Marc Lacroix (biochemist)

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Marc Guy Albert Marie Lacroix [pronunciation: "mɑːk lakʁwa"] is a biochemist (educated at University of Liège) and a researcher (born 28 April 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). He lives in Baelen

Earlier work[edit]

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 (Laboratoire Jean-Claude Heuson de Cancérologie Mammaire, 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[edit]

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 overlaid 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)[edit]

  1. ^ Siwek, B; Larsimont D; Lacroix M; Body JJ (1998). "Establishment and characterization of three new breast-cancer cell lines". International Journal of Cancer. 76 (5): 677–683. doi:10.1002/(SICI)1097-0215(19980529)76:5<677::AID-IJC11>3.0.CO;2-1. PMID 9610725.
  2. ^ Lacroix, M; Zammatteo N; Remacle J; Leclercq G. (2002). "A low-density DNA microarray for analysis of markers in breast cancer". International Journal of Biological Markers. 17 (1): 5–23. doi:10.1177/172460080201700102. PMID 11936587.
  3. ^ Lacroix, M; Leclercq G. (2004). "Relevance of breast cancer cell lines as models for breast tumours: an update". Breast Cancer Research and Treatment. 83 (3): 249–289. doi:10.1023/ PMID 14758095.
  4. ^ Lacroix, M; Haibe-Kains B; Hennuy B; Laes JF; Lallemand F; Gonze I; Cardoso F; Piccart M; Leclercq G; Sotiriou C. (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 (4): 701–707. doi:10.3892/or.12.4.701. PMID 15375488. S2CID 21227327.
  5. ^ Lacroix, M; Leclercq G; et al. (BreastMed Consortium) (2005). "The "portrait" of hereditary breast cancer". Breast Cancer Research and Treatment. 89 (3): 297–304. doi:10.1007/s10549-004-2172-4. PMID 15754129.
  6. ^ De Longueville F, Lacroix M, Barbuto AM, Bertholet V, Gallo D, Larsimont D, Marcq L, Zammatteo N, Boffe S, Leclercq G, Remacle J (2005). "Molecular characterization of breast cancer cell lines by a low-density microarray". International Journal of Oncology. 27 (4): 881–892. PMID 16142302.
  7. ^ Lacroix, M; Toillon RA; Leclercq G. (2006). "P53 and breast cancer, an update". Endocrine-Related Cancer. 13 (2): 293–325. doi:10.1677/erc.1.01172. PMID 16728565.
  8. ^ Lacroix., M (2006). "Significance, detection and markers of disseminated breast cancer cells". Endocrine-Related Cancer. 13 (4): 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): 1–4. doi:10.1002/ijc.23233. PMID 17960586.
  10. ^ Lacroix, M; Siwek B; Marie PJ; Body JJ. (1998). "Production and regulation of interleukin-11 by breast cancer cells". Cancer Letters. 127 (1–2): 29–35. doi:10.1016/S0304-3835(97)00542-9. PMID 9619855.
  11. ^ Sotiriou C, Lacroix M, Lagneaux L, Berchem G, Body JJ (1999). "The aspirin metabolite salicylate inhibits breast cancer cells growth and their synthesis of the osteolytic cytokines interleukins-6 and-11". Anticancer Research. 19 (4B): 2997–3006. PMID 10652584.
  12. ^ Sotiriou, C; Lacroix M; Lespagnard L; Larsimont D; Paesmans M; Body JJ. (2001). "Interleukins-6 and-11 expression in primary breast cancer and subsequent development of bone metastases". Cancer Letters. 169 (1): 87–95. doi:10.1016/S0304-3835(01)00524-9. PMID 11410329.
  13. ^ Lacroix, M; Siwek B; Body JJ. (1996). "Effects of secretory products of breast cancer cells on osteoblast-like cells". Breast Cancer Research and Treatment. 38 (2): 209–216. doi:10.1007/BF01806675. PMID 8861839.
  14. ^ Siwek, B; Lacroix M; DePollak C; Marie P; Body JJ. (1997). "Secretory products of breast cancer cells specifically affect human osteoblastic cells: Partial characterization of active factors". Journal of Bone and Mineral Research. 12 (4): 552–560. doi:10.1359/jbmr.1997.12.4.552. PMID 9101366.
  15. ^ Lacroix, M; Lacroix M; Marie PJ; Body JJ. (2000). "Protein production by osteoblasts: modulation by breast cancer cell-derived factors". Breast Cancer Research and Treatment. 61 (1): 59–67. doi:10.1023/A:1006408916224. PMID 10930090.
  16. ^ Lacroix, M; Body JJ. (1997). "Regulation of c-fos and c-jun expression by calcitonin in human breast cancer cells". Calcified Tissue International. 60 (6): 513–519. doi:10.1007/s002239900273. PMID 9164825.
  17. ^ Lacroix, M; Siwek B; Body JJ. (1998). "Breast cancer cell response to calcitonin: Modulation by growth-regulating agents". European Journal of Pharmacology. 344 (2–3): 279–286. doi:10.1016/S0014-2999(97)01578-1. PMID 9600664.
  18. ^ Jin, L; Borras M; Lacroix M; Legros N; Leclercq G. (1995). "Antiestrogenic activity of 2 11-beta-estradiol derivatives on MCF-7 breast cancer cells". Steroids. 60 (8): 512–518. doi:10.1016/0039-128X(95)00079-6. PMID 8539793.
  19. ^ Borras, M; Lacroix M; Legros N; Leclercq G. (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 (1): 23–30. doi:10.1016/S0304-3835(97)00285-1. PMID 9570382.
  20. ^ Maaroufi, Y; Lacroix M; Lespagnard L; Journe F; Larsimont D; Leclercq G. (2000). "Estrogen receptor of primary breast cancers: evidence for intracellular proteolysis". Breast Cancer Research. 2 (6): 444–454. doi:10.1186/bcr92. PMC 13922. PMID 11056692.
  21. ^ Lacroix, M; Querton G; Hennebert P; Larsimont D; Leclercq G. (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 (3): 263–271. doi:10.1023/A:1017946810277. PMID 11561772.
  22. ^ Rivas, A; Lacroix M; Olea-Serrano F; Laios I; Leclercq G; Olea N. (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 (1): 45–53. doi:10.1016/S0960-0760(02)00146-2. PMID 12429138.
  23. ^ Lacroix, M; Leclercq G. (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 (1–2): 1–7. doi:10.1016/j.mce.2004.02.021. PMID 15149721.
  24. ^ Toillon RA, Magné N, Laios I, Lacroix M, Duvillier H, Lagneaux L, Devriendt D, Van Houtte P, Leclercq G (2005). "Interaction between estrogen receptor alpha, ionizing radiation and (anti-) estrogens in breast cancer cells". Breast Cancer Research and Treatment. 93 (3): 207–215. doi:10.1007/s10549-005-5148-0. PMID 16136271.
  25. ^ Leclercq, G; Lacroix M; Laïos I; Laurent G. (2006). "Estrogen receptor alpha: impact of ligands on intracellular shuttling and turnover rate in breast cancer cells". Current Cancer Drug Targets. 6 (1): 39–64. CiteSeerX doi:10.2174/156800906775471716. PMID 16475975.
  26. ^ Toillon RA, Magné N, Laïos I, Castadot P, Kinnaert E, Van Houtte P, Desmedt C, Leclercq G, Lacroix M (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 (4): 1187–1200. doi:10.1016/j.ijrobp.2006.11.040. PMID 17336220.
  27. ^ Lacroix, M; Toillon RA; Leclercq G. (2004). "Stable 'portrait' of breast tumors during progression: data from biology, pathology and genetics". Endocrine-Related Cancer. 11 (3): 497–522. doi:10.1677/erc.1.00758. PMID 15369451.

Bibliography: collaborative books - invited chapters[edit]

Bibliography: books[edit]


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

External links[edit]