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'''Marc Lacroix''' is a [[biochemist]] (educated at [[University of Liège]]) and a [[researcher]] (born [[1963]] in [[Verviers]], [[Wallonia]], [[Belgium]]) who specializes in [[breast cancer]] [[biology]], [[metastasis]] and therapy <ref name="Siwek2">{{cite journal | first=B | last= Siwek | coauthors= Larsimont D, Lacroix M, Body JJ, | title= Establishment and characterization of three new breast-cancer cell lines | journal= [[International Journal of Cancer]] | year=1998 | volume=76 |pages=677 – 683 | id=PMID 9610725}}</ref><ref name="Lacroix8">{{cite journal | first=M | last= Lacroix | coauthors= Zammatteo N, Remacle J, Leclercq G. | title= A low-density DNA [[microarray]] for analysis of markers in breast cancer | journal= [[International Journal of Biological Markers]] | year=2002 | volume=17 |pages=5 – 23 | id=PMID 11936587}}</ref><ref name="Lacroix9">{{cite journal | first=M | last= Lacroix | coauthors= Leclercq G. | title= Relevance of breast cancer cell lines as models for breast tumours: an update | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2004 | volume=83 |pages=249 – 289 | id=PMID 14758095}}</ref><ref name="Lacroix12">{{cite journal | first=M | last= Lacroix | coauthors= Haibe-Kains B, Hennuy B, Laes JF, Lallemand F, Gonze I, Cardoso F, Piccart M, Leclercq G, Sotiriou C. | title= Gene regulation by phorbol 12-myristate 13-acetate in MCF-7 and MDA-MB-231, two breast cancer cell lines exhibiting highly different phenotypes | journal= [[Oncology Reports]] | year=2004 | volume=12 |pages=701 – 707 | id=PMID 15375488}}</ref><ref name="Lacroix13">{{cite journal | first=M | last= Lacroix | coauthors= Leclercq G, on behalf of BreastMed Consortium. | title= The "portait" of hereditary breast cancer | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2005 | volume=89 |pages=297 – 304 | id=PMID 15754129}}</ref><ref name="De Longueville1">{{cite journal | first=F | last= De Longueville | coauthors= Lacroix M (co-first author), Barbuto AM, Bertholet V, Gallo D, Larsimont D, Marcq L, Zammatteo N, Boffe S, Leclercq G, Remacle J. | title= Molecular characterization of breast cancer cell lines by a low-density microarray | journal= [[International Journal of Oncology]] | year=2005 | volume=27 |pages=881 – 892 | id=PMID 16142302}}</ref><ref name="Lacroix14">{{cite journal | first=M | last=Lacroix | coauthors= Toillon RA, Leclercq G. | title= P53 and breast cancer, an update | journal= [[Endocrine-Related Cancer]] | year=2006 | volume=13 |pages=293 – 325 |id=PMID 16728565}}</ref><ref name="Lacroix15">{{cite journal | first=M | last=Lacroix. | title= Significance, detection and markers of disseminated breast cancer cells | journal= [[Endocrine-Related Cancer]] | year=2006 | volume=13 |pages=1033-1067 |id=PMID 17158753}}</ref><ref name="Lacroix16">{{cite journal | first=M | last=Lacroix. | title= Persistent use of "false" cell lines | journal= [[International Journal of Cancer]] | year=2008 | volume=122 |pages=1 – 4 |id=PMID 17960586}}</ref> .<BR>
'''Marc Lacroix''' is a [[biochemist]] (educated at [[University of Liège]]) and a [[researcher]] (born [[1963]] in [[Verviers]], [[Wallonia]], [[Belgium]]) who specializes in [[breast cancer]] [[biology]], [[metastasis]] and therapy <ref name="Siwek2">{{cite journal | first=B | last= Siwek | coauthors= Larsimont D, Lacroix M, Body JJ, | title= Establishment and characterization of three new breast-cancer cell lines | journal= [[International Journal of Cancer]] | year=1998 | volume=76 |pages=677 – 683 | pmid=9610725 | doi= 10.1002/(SICI)1097-0215(19980529)76:5<677::AID-IJC11>3.0.CO;2-1 | doilabel= 10.1002/(SICI)1097-0215(19980529)76:5&#60;677::AID-IJC11&#62;3.0.CO;2-1}}</ref><ref name="Lacroix8">{{cite journal | first=M | last= Lacroix | coauthors= Zammatteo N, Remacle J, Leclercq G. | title= A low-density DNA [[microarray]] for analysis of markers in breast cancer | journal= [[International Journal of Biological Markers]] | year=2002 | volume=17 |pages=5 – 23 | pmid=11936587}}</ref><ref name="Lacroix9">{{cite journal | first=M | last= Lacroix | coauthors= Leclercq G. | title= Relevance of breast cancer cell lines as models for breast tumours: an update | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2004 | volume=83 |pages=249 – 289 | pmid=14758095 | doi= 10.1023/B:BREA.0000014042.54925.cc}}</ref><ref name="Lacroix12">{{cite journal | first=M | last= Lacroix | coauthors= Haibe-Kains B, Hennuy B, Laes JF, Lallemand F, Gonze I, Cardoso F, Piccart M, Leclercq G, Sotiriou C. | title= Gene regulation by phorbol 12-myristate 13-acetate in MCF-7 and MDA-MB-231, two breast cancer cell lines exhibiting highly different phenotypes | journal= [[Oncology Reports]] | year=2004 | volume=12 |pages=701 – 707 | pmid=15375488}}</ref><ref name="Lacroix13">{{cite journal | first=M | last= Lacroix | coauthors= Leclercq G, on behalf of BreastMed Consortium. | title= The "portait" of hereditary breast cancer | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2005 | volume=89 |pages=297 – 304 | pmid=15754129 | doi= 10.1007/s10549-004-2172-4}}</ref><ref name="De Longueville1">{{cite journal | first=F | last= De Longueville | coauthors= Lacroix M (co-first author), Barbuto AM, Bertholet V, Gallo D, Larsimont D, Marcq L, Zammatteo N, Boffe S, Leclercq G, Remacle J. | title= Molecular characterization of breast cancer cell lines by a low-density microarray | journal= [[International Journal of Oncology]] | year=2005 | volume=27 |pages=881 – 892 | pmid=16142302}}</ref><ref name="Lacroix14">{{cite journal | first=M | last=Lacroix | coauthors= Toillon RA, Leclercq G. | title= P53 and breast cancer, an update | journal= [[Endocrine-Related Cancer]] | year=2006 | volume=13 |pages=293 – 325 |pmid=16728565 | doi= 10.1677/erc.1.01172}}</ref><ref name="Lacroix15">{{cite journal | first=M | last=Lacroix. | title= Significance, detection and markers of disseminated breast cancer cells | journal= [[Endocrine-Related Cancer]] | year=2006 | volume=13 |pages=1033–1067 |pmid=17158753 | doi= 10.1677/ERC-06-0001}}</ref><ref name="Lacroix16">{{cite journal | first=M | last=Lacroix. | title= Persistent use of "false" cell lines | journal= [[International Journal of Cancer]] | year=2008 | volume=122 |pages=1 – 4 |pmid=17960586 | doi= 10.1002/ijc.23233}}</ref> .<BR>
He works at [[Institut Jules Bordet]] ([[Brussels]], [[Belgium]]).
He works at [[Institut Jules Bordet]] ([[Brussels]], [[Belgium]]).


== Earlier work ==
== Earlier work ==
Breast cancer cells (BCC) frequently metastasize to the [[skeleton]], where they lead to tumor-induced osteolysis and subsequent morbidity. Marc Lacroix has investigated the interrelationships between BCC and bone cells ([[osteoblast|osteoblasts]], the bone-building cells, and [[osteoclast|osteoclasts]], the bone-degrading cells). With colleagues, he discovered that BCC produce soluble factors increasing osteoclast activity, notably interleukin-11, the production of which is reduced by the cyclooxygenase inhibitor [[aspirin]] <ref name="Lacroix5">{{cite journal | first=M | last= Lacroix | coauthors= Siwek B, Marie PJ, Body JJ. | title= Production and regulation of [[Interleukin 11|interleukin-11]] by breast cancer cells | journal= [[Cancer Letters]] | year=1998 | volume=127 |pages=29 – 35 | id=PMID 9619855}}</ref><ref name="Sotiriou1">{{cite journal | first=C | last= Sotiriou | coauthors= Lacroix M (co-first author), Lagneaux L, Berchem G, Body JJ. | title= The [[aspirin]] [[metabolite]] salicylate inhibits breast cancer cells growth and their synthesis of the osteolytic [[cytokine]]s interleukins-6 and-11 | journal= [[Anticancer Research]] | year=1999 | volume=19 |pages=2997 – 3006 | id=PMID 10652584}}</ref><ref name="Sotiriou2">{{cite journal | first=C | last= Sotiriou | coauthors= Lacroix M, Lespagnard L, Larsimont D, Paesmans M, Body JJ. | title= Interleukins-6 and-11 expression in primary breast cancer and subsequent development of bone metastases | journal= [[Cancer Letters]] | year=2001 | volume=169 |pages=87 – 95 | id=PMID 11410329}}</ref>. BCC also reduce the proliferation of osteoblasts and their production of collagen, the main protein component of bone <ref name="Lacroix2">{{cite journal | first=M | last= Lacroix | coauthors= Siwek B, Body JJ. | title= Effects of secretory products of breast cancer cells on [[osteoblast]]-like cells | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=1996 | volume=38 |pages=209 – 216| id=PMID 8861839}}</ref><ref name="Siwek1">{{cite journal | first=B | last= Siwek | coauthors= Lacroix M, DePollak C, Marie P, Body JJ. | title= Secretory products of breast cancer cells specifically affect human osteoblastic cells: Partial characterization of active factors | journal= [[Journal of Bone and Mineral Research]] | year=1997 | volume=12 |pages=552 – 560| id=PMID 9101366}}</ref><ref name="Lacroix6">{{cite journal | first=M | last= Lacroix | coauthors= Lacroix M, Marie PJ, Body JJ. | title= Protein production by osteoblasts: modulation by breast cancer cell-derived factors | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2000 | volume=61 |pages=59 – 67 | id=PMID 10930090}}</ref>. Marc Lacroix also examined the response BCC to the anti-osteolytic agent [[calcitonin]] <ref name="Lacroix3">{{cite journal | first=M | last= Lacroix | coauthors= Body JJ. | title= Regulation of [[C-Fos|c-fos]] and c-jun expression by [[calcitonin]] in human breast cancer cells | journal= [[Calcified Tissue International]] | year=1997 | volume=60 |pages=513 – 519| id=PMID 9164825}}</ref><ref name="Lacroix4">{{cite journal | first=M | last= Lacroix | coauthors= Siwek B, Body JJ. | title= Breast cancer cell response to [[calcitonin]]: Modulation by growth-regulating agents | journal= [[European Journal of Pharmacology]] | year=1998 | volume=344 |pages=279 – 286| id=PMID 9600664}}</ref>.
Breast cancer cells (BCC) frequently metastasize to the [[skeleton]], where they lead to tumor-induced osteolysis and subsequent morbidity. Marc Lacroix has investigated the interrelationships between BCC and bone cells ([[osteoblast|osteoblasts]], the bone-building cells, and [[osteoclast|osteoclasts]], the bone-degrading cells). With colleagues, he discovered that BCC produce soluble factors increasing osteoclast activity, notably interleukin-11, the production of which is reduced by the cyclooxygenase inhibitor [[aspirin]] <ref name="Lacroix5">{{cite journal | first=M | last= Lacroix | coauthors= Siwek B, Marie PJ, Body JJ. | title= Production and regulation of [[Interleukin 11|interleukin-11]] by breast cancer cells | journal= [[Cancer Letters]] | year=1998 | volume=127 |pages=29 – 35 | pmid=9619855 | doi= 10.1016/S0304-3835(97)00542-9}}</ref><ref name="Sotiriou1">{{cite journal | first=C | last= Sotiriou | coauthors= Lacroix M (co-first author), Lagneaux L, Berchem G, Body JJ. | title= The [[aspirin]] [[metabolite]] salicylate inhibits breast cancer cells growth and their synthesis of the osteolytic [[cytokine]]s interleukins-6 and-11 | journal= [[Anticancer Research]] | year=1999 | volume=19 |pages=2997 – 3006 | pmid=10652584}}</ref><ref name="Sotiriou2">{{cite journal | first=C | last= Sotiriou | coauthors= Lacroix M, Lespagnard L, Larsimont D, Paesmans M, Body JJ. | title= Interleukins-6 and-11 expression in primary breast cancer and subsequent development of bone metastases | journal= [[Cancer Letters]] | year=2001 | volume=169 |pages=87 – 95 | pmid=11410329 | doi= 10.1016/S0304-3835(01)00524-9}}</ref>. BCC also reduce the proliferation of osteoblasts and their production of collagen, the main protein component of bone <ref name="Lacroix2">{{cite journal | first=M | last= Lacroix | coauthors= Siwek B, Body JJ. | title= Effects of secretory products of breast cancer cells on [[osteoblast]]-like cells | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=1996 | volume=38 |pages=209 – 216| pmid=8861839 | doi= 10.1007/BF01806675}}</ref><ref name="Siwek1">{{cite journal | first=B | last= Siwek | coauthors= Lacroix M, DePollak C, Marie P, Body JJ. | title= Secretory products of breast cancer cells specifically affect human osteoblastic cells: Partial characterization of active factors | journal= [[Journal of Bone and Mineral Research]] | year=1997 | volume=12 |pages=552 – 560| pmid=9101366 | doi= 10.1359/jbmr.1997.12.4.552}}</ref><ref name="Lacroix6">{{cite journal | first=M | last= Lacroix | coauthors= Lacroix M, Marie PJ, Body JJ. | title= Protein production by osteoblasts: modulation by breast cancer cell-derived factors | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2000 | volume=61 |pages=59 – 67 | pmid=10930090 | doi= 10.1023/A:1006408916224}}</ref>. Marc Lacroix also examined the response BCC to the anti-osteolytic agent [[calcitonin]] <ref name="Lacroix3">{{cite journal | first=M | last= Lacroix | coauthors= Body JJ. | title= Regulation of [[C-Fos|c-fos]] and c-jun expression by [[calcitonin]] in human breast cancer cells | journal= [[Calcified Tissue International]] | year=1997 | volume=60 |pages=513 – 519| pmid=9164825 | doi= 10.1007/s002239900273}}</ref><ref name="Lacroix4">{{cite journal | first=M | last= Lacroix | coauthors= Siwek B, Body JJ. | title= Breast cancer cell response to [[calcitonin]]: Modulation by growth-regulating agents | journal= [[European Journal of Pharmacology]] | year=1998 | volume=344 |pages=279 – 286| pmid=9600664 | doi= 10.1016/S0014-2999(97)01578-1}}</ref>.
In close collaboration with Prof. Guy Leclercq (Institut Jules Bordet, Belgium), Marc Lacroix has studied various aspects of [[estrogen receptor]] biology, ligand-binding and transcriptional activity, and life-cycle <ref name="Jin1">{{cite journal | first=L | last= Jin | coauthors= Borras M, Lacroix M, Legros N, Leclercq G. | title= Antiestrogenic activity of 2 11-beta-estradiol derivatives on [[MCF-7]] breast cancer cells | journal= [[Steroids]] | year=1995 | volume=60 |pages=512 – 518| id=PMID 8539793}}</ref><ref name="Borras1">{{cite journal | first=M | last= Borras | coauthors= Lacroix M, Legros N, Leclercq G. | title= [[Estrogen receptor]]-negative/progesterone receptor-positive Evsa-T mammary tumor cells: a model for assessing the biological property of this peculiar [[phenotype]] of breast cancers | journal= [[Cancer Letters]] | year=1997 | volume=120 |pages=23 – 30| id=PMID 9570382}}</ref><ref name="Maaroufi1">{{cite journal | first=Y | last= Maaroufi | coauthors= Lacroix M, Lespagnard L, Journe F, Larsimont D, Leclercq G. | title= [[Estrogen receptor]] of primary breast cancers: evidence for intracellular proteolysis | journal= [[Breast Cancer Research]] | year=2000 | volume=2 |pages=444 – 454 | id=PMID 11056692}}</ref><ref name="Lacroix7">{{cite journal | first=M | last= Lacroix | coauthors= Querton G, Hennebert P, Larsimont D, Leclercq G. | title= Estrogen receptor analysis in primary breast tumors by ligand-binding assay, immmocytochemical assay, and northern blot: a comparison | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2001 | volume=67 |pages=263 – 271 | id=PMID 11561772}}</ref><ref name="Rivas2">{{cite journal | first=A | last= Rivas | coauthors= Lacroix M, Olea-Serrano F, Laios I, Leclercq G, Olea N. | title= Estrogenic effect of a series of bisphenol analogues on gene and protein expression in MCF-7 breast cancer cells | journal= [[Journal of Steroid Biochemistry and Molecular Biology]] | year=2002 | volume=82 |pages=45 – 53 | id=PMID 12429138}}</ref><ref name="Lacroix10">{{cite journal | first=M | last= Lacroix | coauthors= Leclercq G. | title= About GATA3, HNF3A, and XBP1, three genes co-expressed with the oestrogen receptor-alpha gene (ESR1) in breast cancer | journal= [[Molecular and Cellular Endocrinology]] | year=2004 | volume=219 |pages=1 – 7 | id=PMID 15149721}}</ref><ref name="Toillon1">{{cite journal | first=RA | last=Toillon | coauthors= Magné N, Laios I, Lacroix M, Duvillier H, Lagneaux L, Devriendt D, Van Houtte P, Leclercq G. | title= Interaction between estrogen receptor alpha, ionizing radiation and (anti-) estrogens in breast cancer cells | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2005 | volume=93 |pages=207 – 215 | id=PMID 16136271}}</ref><ref name="Leclercq1">{{cite journal | first=G | last=Leclercq | coauthors= Lacroix M, Laïos I, Laurent G. | title= Estrogen receptor alpha: impact of ligands on intracellular shuttling and turnover rate in breast cancer cells | journal= [[Current Cancer Drug Targets]] | year=2006 | volume=6 |pages=39 – 64 | id=PMID 16475975}}</ref><ref name="Toillon2">{{cite journal | first=RA | last=Toillon | coauthors=Magné N, Laïos I, Castadot P, Kinnaert E, Van Houtte P, Desmedt C, Leclercq G, Lacroix M. | title= Estrogens decrease gamma-rays induced senescence and maintain cell cycle progression in breast cancer cells independently of p53 | journal= [[International Journal of Radiation Oncology, Biology, Physics]] | year=2007 | volume=67 |pages=1187 – 1200 | id=PMID 17336220}}</ref>.
In close collaboration with Prof. Guy Leclercq (Institut Jules Bordet, Belgium), Marc Lacroix has studied various aspects of [[estrogen receptor]] biology, ligand-binding and transcriptional activity, and life-cycle <ref name="Jin1">{{cite journal | first=L | last= Jin | coauthors= Borras M, Lacroix M, Legros N, Leclercq G. | title= Antiestrogenic activity of 2 11-beta-estradiol derivatives on [[MCF-7]] breast cancer cells | journal= [[Steroids]] | year=1995 | volume=60 |pages=512 – 518| pmid=8539793 | doi= 10.1016/0039-128X(95)00079-6}}</ref><ref name="Borras1">{{cite journal | first=M | last= Borras | coauthors= Lacroix M, Legros N, Leclercq G. | title= [[Estrogen receptor]]-negative/progesterone receptor-positive Evsa-T mammary tumor cells: a model for assessing the biological property of this peculiar [[phenotype]] of breast cancers | journal= [[Cancer Letters]] | year=1997 | volume=120 |pages=23 – 30| pmid=9570382 | doi= 10.1016/S0304-3835(97)00285-1}}</ref><ref name="Maaroufi1">{{cite journal | first=Y | last= Maaroufi | coauthors= Lacroix M, Lespagnard L, Journe F, Larsimont D, Leclercq G. | title= [[Estrogen receptor]] of primary breast cancers: evidence for intracellular proteolysis | journal= [[Breast Cancer Research]] | year=2000 | volume=2 |pages=444 – 454 | pmid=11056692 | doi= 10.1186/bcr92}}</ref><ref name="Lacroix7">{{cite journal | first=M | last= Lacroix | coauthors= Querton G, Hennebert P, Larsimont D, Leclercq G. | title= Estrogen receptor analysis in primary breast tumors by ligand-binding assay, immmocytochemical assay, and northern blot: a comparison | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2001 | volume=67 |pages=263 – 271 | pmid=11561772 | doi= 10.1023/A:1017946810277}}</ref><ref name="Rivas2">{{cite journal | first=A | last= Rivas | coauthors= Lacroix M, Olea-Serrano F, Laios I, Leclercq G, Olea N. | title= Estrogenic effect of a series of bisphenol analogues on gene and protein expression in MCF-7 breast cancer cells | journal= [[Journal of Steroid Biochemistry and Molecular Biology]] | year=2002 | volume=82 |pages=45 – 53 | pmid=12429138 | doi= 10.1016/S0960-0760(02)00146-2}}</ref><ref name="Lacroix10">{{cite journal | first=M | last= Lacroix | coauthors= Leclercq G. | title= About GATA3, HNF3A, and XBP1, three genes co-expressed with the oestrogen receptor-alpha gene (ESR1) in breast cancer | journal= [[Molecular and Cellular Endocrinology]] | year=2004 | volume=219 |pages=1 – 7 | pmid=15149721 | doi= 10.1016/j.mce.2004.02.021}}</ref><ref name="Toillon1">{{cite journal | first=RA | last=Toillon | coauthors= Magné N, Laios I, Lacroix M, Duvillier H, Lagneaux L, Devriendt D, Van Houtte P, Leclercq G. | title= Interaction between estrogen receptor alpha, ionizing radiation and (anti-) estrogens in breast cancer cells | journal= [[Breast Cancer Research and Treatment (journal)|Breast Cancer Research and Treatment]] | year=2005 | volume=93 |pages=207 – 215 | pmid=16136271 | doi= 10.1007/s10549-005-5148-0}}</ref><ref name="Leclercq1">{{cite journal | first=G | last=Leclercq | coauthors= Lacroix M, Laïos I, Laurent G. | title= Estrogen receptor alpha: impact of ligands on intracellular shuttling and turnover rate in breast cancer cells | journal= [[Current Cancer Drug Targets]] | year=2006 | volume=6 |pages=39 – 64 | pmid=16475975 | doi= 10.2174/156800906775471716}}</ref><ref name="Toillon2">{{cite journal | first=RA | last=Toillon | coauthors=Magné N, Laïos I, Castadot P, Kinnaert E, Van Houtte P, Desmedt C, Leclercq G, Lacroix M. | title= Estrogens decrease gamma-rays induced senescence and maintain cell cycle progression in breast cancer cells independently of p53 | journal= [[International Journal of Radiation Oncology, Biology, Physics]] | year=2007 | volume=67 |pages=1187 – 1200 | pmid=17336220}}</ref>.




== Recent work ==
== Recent work ==
The amount of data on [[breast cancer]] available for the scientific and medical community is growing rapidly. According to [[PubMed]], a search engine offering access to the [[MEDLINE]] [[bibliographic database|database]] of citations and abstracts of biomedical research articles, 7918 papers containing the expression «breast cancer» were published in 2006. Their number was 3592 in 1996, 1455 in 1986 and only 626 in 1976. In general, the older information is overlayed by more recent data and forgotten to some extent. In 2004, Lacroix and colleagues collected and assembled data from hundreds of articles related to the biology, pathology and genetics of ''in situ'', invasive and metastatic breast cancers. These papers were covering a time period of about 25 years. Lacroix ''et al.'' concluded that despite undergoing increasing genetic alteration, most individual breast cancers rather surprisingly maintain their phenotype when they evolve from ''in situ'' to the metastatic state <ref name="Lacroix11">{{cite journal | first=M | last= Lacroix | coauthors= Toillon RA, Leclercq G. | title= Stable 'portrait' of breast tumors during progression: data from biology, pathology and genetics | journal= [[Endocrine-Related Cancer]] | year=2004 | volume=11 |pages=497 – 522 | id=PMID 15369451}}</ref>. This conclusion was in opposition to a progression model widely accepted at that time, which was suggesting that carcinoma ''in situ'' could evolve into invasive carcinoma and subsequently produce metastases through an accumulation of molecular abnormalities possibly allowing extensive phenotype changes and subsequent gain of aggressiveness.
The amount of data on [[breast cancer]] available for the scientific and medical community is growing rapidly. According to [[PubMed]], a search engine offering access to the [[MEDLINE]] [[bibliographic database|database]] of citations and abstracts of biomedical research articles, 7918 papers containing the expression «breast cancer» were published in 2006. Their number was 3592 in 1996, 1455 in 1986 and only 626 in 1976. In general, the older information is overlayed by more recent data and forgotten to some extent. In 2004, Lacroix and colleagues collected and assembled data from hundreds of articles related to the biology, pathology and genetics of ''in situ'', invasive and metastatic breast cancers. These papers were covering a time period of about 25 years. Lacroix ''et al.'' concluded that despite undergoing increasing genetic alteration, most individual breast cancers rather surprisingly maintain their phenotype when they evolve from ''in situ'' to the metastatic state <ref name="Lacroix11">{{cite journal | first=M | last= Lacroix | coauthors= Toillon RA, Leclercq G. | title= Stable 'portrait' of breast tumors during progression: data from biology, pathology and genetics | journal= [[Endocrine-Related Cancer]] | year=2004 | volume=11 |pages=497 – 522 | pmid=15369451 | doi= 10.1677/erc.1.00758}}</ref>. This conclusion was in opposition to a progression model widely accepted at that time, which was suggesting that carcinoma ''in situ'' could evolve into invasive carcinoma and subsequently produce metastases through an accumulation of molecular abnormalities possibly allowing extensive phenotype changes and subsequent gain of aggressiveness.


== Bibliography: articles in scientific and medical journals (excerpt)==
== Bibliography: articles in scientific and medical journals (excerpt)==

Revision as of 15:43, 7 June 2008


Marc Lacroix is a biochemist (educated at University of Liège) and a researcher (born 1963 in Verviers, Wallonia, Belgium) who specializes in breast cancer biology, metastasis and therapy [1][2][3][4][5][6][7][8][9] .
He works at Institut Jules Bordet (Brussels, Belgium).

Earlier work

Breast cancer cells (BCC) frequently metastasize to the skeleton, where they lead to tumor-induced osteolysis and subsequent morbidity. Marc Lacroix has investigated the interrelationships between BCC and bone cells (osteoblasts, the bone-building cells, and osteoclasts, the bone-degrading cells). With colleagues, he discovered that BCC produce soluble factors increasing osteoclast activity, notably interleukin-11, the production of which is reduced by the cyclooxygenase inhibitor aspirin [10][11][12]. BCC also reduce the proliferation of osteoblasts and their production of collagen, the main protein component of bone [13][14][15]. Marc Lacroix also examined the response BCC to the anti-osteolytic agent calcitonin [16][17]. In close collaboration with Prof. Guy Leclercq (Institut Jules Bordet, Belgium), Marc Lacroix has studied various aspects of estrogen receptor biology, ligand-binding and transcriptional activity, and life-cycle [18][19][20][21][22][23][24][25][26].


Recent work

The amount of data on breast cancer available for the scientific and medical community is growing rapidly. According to PubMed, a search engine offering access to the MEDLINE database of citations and abstracts of biomedical research articles, 7918 papers containing the expression «breast cancer» were published in 2006. Their number was 3592 in 1996, 1455 in 1986 and only 626 in 1976. In general, the older information is overlayed by more recent data and forgotten to some extent. In 2004, Lacroix and colleagues collected and assembled data from hundreds of articles related to the biology, pathology and genetics of in situ, invasive and metastatic breast cancers. These papers were covering a time period of about 25 years. Lacroix et al. concluded that despite undergoing increasing genetic alteration, most individual breast cancers rather surprisingly maintain their phenotype when they evolve from in situ to the metastatic state [27]. This conclusion was in opposition to a progression model widely accepted at that time, which was suggesting that carcinoma in situ could evolve into invasive carcinoma and subsequently produce metastases through an accumulation of molecular abnormalities possibly allowing extensive phenotype changes and subsequent gain of aggressiveness.

Bibliography: articles in scientific and medical journals (excerpt)

  1. ^ Siwek, B (1998). "Establishment and characterization of three new breast-cancer cell lines". International Journal of Cancer. 76: 677–683. doi:10.1002/(SICI)1097-0215(19980529)76:5<677::AID-IJC11>3.0.CO;2-1. PMID 9610725. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |doilabel= ignored (help)CS1 maint: extra punctuation (link)
  2. ^ Lacroix, M (2002). "A low-density DNA microarray for analysis of markers in breast cancer". International Journal of Biological Markers. 17: 5–23. PMID 11936587. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  3. ^ Lacroix, M (2004). "Relevance of breast cancer cell lines as models for breast tumours: an update". Breast Cancer Research and Treatment. 83: 249–289. doi:10.1023/B:BREA.0000014042.54925.cc. PMID 14758095. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  4. ^ Lacroix, M (2004). "Gene regulation by phorbol 12-myristate 13-acetate in MCF-7 and MDA-MB-231, two breast cancer cell lines exhibiting highly different phenotypes". Oncology Reports. 12: 701–707. PMID 15375488. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  5. ^ Lacroix, M (2005). "The "portait" of hereditary breast cancer". Breast Cancer Research and Treatment. 89: 297–304. doi:10.1007/s10549-004-2172-4. PMID 15754129. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  6. ^ De Longueville, F (2005). "Molecular characterization of breast cancer cell lines by a low-density microarray". International Journal of Oncology. 27: 881–892. PMID 16142302. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  7. ^ Lacroix, M (2006). "P53 and breast cancer, an update". Endocrine-Related Cancer. 13: 293–325. doi:10.1677/erc.1.01172. PMID 16728565. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  8. ^ Lacroix., M (2006). "Significance, detection and markers of disseminated breast cancer cells". Endocrine-Related Cancer. 13: 1033–1067. doi:10.1677/ERC-06-0001. PMID 17158753.
  9. ^ Lacroix., M (2008). "Persistent use of "false" cell lines". International Journal of Cancer. 122: 1–4. doi:10.1002/ijc.23233. PMID 17960586.
  10. ^ Lacroix, M (1998). "Production and regulation of interleukin-11 by breast cancer cells". Cancer Letters. 127: 29–35. doi:10.1016/S0304-3835(97)00542-9. PMID 9619855. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  11. ^ Sotiriou, C (1999). "The aspirin metabolite salicylate inhibits breast cancer cells growth and their synthesis of the osteolytic cytokines interleukins-6 and-11". Anticancer Research. 19: 2997–3006. PMID 10652584. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  12. ^ Sotiriou, C (2001). "Interleukins-6 and-11 expression in primary breast cancer and subsequent development of bone metastases". Cancer Letters. 169: 87–95. doi:10.1016/S0304-3835(01)00524-9. PMID 11410329. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  13. ^ Lacroix, M (1996). "Effects of secretory products of breast cancer cells on osteoblast-like cells". Breast Cancer Research and Treatment. 38: 209–216. doi:10.1007/BF01806675. PMID 8861839. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  14. ^ Siwek, B (1997). "Secretory products of breast cancer cells specifically affect human osteoblastic cells: Partial characterization of active factors". Journal of Bone and Mineral Research. 12: 552–560. doi:10.1359/jbmr.1997.12.4.552. PMID 9101366. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  15. ^ Lacroix, M (2000). "Protein production by osteoblasts: modulation by breast cancer cell-derived factors". Breast Cancer Research and Treatment. 61: 59–67. doi:10.1023/A:1006408916224. PMID 10930090. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  16. ^ Lacroix, M (1997). "Regulation of c-fos and c-jun expression by calcitonin in human breast cancer cells". Calcified Tissue International. 60: 513–519. doi:10.1007/s002239900273. PMID 9164825. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  17. ^ Lacroix, M (1998). "Breast cancer cell response to calcitonin: Modulation by growth-regulating agents". European Journal of Pharmacology. 344: 279–286. doi:10.1016/S0014-2999(97)01578-1. PMID 9600664. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  18. ^ Jin, L (1995). "Antiestrogenic activity of 2 11-beta-estradiol derivatives on MCF-7 breast cancer cells". Steroids. 60: 512–518. doi:10.1016/0039-128X(95)00079-6. PMID 8539793. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  19. ^ Borras, M (1997). "Estrogen receptor-negative/progesterone receptor-positive Evsa-T mammary tumor cells: a model for assessing the biological property of this peculiar phenotype of breast cancers". Cancer Letters. 120: 23–30. doi:10.1016/S0304-3835(97)00285-1. PMID 9570382. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  20. ^ Maaroufi, Y (2000). "Estrogen receptor of primary breast cancers: evidence for intracellular proteolysis". Breast Cancer Research. 2: 444–454. doi:10.1186/bcr92. PMID 11056692. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: unflagged free DOI (link)
  21. ^ Lacroix, M (2001). "Estrogen receptor analysis in primary breast tumors by ligand-binding assay, immmocytochemical assay, and northern blot: a comparison". Breast Cancer Research and Treatment. 67: 263–271. doi:10.1023/A:1017946810277. PMID 11561772. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  22. ^ Rivas, A (2002). "Estrogenic effect of a series of bisphenol analogues on gene and protein expression in MCF-7 breast cancer cells". Journal of Steroid Biochemistry and Molecular Biology. 82: 45–53. doi:10.1016/S0960-0760(02)00146-2. PMID 12429138. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  23. ^ Lacroix, M (2004). "About GATA3, HNF3A, and XBP1, three genes co-expressed with the oestrogen receptor-alpha gene (ESR1) in breast cancer". Molecular and Cellular Endocrinology. 219: 1–7. doi:10.1016/j.mce.2004.02.021. PMID 15149721. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  24. ^ Toillon, RA (2005). "Interaction between estrogen receptor alpha, ionizing radiation and (anti-) estrogens in breast cancer cells". Breast Cancer Research and Treatment. 93: 207–215. doi:10.1007/s10549-005-5148-0. PMID 16136271. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  25. ^ Leclercq, G (2006). "Estrogen receptor alpha: impact of ligands on intracellular shuttling and turnover rate in breast cancer cells". Current Cancer Drug Targets. 6: 39–64. doi:10.2174/156800906775471716. PMID 16475975. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  26. ^ Toillon, RA (2007). "Estrogens decrease gamma-rays induced senescence and maintain cell cycle progression in breast cancer cells independently of p53". International Journal of Radiation Oncology, Biology, Physics. 67: 1187–1200. PMID 17336220. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  27. ^ Lacroix, M (2004). "Stable 'portrait' of breast tumors during progression: data from biology, pathology and genetics". Endocrine-Related Cancer. 11: 497–522. doi:10.1677/erc.1.00758. PMID 15369451. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)

Bibliography: invited chapters in thematic books

  • Leclercq G, Lacroix M, Seo HS, Larsimont D. "Mechanisms regulating oestrogen receptor alpha expression in breast cancer.", in "Molecular Mechanisms of Action of Steroid Hormone Receptors" 65-75 (2002). Editors: Marija Krstic-Demonacos & Constantinos Demonacos, Research Signpost Publishers, Trivandrum, India, ISBN 81-7736-129-5, http://www.ressign.com/
  • Sotiriou C, Desmedt C, Durbecq V, Dal Lago L, Lacroix M, Cardoso F, Piccart M. "Genomic and molecular classification of breast cancer.", in "Molecular Oncology of Breast Cancer" 81-95 (2004). Editors: Jeffrey S. Ross and Gabriel N. Hortobagy, Jones and Bartlett Publishers, 40 Tall Pine Drive, Sudbury, MA 01776 USA, ISBN 0-76374-810-2, http://www.jbpub.com/catalog/0763748102/table_of_contents.htm

Bibliography: book

References

Over the years, Marc Lacroix has been refereeing for several international scientific and clinical journals:

External links

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