.D., Goodman P., Moya L., Srinivasan S., Kedda M.-A., Yeadon T., Eckert A., Eklund M., Cavalli-Bjoerkman C., Dunning A.M., Sipeky C., Hakansson N., Elliott R., Ranu H., Giovannucci E., Turman C., Hunter D.J., Cussenot O., Orntoft T.F., Lane A., Lewis S.J., Davis M., Key T.J., Brown P., Kulkarni G.S., Zlotta A.R., Fleshner N.E., Finelli A., Mao X., Marzec J., MacInnis R.J., Milne R., Hopper J.L., Aguado M., Bustamante M., Castano-Vinyals G., Gracia-Lavedan E., Cecchini L., Stampfer M., Ma J., Sellers T.A., Geybels M.S., Park H., Zachariah B., Kolb S., Wokolorczyk D., Lubinski J., Kluzniak W., Nielsen S.F., Weisher M., Cuk K., Vogel W., Luedeke M., Logothetis C.J., Paulo P., Cardoso M., Maia S., Silva M.P., Steele L., Ding Y.C., De Meerleer G., De Langhe S., Thierens H., Lim J., Tan M.H., Ong A.T., Lin D.W., Kachakova D., Mitkova A., Mitev V., Parliament M., Jenster G., Bangma C., Schroder F.H., Truong T., Koudou Y.A., Michael A., Kierzek A., Karlsson A., Broms M., Wu H., Aukim-Hastie C., Tillmans L., Riska S., McDonnell S.K., Dearnaley D., Spurdle A., Gardiner R., Hayes V., Butler L., Taylor R., Saunders P., Kujala P., Talala K., Taari K., Bentzen S., Hicks B., Vogt A., Cox A., George A., Toi A., Evans A., van der Kwast T.H., Imai T., Saito S., Zhao S.-C., Ren G., Zhang Y., Yu Y., Wu Y., Wu J., Zhou B., Pedersen J., Lobato-Busto R., Ruiz-Dominguez J.M., Mengual L., Alcaraz A., Pow-Sang J., Herkommer K., Vlahova A., Dikov T., Christova S., Carracedo A., Tretarre B., Rebillard X., Mulot C., Adolfsson J., Stattin P., Johansson J.-E., Martin R.M., Thompson I.M., Chambers S., Aitken J., Horvath L., Haynes A.-M., Tilley W., Risbridger G., Aly M., Nordstrom T., Pharoah P., Tammela T.L.J., Murtola T., Auvinen A., Burnet N., Barnett G., Andriole G., Klim A., Drake B.F., Borre M., Kerns S., Ostrer H., Zhang H.-W., Cao G., Lin J., Li M., Feng N., Li J., He W., Guo X., Sun Z., Guo J., Southey M.C., FitzGerald L.M., Marsden G., Gomez-Caamano A., Carballo A., Peleteiro P., Calvo P., Szulkin R., Llorca J., Dierssen-Sotos T., Gomez-Acebo I., Lin H.-Y., Ostrander E.A., Bisbjerg R., Klarskov P., Roder M.A., Iversen P., Holleczek B., Stegmaier C., Schnoeller T., Bohnert P., John E.M., Ost P., Teo S.-H., Gamulin M., and Kulis T.

Abstract

The original version of this Article contained an error in the spelling of the author Manuela Gago-Dominguez, which was incorrectly given as Manuela G. Dominguez. This has now been corrected in both the PDF and HTML versions of the Article.Copyright © 2019, The Author(s).

Published
2019

3. Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants.

Author

Stampfer M., Ranu H., Hicks B., Vogt A., Cox A., Davis M., Brown P., George A., Marsden G., Lane A., Lewis S.J., Berry C., Kulkarni G.S., Toi A., Evans A., Zlotta A.R., Van Der Kwast T.H., Imai T., Saito S., Marzec J., Cao G., Lin J., Li M., Zhao S.-C., Ren G., Yu Y., Wu Y., Wu J., Zhou B., Zhang Y., Li J., He W., Guo J., Pedersen J., Hopper J.L., Milne R., Klim A., Carballo A., Lobato-Busto R., Peleteiro P., Calvo P., Aguado M., Ruiz-Dominguez J.M., Cecchini L., Mengual L., Alcaraz A., Bustamante M., Gracia-Lavedan E., Dierssen-Sotos T., Gomez-Acebo I., Pow-Sang J., Park H., Zachariah B., Kluzniak W., Kolb S., Klarskov P., Stegmaier C., Vogel W., Herkommer K., Bohnert P., Maia S., Silva M.P., De Langhe S., Thierens H., Tan M.H., Ong A.T., Kastelan Z., Popov E., Kachakova D., Mitkova A., Vlahova A., Dikov T., Christova S., Carracedo A., Bangma C., Schroder F.H., Cenee S., Tretarre B., Rebillard X., Mulot C., Sanchez M., Adolfsson J., Stattin P., Johansson J.-E., Cavalli-Bjoerkman C., Karlsson A., Broms M., Wu H., Tillmans L., Riska S., Freedman M., Wiklund F., Chanock S., Henderson B.E., Easton D.F., Haiman C.A., Eeles R.A., Conti D.V., Kote-Jarai Z., Hutchinson A., Ling J., Papargiris M., Dadaev T., Saunders E.J., Newcombe P.J., Anokian E., Leongamornlert D.A., Brook M.N., Cieza-Borrella C., Mijuskovic M., Wakerell S., Olama A.A.A., Schumacher F.R., Berndt S.I., Benlloch S., Ahmed M., Goh C., Sheng X., Zhang Z., Muir K., Govindasami K., Lophatananon A., Stevens V.L., Gapstur S.M., Carter B.D., Tangen C.M., Goodman P., Thompson I.M., Batra J., Chambers S., Moya L., Clements J., Horvath L., Tilley W., Risbridger G., Gronberg H., Aly M., Nordstrom T., Pharoah P., Pashayan N., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Albanes D., Weinstein S., Wolk A., Hakansson N., West C., Dunning A.M., Burnet N., Mucci L., Giovannucci E., Andriole G., Cussenot O., Cancel-Tassin G., Koutros S., Freeman L.E.B., Sorensen K.D., Orntoft T.F., Borre M., Maehle L., Grindedal E.M., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Travis R.C., Key T.J., Hamilton R.J., Fleshner N.E., Finelli A., Ingles S.A., Stern M.C., Rosenstein B., Kerns S., Ostrer H., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Guo X., Wang G., Sun Z., Giles G.G., Southey M.C., MacInnis R.J., Fitzgerald L.M., Kibel A.S., Drake B.F., Vega A., Gomez-Caamano A., Fachal L., Szulkin R., Eklund M., Kogevinas M., Llorca J., Castano-Vinyals G., Penney K.L., Park J.Y., Sellers T.A., Lin H.-Y., Stanford J.L., Cybulski C., Wokolorczyk D., Lubinski J., Ostrander E.A., Geybels M.S., Nordestgaard Bo.G., Nielsen S.F., Weisher M., Bisbjerg R., Roder M.A., Iversen P., Brenner H., Cuk K., Holleczek B., Maier C., Luedeke M., Schnoeller T., Kim J., Logothetis C.J., John E.M., Teixeira M.R., Paulo P., Cardoso M., Neuhausen S.L., Steele L., Ding Y.C., De Ruyck K., De Meerleer G., Ost P., Razack A., Lim J., Teo S.-H., Lin D.W., Newcomb L.F., Lessel D., Gamulin M., Kulis T., Kaneva R., Usmani N., Slavov C., Mitev V., Parliament M., Singhal S., Claessens F., Joniau S., Van Den Broeck T., Larkin S., Townsend P.A., Aukim-Hastie C., Gago-Dominguez M., Castelao J.E., Martinez M.E., Roobol M.J., Jenster G., Van Schaik R.H.N., Menegaux F., Truong T., Koudou Y.A., Xu J., Khaw K.-T., Cannon-Albright L., Pandha H., Michael A., Kierzek A., Thibodeau S.N., McDonnell S.K., Schaid D.J., Lindstrom S., Turman C., Ma J., Hunter D.J., Riboli E., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Hoover R.N., Machiela M.J., Kraft P., Cook M., Thwaites A., Guy M., Whitmore I., Morgan A., Fisher C., Hazel S., Livni N., Spurdle A., Srinivasan S., Kedda M.-A., Aitken J., Gardiner R., Hayes V., Butler L., Taylor R., Yeadon T., Eckert A., Saunders P., Haynes A.-M., Kujala P., Talala K., Murtola T., Taari K., Dearnaley D., Barnett G., Bentzen So., Elliott R., Stampfer M., Ranu H., Hicks B., Vogt A., Cox A., Davis M., Brown P., George A., Marsden G., Lane A., Lewis S.J., Berry C., Kulkarni G.S., Toi A., Evans A., Zlotta A.R., Van Der Kwast T.H., Imai T., Saito S., Marzec J., Cao G., Lin J., Li M., Zhao S.-C., Ren G., Yu Y., Wu Y., Wu J., Zhou B., Zhang Y., Li J., He W., Guo J., Pedersen J., Hopper J.L., Milne R., Klim A., Carballo A., Lobato-Busto R., Peleteiro P., Calvo P., Aguado M., Ruiz-Dominguez J.M., Cecchini L., Mengual L., Alcaraz A., Bustamante M., Gracia-Lavedan E., Dierssen-Sotos T., Gomez-Acebo I., Pow-Sang J., Park H., Zachariah B., Kluzniak W., Kolb S., Klarskov P., Stegmaier C., Vogel W., Herkommer K., Bohnert P., Maia S., Silva M.P., De Langhe S., Thierens H., Tan M.H., Ong A.T., Kastelan Z., Popov E., Kachakova D., Mitkova A., Vlahova A., Dikov T., Christova S., Carracedo A., Bangma C., Schroder F.H., Cenee S., Tretarre B., Rebillard X., Mulot C., Sanchez M., Adolfsson J., Stattin P., Johansson J.-E., Cavalli-Bjoerkman C., Karlsson A., Broms M., Wu H., Tillmans L., Riska S., Freedman M., Wiklund F., Chanock S., Henderson B.E., Easton D.F., Haiman C.A., Eeles R.A., Conti D.V., Kote-Jarai Z., Hutchinson A., Ling J., Papargiris M., Dadaev T., Saunders E.J., Newcombe P.J., Anokian E., Leongamornlert D.A., Brook M.N., Cieza-Borrella C., Mijuskovic M., Wakerell S., Olama A.A.A., Schumacher F.R., Berndt S.I., Benlloch S., Ahmed M., Goh C., Sheng X., Zhang Z., Muir K., Govindasami K., Lophatananon A., Stevens V.L., Gapstur S.M., Carter B.D., Tangen C.M., Goodman P., Thompson I.M., Batra J., Chambers S., Moya L., Clements J., Horvath L., Tilley W., Risbridger G., Gronberg H., Aly M., Nordstrom T., Pharoah P., Pashayan N., Schleutker J., Tammela T.L.J., Sipeky C., Auvinen A., Albanes D., Weinstein S., Wolk A., Hakansson N., West C., Dunning A.M., Burnet N., Mucci L., Giovannucci E., Andriole G., Cussenot O., Cancel-Tassin G., Koutros S., Freeman L.E.B., Sorensen K.D., Orntoft T.F., Borre M., Maehle L., Grindedal E.M., Neal D.E., Donovan J.L., Hamdy F.C., Martin R.M., Travis R.C., Key T.J., Hamilton R.J., Fleshner N.E., Finelli A., Ingles S.A., Stern M.C., Rosenstein B., Kerns S., Ostrer H., Lu Y.-J., Zhang H.-W., Feng N., Mao X., Guo X., Wang G., Sun Z., Giles G.G., Southey M.C., MacInnis R.J., Fitzgerald L.M., Kibel A.S., Drake B.F., Vega A., Gomez-Caamano A., Fachal L., Szulkin R., Eklund M., Kogevinas M., Llorca J., Castano-Vinyals G., Penney K.L., Park J.Y., Sellers T.A., Lin H.-Y., Stanford J.L., Cybulski C., Wokolorczyk D., Lubinski J., Ostrander E.A., Geybels M.S., Nordestgaard Bo.G., Nielsen S.F., Weisher M., Bisbjerg R., Roder M.A., Iversen P., Brenner H., Cuk K., Holleczek B., Maier C., Luedeke M., Schnoeller T., Kim J., Logothetis C.J., John E.M., Teixeira M.R., Paulo P., Cardoso M., Neuhausen S.L., Steele L., Ding Y.C., De Ruyck K., De Meerleer G., Ost P., Razack A., Lim J., Teo S.-H., Lin D.W., Newcomb L.F., Lessel D., Gamulin M., Kulis T., Kaneva R., Usmani N., Slavov C., Mitev V., Parliament M., Singhal S., Claessens F., Joniau S., Van Den Broeck T., Larkin S., Townsend P.A., Aukim-Hastie C., Gago-Dominguez M., Castelao J.E., Martinez M.E., Roobol M.J., Jenster G., Van Schaik R.H.N., Menegaux F., Truong T., Koudou Y.A., Xu J., Khaw K.-T., Cannon-Albright L., Pandha H., Michael A., Kierzek A., Thibodeau S.N., McDonnell S.K., Schaid D.J., Lindstrom S., Turman C., Ma J., Hunter D.J., Riboli E., Siddiq A., Canzian F., Kolonel L.N., Le Marchand L., Hoover R.N., Machiela M.J., Kraft P., Cook M., Thwaites A., Guy M., Whitmore I., Morgan A., Fisher C., Hazel S., Livni N., Spurdle A., Srinivasan S., Kedda M.-A., Aitken J., Gardiner R., Hayes V., Butler L., Taylor R., Yeadon T., Eckert A., Saunders P., Haynes A.-M., Kujala P., Talala K., Murtola T., Taari K., Dearnaley D., Barnett G., Bentzen So., and Elliott R.

Abstract

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling.Copyright © 2018 The Author(s).

Published
2018

4. Short-term versus long-term addition of cyproterone acetate to buserelin therapy in comparison with orchidectomy in the treatment of metastatic prostate cancer

Author

Klijn, J.G.M., Voogt, H.J. de, Studer, U.E., Schroder, F.H., Sylvester, R., and De Pauw, M.

Subjects
Prostate cancer -- Care and treatment, Metastasis -- Care and treatment, Antiandrogens -- Evaluation, Orchiectomy -- Evaluation, Health
Abstract

In an open, multicenter, three-armed, randomized study, we compared the effects of short-term (2 weeks) and continuous addition of the antiandrogen cyproterone acetate to the luteinizing hormone-releasing hormone agonist buserelin to those of orchidectomy in patients with advanced prostate cancer. No significant differences among the three treatment arms with respect to response rate, subjective response, time-to-progression, overall survival, and cancer deaths were observed. It was concluded that the short-term or continuous addition of cyproterone acetate to buserelin administered intranasally did not improve treatment results compared to orchidectomy only.

Published
1993

6. Extracorporeal shock wave treatment of common bile duct stones: experience with two different lithotriptors at a single institution

Author

den Toom, R., Nijs, H.G.T., van Blankenstein, M., Lameris, J.S., Schroder, F.H., and Terpstra, O.T.

Subjects
Common bile duct calculi -- Care and treatment, Ultrasonic lithotripsy -- Cases, Health
Abstract

Gallstones in the common bile duct, conduit for bile from the gallbladder to the duodenal portion of the small intestine, can be removed by surgical exploration of the common duct. However, for elderly or high-risk patients, this procedure is associated with severe morbidity and mortality. Extracorporeal shock wave lithotripsy can be used to noninvasively treat retained common bile duct stones. This procedure uses shock waves focused on the gallstone to break up the stone. A report is presented of treatment of 62 patients with retained common duct stones using a first and second generation lithotriptor. Thirteen patients were treated using the earlier electrohydraulic lithotriptor, and 43 were treated using the second generation electromagnetic lithotriptor. General anesthesia was used for all of the patients treated with the first generation instrument, compared with only l of the 43 patients treated with the newer lithotriptor. More sessions and more shock waves were needed by the patients treated with the newer lithotriptor. Stone fragmentation was achieved in all of the patients using the earlier instrument, compared with 86 percent of those treated with the newer instrument. At follow-up, at an average of 43 months for the earlier lithotriptor group and 18 months for the newer instrument group, no patients had any gallbladder-related complaints. It is concluded that both extracorporeal shock wave devises are safe and effective in treating retained common bile duct stones. This procedure should be considered before surgery is undertaken in elderly or high-risk patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

7. Prostate-cancer mortality at 11 years of follow-up

Author

Schroder, F.H., Hugosson, J., Roobol, M.J., Tammela, T.L.J., Ciatto, S., Nelen, V., Kwiatkowski, M., Lujan, M., Lilja, H., Zappa, M., Denis, L.J., Recker, F., Paez, A., Maattanen, L., Bangma, C.H., Aus, G., Carlsson, S., Villers, A., Rebillard, X., Kwast, T. van der, Kujala, P.M., Blijenberg, B.G., Stenman, U.H., Huber, A., Taari, K., Hakama, M., Moss, S.M., Koning, H.J. de, Auvinen, A., Raaijmakers, R., Urology, Pathology, Clinical Chemistry, and Public Health

Subjects
Male, Risk, medicine.medical_specialty, Randomization, Prostate-Specific Antigen/blood, Kaplan-Meier Estimate, Rate ratio, law.invention, Prostate cancer, SDG 3 - Good Health and Well-being, Randomized controlled trial, law, Cause of Death, Internal medicine, medicine, Humans, Early Detection of Cancer, Renal disorder [IGMD 9], Aged, Cause of death, Prostatic Neoplasms/diagnosis, Gynecology, business.industry, Hormonal regulation [IGMD 6], Age Factors, Prostate cancer mortality, General Medicine, Middle Aged, medicine.disease, Confidence interval, Risk of death, business, Follow-Up Studies
Abstract

Item does not contain fulltext BACKGROUND: Several trials evaluating the effect of prostate-specific antigen (PSA) testing on prostate-cancer mortality have shown conflicting results. We updated prostate-cancer mortality in the European Randomized Study of Screening for Prostate Cancer with 2 additional years of follow-up. METHODS: The study involved 182,160 men between the ages of 50 and 74 years at entry, with a predefined core age group of 162,388 men 55 to 69 years of age. The trial was conducted in eight European countries. Men who were randomly assigned to the screening group were offered PSA-based screening, whereas those in the control group were not offered such screening. The primary outcome was mortality from prostate cancer. RESULTS: After a median follow-up of 11 years in the core age group, the relative reduction in the risk of death from prostate cancer in the screening group was 21% (rate ratio, 0.79; 95% confidence interval [CI], 0.68 to 0.91; P=0.001), and 29% after adjustment for noncompliance. The absolute reduction in mortality in the screening group was 0.10 deaths per 1000 person-years or 1.07 deaths per 1000 men who underwent randomization. The rate ratio for death from prostate cancer during follow-up years 10 and 11 was 0.62 (95% CI, 0.45 to 0.85; P=0.003). To prevent one death from prostate cancer at 11 years of follow-up, 1055 men would need to be invited for screening and 37 cancers would need to be detected. There was no significant between-group difference in all-cause mortality. CONCLUSIONS: Analyses after 2 additional years of follow-up consolidated our previous finding that PSA-based screening significantly reduced mortality from prostate cancer but did not affect all-cause mortality. (Current Controlled Trials number, ISRCTN49127736.).

Published
2012

8. Prospective Study of Diagnostic Accuracy Comparing Prostate Cancer Detection by Transrectal Ultrasound-Guided Biopsy Versus Magnetic Resonance (MR) Imaging with Subsequent MR-guided Biopsy in Men Without Previous Prostate Biopsies

Author

Pokorny, M.R., Rooij, M. de, Duncan, E., Schroder, F.H., Parkinson, R., Barentsz, J.O., Thompson, L.C., Pokorny, M.R., Rooij, M. de, Duncan, E., Schroder, F.H., Parkinson, R., Barentsz, J.O., and Thompson, L.C.

Abstract

Item does not contain fulltext, BACKGROUND: The current diagnosis of prostate cancer (PCa) uses transrectal ultrasound-guided biopsy (TRUSGB). TRUSGB leads to sampling errors causing delayed diagnosis, overdetection of indolent PCa, and misclassification. Advances in multiparametric magnetic resonance imaging (mpMRI) suggest that imaging and selective magnetic resonance (MR)-guided biopsy (MRGB) may be superior to TRUSGB. OBJECTIVE: To compare the diagnostic efficacy of the magnetic resonance imaging (MRI) pathway with TRUSGB. DESIGN, SETTING, AND PARTICIPANTS: A total of 223 consecutive biopsy-naive men referred to a urologist with elevated prostate-specific antigen participated in a single-institution, prospective, investigator-blinded, diagnostic study from July 2012 through January 2013. INTERVENTION: All participants had mpMRI and TRUSGB. Men with equivocal or suspicious lesions on mpMRI also underwent MRGB. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: The primary outcome was PCa detection. Secondary outcomes were histopathologic details of biopsy and radical prostatectomy specimens, adverse events, and MRI reader performance. Sensitivity, specificity, negative predictive values (NPVs), and positive predictive values were estimated and basic statistics presented by number (percentage) or median (interquartile range). RESULTS AND LIMITATIONS: Of 223 men, 142 (63.7%) had PCa. TRUSGB detected 126 cases of PCa in 223 men (56.5%) including 47 (37.3%) classed as low risk. MRGB detected 99 cases of PCa in 142 men (69.7%) with equivocal or suspicious mpMRI, of which 6 (6.1%) were low risk. The MRGB pathway reduced the need for biopsy by 51%, decreased the diagnosis of low-risk PCa by 89.4%, and increased the detection of intermediate/high-risk PCa by 17.7%. The estimated NPVs of TRUSGB and MRGB for intermediate/high-risk disease were 71.9% and 96.9%, respectively. The main limitation is the lack of long follow-up. CONCLUSIONS: We found that mpMRI/MRGB reduces the detection of low-risk PCa and reduc

Published
2014

9. Prevention and early detection of prostate cancer

Author

Cuzick, J., Thorat, M.A., Andriole, G., Brawley, O.W., Brown, P.H., Culig, Z., Eeles, R.A., Ford, L.G., Hamdy, F.C., Holmberg, L., Ilic, D., Key, T.J., Vecchia, C. La, Lilja, H., Marberger, M., Meyskens, F.L., Minasian, L.M., Parker, C., Parnes, H.L., Perner, S., Rittenhouse, H., Schalken, J.A., Schmid, H.P., Schmitz-Drager, B.J., Schroder, F.H., Stenzl, A., Tombal, B., Wilt, T.J., Wolk, A., Cuzick, J., Thorat, M.A., Andriole, G., Brawley, O.W., Brown, P.H., Culig, Z., Eeles, R.A., Ford, L.G., Hamdy, F.C., Holmberg, L., Ilic, D., Key, T.J., Vecchia, C. La, Lilja, H., Marberger, M., Meyskens, F.L., Minasian, L.M., Parker, C., Parnes, H.L., Perner, S., Rittenhouse, H., Schalken, J.A., Schmid, H.P., Schmitz-Drager, B.J., Schroder, F.H., Stenzl, A., Tombal, B., Wilt, T.J., and Wolk, A.

Abstract

Contains fulltext : 139211.pdf (publisher's version ) (Closed access), Prostate cancer is a common malignancy in men and the worldwide burden of this disease is rising. Lifestyle modifications such as smoking cessation, exercise, and weight control offer opportunities to reduce the risk of developing prostate cancer. Early detection of prostate cancer by prostate-specific antigen (PSA) screening is controversial, but changes in the PSA threshold, frequency of screening, and the use of other biomarkers have the potential to minimise the overdiagnosis associated with PSA screening. Several new biomarkers for individuals with raised PSA concentrations or those diagnosed with prostate cancer are likely to identify individuals who can be spared aggressive treatment. Several pharmacological agents such as 5alpha-reductase inhibitors and aspirin could prevent development of prostate cancer. In this Review, we discuss the present evidence and research questions regarding prevention, early detection of prostate cancer, and management of men either at high risk of prostate cancer or diagnosed with low-grade prostate cancer.

Published
2014

10. International Organizing Committee

Author

JAMES, V.H.T., primary, LAUMAS, K.R., additional, VOIGT, K.D., additional, LINDNER, H.R., additional, DOMINGUEZ, O.V., additional, LIPSETT, M.B., additional, JENSEN, E.V., additional, MARTINI, L., additional, ADLERCREUTZ, W., additional, LIPPMAN, M.E., additional, BARDIN, C.W., additional, MAINWARING, W.I.P., additional, BLAQUIER, J., additional, MATHIEU, J., additional, BURGER, H.G., additional, MILGROM, E., additional, DE KRETSER, D., additional, MOTTA, M., additional, DE LUCA, H., additional, NIESCHLAG, E., additional, DENEF, C., additional, ROCHEFORT, H., additional, FINDLAY, J.L., additional, SCHRODER, F.H., additional, FISHMAN, J., additional, SEKSO, M., additional, FOREST, M., additional, SERIO, M., additional, FRANCE, T., additional, STAIB, W., additional, HOFFMAN, B., additional, STITCH, S.R., additional, IMURA, H., additional, TAKEDA, R., additional, LABRIE, F., additional, TRESGUERRES, J.A.F., additional, LADOSKY, W., additional, VAN DER MOLEN, H., additional, FINKELSTEIN, M., additional, NIMROD, A., additional, MAZUR, Y., additional, LUNENFELD, B., additional, SPITZ, I., additional, and ECKSTEIN, B., additional

Published
1983
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11. Prostate cancer detection and dutasteride: utility and limitations of prostate-specific antigen in men with previous negative biopsies.

Author

Leeuwen, P.J. van, Kolble, K., Huland, H., Hambrock, T., Barentsz, J.O., Schroder, F.H., Leeuwen, P.J. van, Kolble, K., Huland, H., Hambrock, T., Barentsz, J.O., and Schroder, F.H.

Abstract

01 februari 2011, Contains fulltext : 96235.pdf (publisher's version ) (Closed access), CONTEXT: We addressed the question whether the change of serum prostate-specific antigen (PSA) in men who use 5alpha-reductase inhibitor (5-ARI) dutasteride is sensitive for the detection of aggressive prostate cancer (PCa). OBJECTIVE: The case of a man using dutasteride diagnosed with Gleason 7 transition zone cancer at biopsy indicated by a rising PSA is described. The following issues are discussed: (1) Is a rise of PSA in patients using dutasteride predictive of aggressive PCa in men with prior negative biopsies? (2) Is it safe not to biopsy men using dutasteride who do not show a rising PSA? (3) How can we avoid potentially unnecessary biopsies in men using dutasteride without a rising PSA? EVIDENCE ACQUISITION: We reviewed the recent literature addressing our objective that relates to two studies: the Prostate Cancer Prevention Trial and the Reduction by Dutasteride of Prostate Cancer Events trial. EVIDENCE SYNTHESIS: In men using dutasteride, the positive predictive value/detection rate of Gleason 7-10 PCa is 13.2% and 4.0% for men with and without a rising PSA, respectively. However, a substantial proportion of Gleason 7-10 cases (42.9%) would be missed if a rising PSA was used as the only biopsy indication. Currently available data do not provide selective mechanisms to diagnose these cancers. CONCLUSIONS: A rising PSA for a patient using dutasteride should be an indication for prostate biopsies. Currently, in the case of stable PSA a biopsy may still be considered. Options for a selective approach are therefore suggested in this review to avoid unnecessary biopsies and to achieve a more selective PCa detection in men on 5-ARI treatment.

Published
2011

12. Prostate cancer: trends in incidence, survival and mortality in the Netherlands, 1989-2006.

Author

Cremers, R.G.H.M., Karim-Kos, H.E., Houterman, S., Verhoeven, R.H.A., Schroder, F.H., Kwast, T.H. van der, Kil, P.J.M., Coebergh, J.W.W., Kiemeney, L.A.L.M., Cremers, R.G.H.M., Karim-Kos, H.E., Houterman, S., Verhoeven, R.H.A., Schroder, F.H., Kwast, T.H. van der, Kil, P.J.M., Coebergh, J.W.W., and Kiemeney, L.A.L.M.

Abstract

01 juli 2010, Contains fulltext : 89583.pdf (publisher's version ) (Closed access), BACKGROUND: Prostate cancer occurrence and stage distribution changed dramatically during the end of the 20th century. This study aimed to quantify and explain trends in incidence, stage distribution, survival and mortality in the Netherlands between 1989 and 2006. METHODS: Population-based data from the nationwide Netherlands Cancer Registry and Causes of Death Registry were used. Annual incidence and mortality rates were calculated and age-adjusted to the European Standard Population. Trends in rates were evaluated by age, clinical stage and differentiation grade. RESULTS: 120,965 men were newly diagnosed with prostate cancer between 1989 and 2006. Age-adjusted incidence rates increased from 63 to 104 per 100,000 person-years in this period. Two periods of increasing incidence rates could be distinguished with increases predominantly in cT2-tumours between 1989 and 1995 and predominantly in cT1c-tumours since 2001. cT4/N+/M+-tumour incidence rates decreased from 23 in 1993 to 18 in 2006. The trend towards earlier detection was accompanied by a lower mean age at diagnosis (from 74 in 1989 to 70 in 2006), increased frequency of treatment with curative intent and improved 5-year relative survival. Mortality rates decreased from 34 in 1996 to 26 in 2007. CONCLUSIONS: The increase of prostate cancer incidence in the early 1990s was probably caused by increased prostate cancer awareness combined with diagnostic improvements (transrectal ultrasound, (thin) needle biopsies), but not PSA testing. The subsequent peak since 2001 is probably attributable to PSA testing. The decline in prostate cancer mortality from 1996 onwards may be the consequence of increased detection of cT2-tumours between 1989 and 1995. Unfortunately, data on the use of PSA tests and other prostate cancer diagnostics to support these conclusions are lacking.

Published
2010

13. Screening for prostate cancer in Dutch hereditary prostate cancer families.

Author

Kiemeney, L.A.L.M., Broeders, M.J.M., Pelger, M., Kil, P.J.M., Schroder, F.H., Witjes, J.A., Vasen, H.F., Kiemeney, L.A.L.M., Broeders, M.J.M., Pelger, M., Kil, P.J.M., Schroder, F.H., Witjes, J.A., and Vasen, H.F.

Abstract

Contains fulltext : 71069.pdf (publisher's version ) (Closed access), It is common belief that in families with hereditary prostate cancer (HPC), unaffected men should be screened periodically with PSA, but little is known about the effects of such screening. We studied test and tumor characteristics in unaffected 50-75-year-old screenees from HPC families. In the Netherlands, 153 verified HPC families are registered; 132 unaffected men in these families were not under surveillance for prostate cancer and gave informed consent for PSA testing by their GP and referral to a urologist in the case of a PSA level >or= 3.0 ng/ml. Results were compared to published data from the Rotterdam and Goteborg sections of the European Randomized Study of Screening for Prostate Cancer (ERSPC). A PSA >or= 3.0 ng/ml was found in 20 men: referral rate, 15.1% (ERSPC Rotterdam: 20.1%; ERSPC Goteborg: 12.0%). Only 3 cases of prostate cancer were diagnosed in these men: detection rate in the first screening round 2.3% (ERSPC Rotterdam: 5.3%; ERSPC Goteborg: 2.3%). Frequent opportunistic PSA testing made it impossible to estimate the detection rates in subsequent screening rounds. In the first and subsequent PSA screening rounds, 11 cases of cancer were detected. All but 1 had favorable tumor characteristics (cT1c/pT2; Gleason < 7). These results raise the question as to whether men from all HPC families should be considered at high-risk. We suggest that the same PSA testing guidelines should apply to HPC families and the general population. A more aggressive screening policy in HPC families does not seem to be justified.

Published
2008

14. Innovations in serum and urine markers in prostate cancer current European research in the P-Mark project.

Author

Gils, M.P. van, Stenman, U.H., Schalken, J.A., Schroder, F.H., Luider, T.M., Lilja, H., Bjartell, A., Hamdy, F.C., Pettersson, K.S., Bischoff, R., Takalo, H., Nilsson, O., Mulders, P.F.A., Bangma, C.H., Gils, M.P. van, Stenman, U.H., Schalken, J.A., Schroder, F.H., Luider, T.M., Lilja, H., Bjartell, A., Hamdy, F.C., Pettersson, K.S., Bischoff, R., Takalo, H., Nilsson, O., Mulders, P.F.A., and Bangma, C.H.

Abstract

Contains fulltext : 47999schalken.pdf (publisher's version ) (Closed access), An overview is given of serum and urine prostate cancer markers that are currently under investigation and subsequently the P-Mark project is introduced. There are many markers showing promise to overcome the limitations of prostate specific antigen (PSA). Eventually, these markers should be able to increase the specificity in diagnosis, differentiate between harmless and aggressive disease and identify progression towards androgen independence at an early stage. In the P-Mark project, several recently developed, promising markers will be evaluated using clinically well-defined biorepositories. Following successful evaluation, these markers will be validated on a sample set derived from two large, European, prostate cancer studies and used for the identification of special risk groups in the general population. In addition, novel markers will be identified in the same biorepositories by different mass spectrometry techniques.

Published
2005

15. Molecular prostate cancer pathology: current issues and achievements.

Author

Schalken, J.A., Bergh, A. von, Bono, A.V., Foster, C., Gospadarowicz, M., Isaacs, W.B., Rubin, M., Schroder, F.H., Tribukait, B., Tsukamotot, T., Wiklund, P., Schalken, J.A., Bergh, A. von, Bono, A.V., Foster, C., Gospadarowicz, M., Isaacs, W.B., Rubin, M., Schroder, F.H., Tribukait, B., Tsukamotot, T., and Wiklund, P.

Abstract

Contains fulltext : 48847schalken.pdf (publisher's version ) (Closed access), Recent developments in the field of molecular techniques have provided new tools that have led to the discovery of many new promising biomarkers for prostate cancer. These biomarkers may be instrumental in the development of new tests that will have a high specificity for the diagnosis and prognosis of prostate cancer. A biomarker is defined as a molecular test that provides additional information to currently available clinical and pathological tests. Biomarkers should be reproducible (both within and between institutes) and have an impact on clinical management. For diagnostic purposes it is important that potential biomarkers are tested in terms of tissue specificity and their discrimination potential between prostate cancer, normal prostate and benign prostatic hyperplasia. The results of (multiple) biomarker-based assays may enhance the specificity of cancer detection. There is an urgent need for molecular prognostic biomarkers for predicting the biological behavior and outcome of cancer.

Published
2005

16. Report on the consensus workshop on screening and global strategy for prostate cancer

Author

Denis, L., Murphy, D.L., Schroder, F.H., and Witjes, J.A.

Subjects
Gynecology, Oncology, Cancer Research, medicine.medical_specialty, business.industry, Medical screening, Public health, Consensus conference, Urological oncology, Global strategy, medicine.disease, Prostate cancer, medicine.anatomical_structure, Prostate, Internal medicine, Epidemiology, medicine, Urologische oncologie, Prostate disease, business
Abstract

Item does not contain fulltext 20 p.

Published
1995

17. 1013 PREDICTING FAVOURABLE PATHOLOGICAL OUTCOME IN PATIENTS WITH CLINICAL HIGH RISK PROSTATE CANCER. A NOVEL NOMOGRAM BASED ON A MULTI-INSTITUTIONAL ANALYSIS

Author

Briganti, A., primary, Spahn, M., additional, Joniau, S., additional, Gontero, P., additional, Montorsi, F., additional, Marchioro, G., additional, Tombal, B., additional, Frohneberg, D., additional, Isbarn, H., additional, Bangma, C.H., additional, Schroder, F.H., additional, Kneitz, B., additional, Bader, P., additional, Graefen, M., additional, Tizzani, A., additional, and Van Poppel, H., additional

Published
2010
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21. Rapid microwave stimulated fixation of entire prostatectomy specimens

Author

Ruijter, T.E.G., Miller, G.J., Aalders, M.W., Hulsbergen-van de Kaa, C.A., Schalken, J.A., Debruyne, F.M.J., Schroder, F.H., Beeker, G.C.M., Blijenberg, B.G., Boeken Kruger, S.E., Eman, I., Hoedemaeker, R.F., Kirkels, W.J., Kranse, R., Kwast, T.H. van der, Noordzij, M.A., Poel, H.G. van der, Romijn, J.C., Steenbrugge, G.J. van, Trapman, J., Verkaik, N.S., Bussemakers, M.J.G., Hessels, D., Oosterhof, G.O.N., Thomas, C.M.G., Witjes, W.P.J., Haapaniemi, A., Lovgren, T., Ruijter, T.E.G., Miller, G.J., Aalders, M.W., Hulsbergen-van de Kaa, C.A., Schalken, J.A., Debruyne, F.M.J., Schroder, F.H., Beeker, G.C.M., Blijenberg, B.G., Boeken Kruger, S.E., Eman, I., Hoedemaeker, R.F., Kirkels, W.J., Kranse, R., Kwast, T.H. van der, Noordzij, M.A., Poel, H.G. van der, Romijn, J.C., Steenbrugge, G.J. van, Trapman, J., Verkaik, N.S., Bussemakers, M.J.G., Hessels, D., Oosterhof, G.O.N., Thomas, C.M.G., Witjes, W.P.J., Haapaniemi, A., and Lovgren, T.

Abstract

Item does not contain fulltext

Published
1997

24. In Reply

Author

Bangma, C.H., primary, Rietbergen, J.B.W., additional, Kranse, R., additional, Blijenberg, B.G., additional, Petterson, K., additional, and Schroder, F.H., additional

Published
1998
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32. Cancer of the Prostate

Author

Schroder, F.H.

Subjects
Cancer of the Prostate (Book) -- Book reviews, Books -- Book reviews
Published
1993

33. Textbook of Benign Prostatic Hyperplasia

Author

Bosch, J.L.H.R. and Schroder, F.H.

Subjects
Textbook of Benign Prostatic Hyperplasia (Book), Books -- Book reviews, Health
Abstract

Ed Roger Kirby, John D McConnell, John M Fitzpatrick, Claus G Roehrborn, Peter Boyle Isis Medical Media, 99.50 £, pp 566 ISBN 1 899066 24 1 It is some time [...]

Published
1996

35. Androgen receptor and 5 alpha-reductase activity in the epithelium and the stroma of human benign prostatic hyperplasia

Author

OISHI, Kenji, OKADA, Kenichiro, YOSHIDA, Osamu, ROMIJN, J.G., ROMIJN, J. G., BOLT de VRIES, J., SCHRODER, F.H., and SCHRODER, F. H.

Subjects
Androgen receptor, Cell separation, BPH, 494.9, 5a-reductase
Abstract

ヒト前立腺肥大症の組織を上皮と間質に分離する方法を改良し, 上皮細胞は組織1 gあたり平均2千万個得, 95%以上の細胞に酸性フォスファテース活性のあることを組織化学的に証明した.間質は, 酸性フォスファテース活性が上皮に比べ, 単位蛋白あたり約1/10以下であった.また5α-リダクテースはほとんどが間質に存在し, 男性ホルモン受容体は, むしろ間質に多いとの結果を得た, An average of 20 X 10(6) nucleated cells were obtained from 1 g tissue of human benign prostatic hyperplasia by mechanical separation technique. Of these cells, 96.2% showed acid phosphatase activity and this was 10 times higher than the remaining stromal fraction on a protein base. The total activity of 5 alpha-reductase was 81 times higher in stroma than epithelium and the total activity of 3(beta)-oxidoreductase was 29 times higher in stroma. Androgen receptor amount measured in total tissue, epithelium and stroma were 100, 29 and 62 fmol R1881/mg DNA, respectively. These results suggest that androgen metabolism takes place mainly in the stroma of human BPH tissue, and that BPH is probably the disease of prostatic stroma.

Published
1985

37. Progression in Untreated Carcinoma of the Prostate Metastatic to Regional Lymph Nodes (Stage T0 to 4,N1 to 3,M0,D1)

Author

Davidson, P.J.T., Hop, W., Kurth, K.H., Fossa, S.D., Waehre, H., and Schroder, F.H.

Abstract

Purpose: We attempt to contribute to the understanding of the natural history of prostate cancer metastatic to lymph nodes. Materials and Methods: A total of 61 patients with node-positive prostate cancer was prospectively followed without adjuvant treatment for an average of 41 months. The impact of T and P categories, grade, tumor volume and prostate specific antigen change on interval to progression was studied in a univariate and multivariate analysis. Results: Median interval to progression was 18 months, and correlated with grade and prostate specific antigen doubling time. Changes in prostatic volume with time were not predictive. Conclusions: Our study provides insight into the natural history of node-positive disease and identifies relevant prognostic factors that may be used for treatment decisions.

Published
1995
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38. This title is unavailable for guests, please login to see more information.

Author

OISHI, Kenji, OKADA, Kenichiro, YOSHIDA, Osamu, ROMIJN, J. G., BOLT de VRIES, J., SCHRODER, F. H., ROMIJN, J.G., SCHRODER, F.H., OISHI, Kenji, OKADA, Kenichiro, YOSHIDA, Osamu, ROMIJN, J. G., BOLT de VRIES, J., SCHRODER, F. H., ROMIJN, J.G., and SCHRODER, F.H.

Abstract

An average of 20 X 10(6) nucleated cells were obtained from 1 g tissue of human benign prostatic hyperplasia by mechanical separation technique. Of these cells, 96.2% showed acid phosphatase activity and this was 10 times higher than the remaining stromal fraction on a protein base. The total activity of 5 alpha-reductase was 81 times higher in stroma than epithelium and the total activity of 3(beta)-oxidoreductase was 29 times higher in stroma. Androgen receptor amount measured in total tissue, epithelium and stroma were 100, 29 and 62 fmol R1881/mg DNA, respectively. These results suggest that androgen metabolism takes place mainly in the stroma of human BPH tissue, and that BPH is probably the disease of prostatic stroma.

Published
1985

43. The free-to-total serum prostate specific antigen ratio for staging prostate carcinoma

Author

Bangma, C.H., Kranse, R., Blijenberg, P.G., and Schroder, F.H.

Subjects
Prostate cancer -- Diagnosis, Prostate-specific antigen -- Methods, Tumor staging -- Methods, Health, Diagnosis, Methods
Abstract

Bangma, C. H.; Kranse, R.; Blijenberg, P. G.; Schroder, F. H. 'The Free-to-Total Serum Prostate Specific Antigen Ratio for Staging Prostate Carcinoma.' Journal of Urology, February 1997;157(2):544-547. According to the [...]

Published
1997

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