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Searched applicants and owners= \"Cambridge Univ\", \" Univ Cambridge\", \" University of Cambridge\", \" Cambridge University\" , \" Cambridge Enterprise Ltd\" , \"cambridge University Technical\", \" Cambridge Univ Entpr Ltd\" , \"cambri* Univ*\"
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Searched applicants and owners= \"Cambridge Univ\", \" Univ Cambridge\", \" University of Cambridge\", \" Cambridge University\" , \" Cambridge Enterprise Ltd\" , \"cambridge University Technical\", \" Cambridge Univ Entpr Ltd\" , \"cambri* Univ*\"
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Total patents= 5951
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DM, INCE TA, QUADE BJ, SHAFER SA, CROWLEY D, JACKS T.: \"Role of K-ras and Pten in the development of mouse models of endometriosis and endometrioid ovarian cancer.\", NAT MED, vol. 11, no. 1, 26 December 2004 (2004-12-26) - January 2005 (2005-01-01), pages 63 - 70, XP002506011","npl_type":"s","xp_number":"002506011","external_id":["15619626","10.1038/nm1173"],"record_lens_id":"072-260-635-983-77X","lens_id":["156-325-289-035-418","072-260-635-983-77X","173-777-922-827-319"],"sequence":1,"category":["D","A"],"us_category":[],"cited_phase":"ISR","cited_date":"2008-11-28","rel_claims":[],"srep_office":"EP"}},{"npl":{"num":2,"text":"MATZUK MM.: \"Gynecologic diseases get their genes.\", NAT MED., vol. 11, no. 1, January 2005 (2005-01-01), pages 24 - 26, 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for invention","granted":false,"earliest_filing_date":"2008-08-11","has_disclaimer":false,"patent_status":"PENDING","publication_count":1,"has_spc":false,"has_grant_event":false,"has_entry_into_national_phase":false},"abstract":{"en":[{"text":"This invention relates to the production of rodent endometriosis models by implanting into wild type recipient rodents menstruating endometrium from donor rodents in which an oncogene, such as K-ras, has been activated. Rodent endometriosis models and methods of production and use of such models in screening for therapeutics are provided.","lang":"en","source":"WIPO_FULLTEXT","data_format":"ORIGINAL"}],"fr":[{"text":"Cette invention porte sur la production de modèles rongeurs d'endométriose par implantation chez des rongeurs receveurs de type sauvage d'un endomètre menstruel provenant de rongeurs donneurs dans lesquels un oncogène, tel que K-ras, a été activé. L'invention porte ainsi sur des modèles rongeurs d'endométriose ainsi que sur des procédés de production et d'utilisation de tels modèles dans le criblage d'agents thérapeutiques.","lang":"fr","source":"WIPO_FULLTEXT","data_format":"ORIGINAL"}]},"abstract_lang":["en","fr"],"has_abstract":true,"claim":{"en":[{"text":"Claims : 1. A method of producing a rodent endometriosis model comprising providing a female donor rodent having an activatable oncogenic nucleic acid sequence, activating the oncogenic nucleic acid sequence, inducing menstruation of endometrium comprising activated oncogenic nucleic acid sequence from the donor rodent, and implanting the menstruating endometrium into a female recipient rodent. 2. A method according to claim 1 wherein the oncogenic nucleic acid sequence is an oncogenic K-ras nucleic acid sequence 3. A method according to claim 1 or claim 2 wherein the oncogenic nucleic acid sequence is activated by expression of site-specific recombinase. 4. A method according to claim 3 wherein the female donor rodent has a nucleotide sequence encoding a site-specific recombinase. 5. A method according to claim 4 wherein the site-specific recombinase is Cre recombinase. 6. A method according to claim 4 or claim 5 wherein the nucleotide sequence encoding the site-specific recombinase is operably linked to a tissue-specific promoter. 7. A method according to any one of claims 4 to 6 wherein the nucleotide sequence encoding the site-specific recombinase is operably linked to an inducible promoter. 8. A method according to claim 7 comprising inducing expression of the nucleotide sequence encoding the site-specific recombinase from the inducible promoter. 9. A method according to any one of claims 3 to 8 wherein the female donor rodent has a first reporter gene which is activated by expression of site-specific recombinase. 10. A method according to claim 9 wherein the female donor rodent has a second reporter gene constitutively expressed. 11. A method according to any one of the preceding claims wherein menstruation is induced by inducing decidualization and lowering progesterone levels in the donor rodent endothelium. 12. A method according to claim 11 wherein the progesterone levels are lowered by withdrawal of progesterone treatment. 13. A method according to claim 11 or claim 12 wherein the progesterone levels are lowered by administration of antiprogesterone . 14. A method according to any one of claims 11 to 13 wherein decidualisation is induced in said donor rodent by administration of oil to the uterus of said rodent. 15. A method according to any one of claims 11 to 14 wherein decidualisation is induced in said donor rodent simultaneously with activation of the oncogenic nucleic acid sequence. 16. A method according to any one of claims 11 to 15 wherein menstruating endometrial tissue is collected from the donor rodent 50 to 70 hours after a final progesterone treatment. 17. A method according to any one of claims 1 to 16 wherein stable endometrial lesions form less than 28 days after said implantation . 18. A method of screening for an agent for use in the treatment of endometriosis comprising producing a rodent endometriosis model by a method according to any one of claims 1 to 17, administering a test compound to the rodent endometriosis model, and determining the effect of said compound on endometriosis in said model. 19. A method according to claim 18 wherein the effect of the compound on the size, amount or composition of endometrial lesions formed by the implanted menstruating endometrium in the recipient rodent is determined. 20. A method according to claim 19 wherein a decrease or reduction in the size or number of endometrial lesions or a change in cellular composition in mice treated with the test compound relative to control mice untreated with the test compound is indicative that the test compound is a putative agent which may be useful in the treatment of endometriosis. 21. A method according to any one of claims 18 to 20 comprising identifying a test compound as useful in the treatment of endometriosis. 22. A rodent endometriosis model comprising: a recipient rodent implanted with menstruating endometrium from a donor rodent, wherein the menstruating endometrium of the donor rodent has an activated oncogenic nucleic acid sequence. 23. A rodent endometriosis model produced by a method according to any one of claims 1 to 17. 24. A method of screening for a gene involved in endometriosis may comprise; altering the expression of a candidate gene in the endometrium of a rodent endometriosis model according to claim 22 or claim 23, and determining the effect of said activation on endometriosis in said model. 25. A method according to claim 24 wherein the expression of the candidate gene is altered in the donor rodent and/or the recipient rodent. 26. A method according to claim 24 or claim 25 wherein the expression of the candidate gene is increased. 27. A method according to claim 24 or claim 25 wherein the expression of the candidate gene is decreased. 28. A method according to any one of claims 24 to 27 wherein the effect on endometriosis is determined by determining the effect on the size, amount or cellular composition of endometriosislesions formed by the implanted menstruating endometrium in the recipient rodent. 29. A method according to claim 28 wherein a change in the size, number or cellular composition of endometrial lesions in mice with altered candidate gene expression relative to control mice with unaltered candidate gene expression is indicative that the gene is involved in endometriosis.","lang":"en","source":"WIPO_FULLTEXT","data_format":"ORIGINAL"}]},"claim_lang":["en"],"has_claim":true,"description":{"en":{"text":"MURINE ENDOMETRIOSIS MODELLED BY K-RAS ACTIVATION OF MENSTRUATING ENDOMETRIUM This invention relates to models of endometriosis, in particular rodent endometriosis models which may be useful, for example, in the development of treatments for this condition. Endometriosis is one of the most common causes of pelvic pain and infertility in women, which afflicts approximately 5-10% of women of reproductive age [1-3] . The pathological diagnosis of endometriosis is characterized by the presence of benign endometrial glands and stroma outside the uterus [1, 4] . The cause of endometriosis is still not clear. The most widely accepted theory is that the disorder originates from retrograde menstruation of endometrial tissue, shed at the time of menstruation, which passes backward along the fallopian tubes and into the peritoneal cavity [2] . However, retrograde menstruation is suggested to occur in nearly all women of reproductive age [3, 5], and little is known about the development and progress of the disease after retrograde menstruation. Ethical considerations limit endometriosis research in man and experimental animal models provide an alternative way to study the pathogenesis of endometriosis and develop drugs . Endometriosis occurs naturally in human and some non-human primates, and non-human primates have been used widely for endometriosis research [6-8] . However, ethical considerations and the cost of keeping non-human primates limit the use of these animal models. On the other hand, although small laboratory animals such as rodents do not naturally menstruate nor develop endometriosis, a model of endometriosis using small laboratory animals is a more ethically and economically attractive option. There are three currently used murine models of endometriosis: an autograft model, an allograft model and a xenograft model. The autotransplantation model of endometriosis, in which pieces of uterine horn are surgically transposed onto connective tissue supplied by the internal mesenteric artery, has been performed in rat and mouse [9-12] ; and has also been applied to rabbit [13] . This model is the most commonly used one among the three existing murine models, however the inclusion of myometrium in the ectopic uterine fragments is different from pathogenesis of human endometriosis and is the main weakness of this model. Transplantation of heterologous murine endometrium from the same strain of mouse has also been successfully achieved in ovarectomised, estrogen-supplemented mice. [14, 15] The subsequent lesions exhibited dilated multicystic glands surrounded by stroma. The main weakness of this model is that it is strongly estrogen-driven. Also, the estrogen treated donor tissue is intact rather than stressed, as is the case during the retrograde menstruating endometrial tissue in humans. However, there are several advantages of using a heterologous mouse model. These include the ability to use anti-mouse antibodies and murine molecular probes to investigate cellular and molecular events in endometriosis-like tissue. Additionally, it provides the potential of using genetically manipulated mice to investigate gene products that are critical to ectopic endometrial lesion development [16] . Implanting human endometrial tissue into xenographic hosts such as nude or SCID mice to induce endometriosis has also been used [17, 18] . Histologically nude mouse implants are characterised by the presence of endometrial glandular acini and stromal cells although lesions can contain necrosis, haemosiderin and an infiltrate of macrophages and other leucocytes. As is the case in the human disease, estrogen supplementation is associated with larger lesions and a proliferative histological pattern whereas danazol resulted in atrophic tissue changes [19] . An unfavourable aspect of the nude mouse model is that the proportion of mice that develop lesions has been documented to vary from 33-100% [18-20] . The SCID mouse model has been reported to show higher success rate in lesion development [21, 22], and this might be due to their defective natural killer cell function [21] . However, when nude mice were compared with non-obese diabetic SCID (NOD-SCID) , little difference in lesion development frequency was observed [23] . Although the xenograft model is the first established endometriosis model using small laboratory animals, it is not as widely used as the homologous model, probably due to the difficulty of collecting human endometrial tissue. In addition, the compromised immune function in host mice is a significant key limitation of this model . The three current murine models of endometriosis all have their limitations. During menstruation, the superficial layer of endometrium breaks down and is sloughed from the basal layer. These tissues are stressed, undergoing degeneration involving many apoptotic cells and the overall tissue is rather fragile. One common difference between the existing models and human endometriosis is that the donor tissues from all these three models are intact rather than stressed and fragile as is the case in menstruating endometrium. However, unlike human and non- human primates, the endometrium of small laboratory animals does not decidualize spontaneously without embryo implantation. Furthermore these species do not menstruate. A murine model of decidualization and menstruation based on Finn and Pope's report has been developed [24, 25] . Using this model, sloughed decidualized endometrium was isolated from a progesterone-withdrawn donor. To our surprise, the menstruating endometrium barely survived when transplanted into immunocompromised nude mice but not at all when transferred to immunocompetent recipients of the same strain. A murine endometriosis model based on the activation of an oncogenic K-ras allele using transgenic mice was reported in 2005 [26] . This model requires the injection of a cre-encoding retrovirus into the ovarian bursa, which is a surgical procedure. The primary target of this is the ovarian epithelium and it is not clear how such a manipulation leads to the development of endometriosis since the bursa is an enclosed space and there is no route for the retrovirus to reach endometrial tissue. Furthermore, the endometriotic lesions only developed in approximately 50% of the animals and even these took eight months to develop. These features severely limit the utility of this model. The present inventors have discovered that the implantation of menstruating endometrium from K-ras activated mice into wild type recipients produces viable endometriosis-like lesions. This allows the production of a rodent model of endometriosis which may be useful in the development of therapeutics . A first aspect of the invention provides a method of producing a rodent endometriosis model comprising providing a female donor rodent having an activatable oncogenic nucleic acid sequence, activating the oncogenic nucleic acid sequence, inducing menstruation of endometrium comprising activated oncogenic nucleic acid sequence from the donor rodent, and implanting the menstruating endometrium into a female recipient rodent. Following implantation, endometrial lesions develop in the recipient rodent. Endometrial lesions are glands of tissue containing both stromal and glandular epithelial cells as well as blood vessels and fibrous collagen structures. The recipient rodent thus represents a model of endometriosis. The donor rodent may be any suitable laboratory species, including mouse, hamster, rat or guinea pig. In preferred embodiments, the rodent may be a mouse. A donor mouse may be of any suitable murine strain. Preferably, the donor rodent is ovariectomised. Preferably, the recipient rodent has intact ovaries, i.e. is not ovariectomised, and/or is not treated with exogenous oestrogen, e.g estradiol. A suitable oncogenic nucleic acid may confer a growth advantage or increased resistance to apoptosis on a host cell expressing the nucleic acid, without causing tumourigenesis An activatable oncogenic nucleic acid sequence is a nucleic acid which is inactive and is not expressed to produce an active product within the donor rodent until a suitable stimulus is applied. Upon exposure to the stimulus, the oncogenic nucleic acid is activated and active product is produced within those cells of the donor rodent which are subjected to the stimulus. Suitable stimuli for activating the oncogenic nucleic acid are described below. The activatable oncogenic nucleic acid sequence may be located extrachromosomally or more preferably within the genome of the donor rodent . Preferably, the oncogenic nucleic acid is an oncogenic K-ras nucleic acid. K-ras protein is a 21-kD GTPase which is a member of the ras signalling pathway and modulates cellular proliferation and differentiation. Wild-type K-ras may be converted into an oncogenic K-ras allele by mutation of one or more amino acids within the wild-type K-ras sequence, typically within the GTPase domain. Oncogenic K-ras alleles cause constitutive activation of ras-signalling pathway, leading to unregulated cellular proliferation and impaired differentiation. An oncogenic K-ras nucleic acid sequence encodes an oncogenic K- ras allele. A suitable sequence may encode the sequence of wild- type K-ras with an oncogenic mutation. Suitable oncogenic mutations include the substitution of GIy at position 12 or 13 in the K-ras sequence. For example, GIy 12 may be substituted for Ser, VaI or Asp. In some preferred embodiments, the GIy 12 may be substituted for VaI (i.e. K-ras V12) . In some embodiments, an oncogenic K-ras nucleic acid may have the murine K-ras sequence with one or more oncogenic mutations . Murine K-ras has an amino acid sequence having the database accession number NP_067259.3 GI: 84370270 and is encoded by a nucleic acid having the database accession number NM_021284.4 GI: 142374722. In other embodiments, the oncogenic K-ras nucleic acid sequence may be a heterologous sequence, for example from a non-murine or non-rodent mammalian species, with one or more oncogene- activating mutations. Suitable heterologous oncogenic K-ras nucleic acids include the human K-ras isoform a which has an amino acid sequence having the database accession number NP_004976.2 GI: 15718761 which is encoded by a nucleic acid having the database accession number NM_004985.3 GI: 34485723 or the human K-ras isoform b which has an amino acid sequence having the database accession number NP_203524.1 GI: 15718763 which is encoded by a nucleic acid having the database accession number NM_033360.2 GI: 34485724 A heterologous nucleic acid is a nucleic acid that is outside its natural environment i.e. it is not naturally occurring within the donor rodent. A heterologous nucleic acid may be recombinant. The heterologous nucleic acid may, for example, have been introduced into the donor rodent or an ancestor thereof by conventional recombinant techniques. The donor rodent may be homozygous or heterozygous for the activatable oncogenic nucleic acid sequence. For example, the donor rodent may be a K-ras +/~ mouse, such as a K-ras vl2+/~ mouse. The activated oncogenic nucleic acid may be operably linked to appropriate regulatory sequences, including promoter sequences, terminator fragments, polyadenylation sequences, enhancer sequences, marker genes and other sequences as appropriate. The regulatory sequences drive the expression of the oncogenic nucleic acid in rodent cells following activation. In some embodiments, tissue-specific regulatory sequences may drive expression of the activated oncogenic nucleic acid sequence in specific tissues, such as the endometrium. The regulatory sequences may be operably linked to the oncogenic nucleic acid sequence before the oncogenic nucleic acid sequence is activated or may only become operably linked to the oncogenic nucleic acid sequence during activation. Activation of the oncogenic nucleic acid may be systemic throughout the rodent or may only occur in specific tissues such as the endometrium. Tissue specific activation may be achieved, for example, by the application of the stimulus to specific tissues . Any suitable stimulus may be employed to activate the oncogenic nucleic acid. For example, the stimulus may be expression of a site specific recombinase. The oncogenic nucleic acid may be activatable by a site specific recombinase. Suitable site specific recombinases include Cre and FLP. Cre recombinase is a Type I topoisomerase from bacteriophage Pl that catalyzes the site-specific recombination of DNA between loxP sites (Abremski, K. and Hoess, R. (1984) J. Biol. Chem., 259, 1509-1514) . The loxP sites which are recognised by Cre recombinase are 34 base pair (bp) sequences comprised of two 13 bp inverted repeats flanking an 8 bp spacer region (Metzger, D. and Feil, R. (1999) Curr. Opin. Biotechnol. 10, 470-476) . Nucleic acid located between directly repeated loxP sites is excised by Cre recombinase in circular form and nucleic acid located between opposing repeated loxP sites is inverted by Cre recombinase. The use of Cre recombinase to mediate recombination between loxP sites is well known in the art (see, for example, Bockamp, E. et al (2002) Physiol. Genomics. 11, 115-132; Cohen-Tannoudji, M. et al (1998) MoI. Hum. Reprod. 4, 929-938; Davey, R. A. & MacLean, H. E. (2006) Am J Physiol Endocrinol Metab. 291, E429- 438; Rajewsky, K. et al (1996) J Clin Invest. 98, 600-3) . Cre recombinase may, for example, have the amino acid sequence having the database accession number YP__006472.1 GI: 46401628. Nucleic acid encoding Cre recombinase may be provided using conventional techniques. The nucleic acid sequence of Cre recombinase is found between nucleotides 436 to 1467 of the Pl phage genome of NC_005856.1 GI: 46401624. FLP recombinase is a site specific integrase from the 2 micron plasmid of S. cerevisiae that catalyzes the site-specific recombination of DNA between FLT sites. The FLT sites which are recognised by FLP recombinase are comprised of three 13 bp repeats and an 8 bp spacer region. The use of FLP recombinase to mediate recombination between FLT sites is well known in the art (see for example Pan et al MoI Cell Biol. (1993) 13(6) 3167- 3175) . FLP recombinase may, for example, have the amino acid sequence having the database accession number NP_040488.1 GI11466068. Nucleic acid encoding FLP recombinase may be provided using conventional techniques. The nucleic acid sequence of FLP recombinase is found between nucleotides 5570 to 6318 and 1 to 523 of the 2 micron plasmid sequence of NC 001398.1 GI11466067. The oncogenic nucleic acid sequence may be associated in the genome of the donor rodent with target sites for the site specific recombinase (e.g. loxP sites or FLT sites) which allow the activation of the oncogenic nucleic acid sequence by the appropriate site specific recombinase (e.g. Cre or FLP) . The oncogenic nucleic acid sequence and target sites may be in any suitable arrangement which causes activation of the oncogenic nucleic acid sequence following recombinase mediated recombination between the target sites. Various arrangements of oncogenic nucleic acid sequence and site specific recombinase target sites are possible. For example, a blocking sequence flanked by target sites may be positioned within the oncogenic nucleic acid. The blocking sequence prevents transcription of active oncogenic nucleic acid. The blocking sequence is excised by recombinase-mediated recombination between the target sites, allowing transcription of the active oncogenic nucleic acid. In some embodiments, a blocking sequence may be positioned between the oncogenic nucleic acid and a promoter. Excision of the blocking sequence operably links the promoter and the oncogenic nucleic acid, allowing transcription of the oncogenic nucleic acid. Alternatively, the oncogenic nucleic acid may be flanked by target sites and positioned in an inverted orientation with respect to its promoter, such that it is not expressed in an active form. The oncogenic nucleic acid is activated by expression of site specific recombinase, which mediates inversion of the oncogenic nucleic acid between the inverted target sites, allowing transcription of the active oncogenic nucleic acid. Alternatively, the oncogenic nucleic acid may comprise a STOP codon flanked by target sites. The STOP codon prevents the translation of active oncogenic protein from the nucleic acid. Site specific recombinase mediates excision of the STOP codon from the nucleic acid, allowing active oncogenic protein to be translated from the oncogenic nucleic acid. Preferably, the donor rodent further comprises a nucleic acid sequence encoding a site specific recombinase such as Cre or FLP. Expression of the nucleic acid produces the site specific recombinase which activates the oncogenic nucleic acid sequence. The nucleic acid encoding site specific recombinase may be operably linked to appropriate regulatory sequences, including promoter sequences, terminator fragments, polyadenylation sequences, enhancer sequences, marker genes and other sequences as appropriate. The regulatory sequences drive the expression of site-specific recombinase in rodent cells. Preferably, expression of the site- specific recombinase is tissue specific. In other words, site- specific recombinase not expressed in all cells of the donor rodent. Site-specific recombinase may, for example, be specifically expressed in epithelial cells, in particular cells of the endometrium. The nucleic acid encoding the site-specific recombinase gene may be operably linked to tissue specific, in particular epithelial cell specific, regulatory sequences, such as promoters. Many suitable epithelial promoters are known in the art and include the Ah promoter . The nucleic acid encoding the site-specific recombinase gene may be operably linked to inducible regulatory sequences, such as promoters . Inducible regulatory sequences may provide expression of the site-specific recombinase only in cells or tissues which are exposed to an inducing agent. Site-specific recombinase is expressed following exposure of cells or tissues to the inducing agent and the expressed site-specific recombinase activates the oncogenic nucleic acid sequence in the cells or tissues of the donor rodent which are exposed to the inducing agent. In some embodiments, the tissue specificity of site-specific recombinase expression may be increased by applying the inducing agent selectively to the uterus and/or endometrium of the donor rodent, such that expression of the site-specific recombinase is only induced in the endometrium and adjacent tissues and not systemically in all tissues of the donor rodent. Many suitable inducible promoters are known in the art and include Ah, Tet-on, ecdysone or tamoxifen controlled promoters. In some preferred embodiments, the site-specific recombinase gene may be operably linked to the Ah promoter, which is induced by administration of β-napthoflavone (β-NF) . The Ah promoter is especially preferred because it is both inducible and epithelial cell specific (Kemp et al Nucl Acid Res 2004 32 e92; Ireland et al (2004) Gastroenterology 126 1236-1246). The inducing agent which induces expression of the site-specific recombinase may be administered systemically, for example by intraperitoneal injection, or may be administered specifically to the uterus and/or endometrium of the donor rodent, for example by injection into one or both horns of the uterus, such that site-specific recombinase expression is induced in the endometrium and adjacent tissues and not systemically in all tissues of the donor rodent. The donor rodent may be heterozygous or, more preferably, homozygous for the nucleic acid encoding site specific recombinase, For example, the donor rodent may be a AhCre +/+ mouse. The donor rodent may further comprise a nucleic acid encoding an activatable first reporter gene. A reporter gene is a nucleic acid which encodes a detectable gene product. For example, a reporter gene may encode an enzyme which mediates a luminescent, fluorescent or chromogenic reaction which produces a detectable signal. Suitable reporter genes are well known in the art and include green fluorescent protein (GFP) , luciferase, and enhanced yellow fluorescent protein (eYFP) and variants thereof, alkaline phosphatase, β- galactosidase (lacZ) , and β-glucuronidase. The reporter gene may be inactive (i.e. not expressed in an active form within the donor rodent) until the stimulus which activates the oncogenic nucleic acid is applied. Upon exposure to this stimulus, the reporter gene is activated and expressed in an active form within tissues of the donor rodent which are subjected to the stimulus, in addition to the oncogenic nucleic acid. Expression of the reporter gene in a tissue or cell is therefore indicative of expression of the oncogenic nucleic acid in the tissue or cell. As described above, the stimulus is preferably expression of site-specific recombinase i.e. expression of the reporter gene may be activatable by site-specific recombinase. The activatable reporter gene may be associated in the genome of the donor rodent with target sites which allow the activation of the reporter gene by site-specific recombinase. The reporter gene and target sites may be in any suitable arrangement which allows activation of the reporter gene by recombination between the target sites. Suitable arrangements are described in more detail above. In some embodiments, a Cre recombinase activatable reporter gene, such as lacZ, may be present at the ROSA26 locus of the donor rodent . The donor rodent may further comprise a nucleic acid encoding a second reporter gene which is expressed consitutively . This allows the tissue implanted into the recipient rodent to be monitored over time. For example, the implanted menstruating endometrium may constitutive express luciferase, and may be detected in the recipient rodent using real-time in vivo imaging techniques (Xenogen Corp, MA USA) . The donor rodent may be heterozygous or, more preferably, homozygous for the activatable reporter gene. For example, the donor rodent may be a ROSA26R-LacZ +/+ mouse. In some preferred embodiments, a suitable donor rodent may comprise an inducible site specific recombinase nucleic acid sequence, a site specific recombinase activatable oncogenic nucleic acid sequence and a site specific recombinase activatable reporter gene. Preferably, the donor rodent is heterozygous for the oncogenic nucleic acid sequence and homozygous for the site specific recombinase and reporter gene. In some preferred embodiments, the donor rodent may be a Jf- ras vl2+/' /AhCre +/+ /ROSA26R-LacZ +/+ mouse. Further genetic modification of the donor and/or recipient rodent may be useful, for example for investigating the mechanism of the pathogenesis or performing proof-of-concept studies. A donor rodent may comprise one or more additional genetic modifications to those set out above. Suitable modifications include deletions, insertions or substitutions of one or more nucleotides. A genetic modification may inactivate or modify the activity of a target sequence. Suitable target sequences include genes which encode chemokines, cytokines, growth factors and their receptors, proteases, protease inhibitors, immune regulators or adhesion molecules. Nucleic acid sequences as described above may be comprised within a vector in the genome of the donor rodent. Vectors may be plasmids, viral e.g. 'phage, or phagemid, as appropriate. For further details see, for example, Molecular Cloning: a Laboratory Manual: 3rd edition, Russell et al., 2001, Cold Spring Harbor Laboratory Press, and Protocols in Molecular Biology, Second Edition, Ausubel et al . eds . John Wiley & Sons, 1992. In some embodiments, a viral vector suitable for expression in rodent cells may be employed. Suitable viral vectors include adenovirus, adeno-associated virus (AAV) , for example AAV serotype 2 virus, retrovirus, lentivirus, recombinant adenovirus, Λ gutless' adenovirus, herpes simplex virus, and poliovirus vectors. A viral vector may be packaged into a viral particle comprising one or more capsid proteins prior to transfection of host cells. Techniques for the introduction of nucleic acid into cells are well established in the art and any suitable technique may be employed, in accordance with the particular circumstances. For eukaryotic cells, suitable techniques may include DEAE-dextran, polyethyleneimine, electroporation, liposome-mediated transfection and transduction using retrovirus or other virus, e.g. adenovirus, AAV, lentivirus or vaccinia. Transgenic donor rodents as described herein may be produced in accordance with standard techniques. For example, a heterologous nucleic acid may be introduced into a rodent germ line cell, and a transgenic rodent generated from said rodent germ line cell. A suitable rodent germ-line cell may include an egg, oocyte or embryonic stem (ES) cell. In some embodiments, the nucleic acid may be introduced into a germ line cell that is comprised in an early stage embryo, such as a blastocyst. The heterologous nucleic acid or vector may be introduced into the germ line cell using any method known in the art, including, for example, pronuclear microinjection; retrovirus mediated gene transfer into germ lines; gene targeting in embryonic stem cells; electroporation of embryos; sperm-mediated gene transfer; calcium phosphate/DNA co-precipitates, microinjection of DNA into the nucleus, bacterial protoplast fusion with intact cells, transfection, and polycations, e.g., polybrene, polyornithine, etc., (See, for example Van der Putten, et al . , 1985, Proc. Natl. Acad. Sci., USA 82:6148-6152; Thompson, et al . , 1989, Cell 56:313-321; Lo, 1983, MoI Cell. Biol. 3:1803-1814; Lavitrano, et al., 1989, Cell, 57 -.111-123 Gordon, 1989, Intl. Rev. Cytol . , 115:171-229; Keown et al . , 1989, Methods in Enzymology; Keown et al., 1990, Methods and Enzymology, Vol. 185, pp. 527-537; Mansour et al., 1988, Nature, 336:348-352) . After the heterologous nucleic acid or vector has been introduced into cells, the cells in which the heterologous nucleic acid has successfully incorporated into the rodent germ- line cell genome may be identified. Cells comprising the heterologous nucleic acid may be identified, for example, by detecting the expression of a marker gene. For example, transformed cells may be treated with a selective agent that selects either cells expressing or cells not expressing the selectable marker. Many suitable selectable markers and agents are known in the art. For example, cells expressing the introduced neomycin resistance gene are resistant to the compound G418, while cells that do not express the neo gene marker are killed by G418. Successful insertion of the heterologous nucleic acid into the genome may be confirmed by analyzing the DNA of the selected cells using routine techniques, such as PCR and/or Southern analysis . A rodent may be generated from a cell comprising the heterologous nucleic acid or vector using standard techniques (see for example Piedrahita et al (1992) PNAS USA 89 4471-4475, Roller et al (1989) PNAS USA 86 8927-8931; Transgenic Animal Technology: A Laboratory Handbook, Pinkert CA (2002) Academic Press) . For example, the cell may be introduced into a blastocyst. The injection of transformed cells injected into a rodent blastocyst may lead to the formation of chimeras (see e.g., Bradley, A. in Teratocarcinomas and Embryonic Stem Cells: A Practical Approach, E. J. Robertson, ed., IRL, Oxford, pp. 113-152 (1987)) . Alternatively, germ-line cells identified as comprising the heterologous nucleic acid may be allowed to aggregate with dissociated rodent embryo cells to form the aggregation chimera. A chimeric embryo can then be implanted into a suitable pseudopregnant female foster rodent and the embryo brought to term. Chimeric progeny harbouring the heterologous nucleic acid in their germ cells can be used to breed mice in which all cells of the rodent comprise the heterologous nucleic acid. Rodents, such as mice, which are produced as described may be crossed with mice of the same or other genotypes to produce descendents . The genotype of the rodent or descendent may be determined. A method may include determining that the rodent or its descendent specifically expresses the heterologous nucleic acid(s). Methods of determining the genotypes of rodents are well-known in the art. Menstruation of the endometrium of the donor rodent may be induced following or simultaneous with activation of the oncogenic nucleic acid. Preferably, menstruation is induced by lowering progesterone levels in the endometrium of the donor rodent. Suitable methods are described in Finn, C. A. & Pope, M. (1984) J Endocrinol. 200, 295-300 and Cheng, C. W., et al (2007) Biol Reprod. 76 871- 883. For example menstruation may be induced by treating the donor rodent with progesterone and oestrogen, for example 17β- oestradial (E2), inducing decidualisation of the donor rodent endothelium and lowering progesterone levels, for example by withdrawing or stopping further progesterone treatment. The rodent may initially be treated with progesterone and oestrogen for a number of days, for example up to 6 days, up to 8 days or up to 10 days. Suitable regimens are described in Finn, C. A. et al (1984) J Endocrinol. 100, 295-300 and Cheng, C. W. et al (2007) Biol Reprod. 76 871-883. Typically, a course of treatment may comprise administration of oestrogen on day 1 and day 2, and administration of progesterone and oestrogen on day 6> day 7, and day 8, as shown in Table 1. Progesterone and oestrogen may be administered by subcutaneous injection. Decidualisation may be induced in the endometrium of the donor rodent by any convenient technique including physical means such as crushing or drawing a .thread through the lumen. In preferred embodiments, decidualisation is induced by administration of oil, such as maize or peanut oil, to the uterus of the donor rodent, for example by injection. Decidualisation may be induced after or simultaneously with activation of the oncogenic nucleic acid. Progesterone levels may be lowered concomitantly with decidualisation or after decidualisation. Progesterone levels may be lowered by withdrawing or stopping progesterone treatment and/or by administering an antiprogesterone. Antiprogesterones include progesterone receptor antagonists such as mifepristone (RU486) and RU38486 and anti-progesterone antibodies. Withdrawing progesterone treatment or administering antiprogesterone has the effect of lowering progesterone levels in the endometrium of the donor rodent, causing degeneration of the donor rodent endometrium and leading to the production of menstruating endometrial tissue. Menstruating endometrial tissue may be collected from the donor rodent 48 to 84 hours, preferably 50 to 70 hours after the final administration of progesterone, more preferably around 60 hours. Menstruating endometrial tissue may be resuspended in a suitable medium, such as a collagen or fibrin gel or matrigel™ (BD Biosciences, Oxford UK), after collection from the donor rodent. Following collection, the menstruating endometrial tissue may be treated with drugs, antibodies and/or subjected to genetic modification, for example by transfection with plasmid or viral vectors or other nucleic acids such as antisense oligonucleotides or RNAi. In some embodiments, the collected menstruating endometrial tissue may be labelled with fluorescent dyes to allow tracking of the tissue after implantation. The menstruating endometrial tissue may be implanted into the recipient rodent by any suitable technique. For example, the tissue may be sub-cutaneously injected into the abdominal side of the recipient rodent. Preferably, the menstruating endometrial tissue is implanted within 30 mins, preferably less than 10 mins of collection from the donor rodent . The recipient rodent may be any suitable laboratory species, including mouse, hamster, rat or guinea pig. In preferred embodiments, the recipient rodent may be a mouse. A recipient mouse may be of any suitable murine strain. Preferably, the recipient rodent is the same species and strain as the donor rodent. The recipient rodent may be an immunocompetent rodent. Suitable strains include C57BL/6 mice In some embodiments, the recipient rodent may be treated with an oestrogen, such as 17β-estradiol, before implantation of the menstruating endometrial tissue. In other embodiments, the recipient rodent is not treated with an oestrogen, such as 17β- estradiol, before implantation of the menstruating endometrial tissue . The recipient rodent may comprise one or more additional genetic modifications to those set out above. Suitable modifications include deletions, insertions or substitutions of one or more nucleotides and may inactivate or modify the activity of a target sequence. Suitable target sequences include genes which encode chemokines, cytokines, growth factors and their receptors, proteases, protease inhibitors, immune regulators or adhesion molecules. Following implantation, endometrial lesions form in the recipient rodent. The lesions may form within 28 days following implantation, typically in 7 to 28 days. The endometrial lesions may be stable in the recipient rodent for 7 days or more, 14 days or more or 21 days or more Endometrial lesions may be detected in the recipient rodent by conventional techniques. In some embodiments, endometrial lesions may be detected in samples obtained from the recipient rodent by standard immunohistochemical techniques. In other embodiments, endometrial lesions may be detected in situ using real time in vivo imaging techniques. Suitable imaging techniques are known in the art (see for example Masuda et al (2007) PNAS 104 1925-1930) and reagents and equipment are available from commercial suppliers (e.g. (Xenogen Corp, MA USA) . Other aspects of the invention relate to the use of a rodent endometriosis model as described above in the screening and identification of compounds which may be useful in treating endometriosis . A method of screening for an agent for use in the treatment of endometriosis may comprise: producing a rodent endometriosis model by a method described above, administering a test compound to the rodent endometriosis model, and determining the effect of said compound on endometriosis in said model. The effect of the compound on the implanted menstruating endometrium may be determined. For example, the size or amount of endometriotic lesions formed by the implanted menstruating endometrium may be determined. In addition, the cellular composition of the lesions can be determined This may be carried out using standard techniques, such as immunohistochemistry or in vivo imaging. A decrease or reduction in the size or number of endometrial lesions in mice treated with the test compound relative to control mice untreated with the test compound is indicative that the test compound is a putative agent which may be useful in the treatment of endometriosis. Test compounds which may be screened using the methods described herein may be natural or synthetic chemical compounds used in drug screening programmes. Extracts of plants, microbes or other organisms which contain several characterised or uncharacterised components may also be used. Combinatorial library technology provides an efficient way of testing a potentially vast number of different compounds for ability to modulate an interaction. Such libraries and their use are known in the art, for all manner of natural products, small molecules and peptides, among others. The use of peptide libraries may be preferred in certain circumstances. The amount of test compound or compound which may be added to a method of the invention will normally be determined by trial and error depending upon the type of compound used. Typically, from about 0.00InM to ImM or more of putative inhibitor compound may be used, for example from 0.0InM to lOOμM, e.g. 0.1 to 50μM, such as about lOμM. Suitable test compounds for screening include small organic molecules, peptides, polypeptides, cells, nucleic acids, and vectors . Suitable polypeptides for screening may include antibodies, antibody derivatives or other specific binding proteins, chemokines, cytokines, growth factors, proteases, protease inhibitors, immune regulators, adhesion molecules. Nucleic acids may include aptamers or sense or anti-sense suppression constructs which reduce or abolish expression of a target gene. Vectors may include plasmid or viral vectors. A vector may comprise a heterologous nucleic acid for expression in the rodent model. A heterologous nucleic acid may encode a polypeptide of interest or mediate the suppression of expression of a gene of interest in the model. A method described herein may comprise identifying a test compound as useful in the treatment of endometriosis. Following identification of a compound using a method described above, the compound may be isolated and/or synthesised. The identified compound may be synthesised using conventional chemical synthesis methodologies. Methods for the development and optimisation of synthetic routes are well known to persons skilled in this field. A compound identified using a method described herein may be assessed or investigated further using one or more secondary screens. For example the toxicology and/or biological effect of the compound may be determined in wild-type non-human animals. Following performance of a method described herein, the donor and or recipient mice may be sacrificed or euthanized. A compound identified using a method described herein may be modified to optimise its pharmaceutical properties. The modified compound may be tested using the methods described herein to see whether it has the target property, or to what extent it is exhibited. Modified compounds include mimetics of the lead compound. Further optimisation or modification can then be carried out to arrive at one or more final compounds for in vivo or clinical testing. The test compound may be used in preparation, i.e. manufacture or formulation, of a composition such as a medicament, pharmaceutical composition or drug. These may be administered to individuals, e.g. for the treatment of a condition described herein. A method may comprise formulating the test compound or the modified test compound in a pharmaceutical composition with a pharmaceutically acceptable excipient, vehicle or carrier. Suitable acceptable excipients, vehicles and carriers are well- known in the art . The term \"pharmaceutically acceptable\" as used herein pertains to compounds, materials, compositions, and/or dosage forms which are, within the scope of sound medical judgement, suitable for use in contact with the tissues of a subject (e.g., human) without excessive toxicity, irritation, allergic response, or other problem or complication, commensurate with a reasonable benefit/risk ratio. Each carrier, excipient, etc. must also be \"acceptable\" in the sense of being compatible with the other ingredients of the formulation. Suitable carriers, excipients, etc. can be found in standard pharmaceutical texts, for example, Remington's Pharmaceutical Sciences, 18th edition, Mack Publishing Company, Easton, Pa., 1990. Other aspects of the invention provide a rodent endometriosis model as described herein. A rodent endometriosis model may comprise: a recipient rodent implanted with menstruating endometrium from a donor rodent, wherein the menstruating endometrium of the donor rodent has an activated oncogenic nucleic acid sequence. A suitable rodent endometriosis model may be obtainable by a method described above. Preferably, a rodent endometriosis models is produced by the methods described above. Menstruating endometrium with an activated oncogenic nucleic acid sequence may be produced from a donor rodent by inducing menstruation in the donor rodent, for example by lowering progesterone levels in the endometrium, and collecting the menstruating endometrium from the donor rodent. The induction of menstruation, collection and implantation of menstruating endometrium from a donor rodent is described in more detail above . The rodent endometriosis model may be useful, for example, in investigating the pathogenesis of endometriosis, identifying target genes or other factors associated with endometriosis and screening for agents useful in the treatment of endometriosis. A method of identifying or screening for a gene involved in endometriosis may comprise; altering the expression of a candidate gene in a rodent endometriosis model as described above; and, determining the effect of said activation on endometriosis in said model. The expression of a candidate gene may be altered in the donor rodent and/or the recipient rodent. In some embodiments, the expression of the candidate gene may be altered in the endometrium of the donor rodent. A gene identified as involved in endometriosis may be a useful therapeutic target for drugs for the treatment of endometriosis. In some embodiments, expression of the candidate gene may be increased, for example by gene activation or overexpression from a recombinant expression vector. In other embodiments, expression of the candidate gene may be decreased or reduced, for example by standard Λ knock out' techniques, or antisense or sense suppression techniques, such as RNAi. In some embodiments, a gene may be inactivated in the donor rodent endometrium by site-specific recombinase-mediated ablation For example, candidate gene suspected of involvement in endometriosis, such as a growth factor, cytokine, protease or other factor, may be inactivated in the donor and/or the recipient rodent and the effect of the inactivation on the development of endometriosis determined relative to controls without the inactivation. The effect on endometriosis may be determined by determining the effect of the alteration in gene expression on the size or amount or cellular composition of endometriotic lesions formed by the implanted menstruating endometrium in the rodent model. This may be carried out, for example, by in vivo imaging or standard immunohistochemical techniques. A change in the size, number or cellular composition of endometrial lesions in mice with altered candidate gene expression relative to control mice with unaltered candidate gene expression is indicative that the gene is involved in endometriosis . A decrease or reduction in the size or number of endometrial lesions in mice with increased candidate gene expression or an increase in the size or number of endometrial lesions in mice with reduced candidate gene expression relative to control mice with unaltered candidate gene expression is indicative that agonists of the candidate gene product may be useful in the treatment of endometriosis. A decrease or reduction in the size or number of endometrial lesions in mice with decreased candidate gene expression or an increase in the size or number of endometrial lesions in mice with increased candidate gene expression, relative to control mice with unaltered candidate gene expression is indicative that antagonists of the product of the candidate gene may be useful in the treatment of endometriosis. A method described herein may comprise identifying a candidate gene as involved in endometriosis. The candidate gene and its product may be characterised further and employed in further research or drug discovery, for example to identify agonists or antagonists of the identified gene product which are useful in the treatment of endometriosis Various further aspects and embodiments of the present invention will be apparent to those skilled in the art in view of the present disclosure. All documents mentioned in this specification are incorporated herein by reference in their entirety. \"and/or\" where used herein is to be taken as specific disclosure of each of the two specified features or components with or without the other. For example \"A and/or B\" is to be taken as specific disclosure of each of (i) A, (ii) B and (iii) A and B, just as if each is set out individually herein. Unless context dictates otherwise, the descriptions and definitions of the features set out above are not limited to any particular aspect or embodiment of the invention and apply equally to all aspects and embodiments which are described. Certain aspects and embodiments of the invention will now be illustrated by way of example and with reference to the figures described above and tables described below. Figure 1 shows haematoxylin/eosin staining of endometriosis lesions collected from murine models. Arrows indicate glandular structure; when using wild type donors, the gland-like structure is disintegrating, however when using K-ras expressed donors, glands are more organized. Vessels are also visible in the K-ras induced lesions, indicated as * signs. Figure 2 shows drug induced Cre-recombinase expression resulted in β-galatosidase gene recombination and expression in murine endometrium. The β-galatosidase positive cells are stained dark. There is tense staining in glandular epithelial cells; however some cells within the stroma area are also stained positively. Figure 3 shows immunohistochemistry results which confirm the presence of glandular epithelial cells and stromal cells. The left panels show positive staining of glandular epithelial cells at different time-points after tissue implantation. The right panels show the staining of stromal cells. Figure 4 shows the staining of blood vessels using an antibody against endothelial cell marker CD31. Figure 5 shows the presence of leukocytes within the lesions using an antibody against leukocyte common antigen CD45 Figure 6 shows collagen and fibrous structure within the lesions using Van Gieson's staining. Figure 7 shows an example of a lesion on the peritoneal surface of a recipient mouse after dissection. The divisions on the ruler are lmm. Lesions were generated in the absence of matrigel, and are sensitive to estadiol ablation through administration of the estrogen receptor antagonist ICI 182,780 (Fulvestrant) . Figure 8 (A) and (B) show endometriotic cysts in induced murine endometriosis. The cells stained dark around the perimeter of the cysts are LacZ positive, indicating ere mediated recombination. Lesions were generated in the absence of matrigel, and are sensitive to estadiol ablation through administration of the estrogen receptor antagonist ICI 182,780 (Fulvestrant) . Figure 9 (A) and (B) show high power images (x400) of glandular structures in murine lesions (H&E stain)_in induced murine endometriosis. Again, lesions were generated in the absence of matrigel, and are sensitive to estadiol ablation through administration of the estrogen receptor antagonist ICI 182,780 (Fulvestrant) . Figure 10 A: shows collagen and fibrous structure within lesions identified using Van Gieson' s staining in human endometriosis. B: shows collagen and fibrous structure within lesions identified using Van Gieson' s stain in induced murine endometriosis. Lesions were generated in the absence of matrigel, and are sensitive to estadiol ablation through administration of the estrogen receptor antagonist ICI 182,780 (Fulvestrant) . In both A and B collagen is visible as elongate fibres, nuclei as darker stained dots and blood cells are stained light gray. Figure 11 shows CD45+ve cells (darker stained) in a murine endometriotic lesion in induced murine endometriosis. Glandular and epithelial cells lining the cyst are also visible. Lesions were generated in the absence of matrigel, and are sensitive to estadiol ablation through administration of the estrogen receptor antagonist ICI 182,780 (Fulvestrant) . Figure 12 shows cytokeratin staining (black) of epithelial cells in the cyst wall of a murine lesion in induced murine endometriosis. Lesions were generated in the absence of matrigel, and are sensitive to estadiol ablation through administration of the estrogen receptor antagonist ICI 182,780 (Fulvestrant) . Figure 13 shows a negative control for immunostaining of a murine endometriotic lesion in induced murine endometriosis using an irrelevant primary antibody. Darker stained regions indicate LacZ +ve cells. This demonstrates that the staining seen in Figure 11 and 12 is specific. Lesions were generated in the absence of, and are sensitive to estadiol ablation through administration of the estrogen receptor antagonist ICI 182,780 (Fulvestrant) . Experiments Materials and Methods Animals All procedures and care of the animals were performed following United Kingdom Home Office regulations. Adult female C57BL/6 mice were purchased (Harlan UK, Oxon, United Kingdom) and K- ras vl2+/~ /AhCre +/+ /ROSA26R-LacZ +/+ transgenic mice were bred on site. All of the mice were maintained in standard housing. The K-ras vl2+/' /AhCre +/+ /ROSA26R-LacZ +/+ transgenic mice allow transient endometrial, (predominantly epithelial), expression of Cre protein, that can mediate recombination of the K-rasV12 transgene and ROSA26R-LacZ reporter gene. K-ras vl2 /AhCre transgenic mice were crossed with Rosa26R mice to generated K- ras vl2+/ -/AhCre +/~ /ROSA26R-LacZ +/~ transgenic mice. We then bred the Fl offspring mice to generate F2 K-ras vl2+/~ /AhCre +/+ /ROSA26R- LacZ +/+ transgenic mice. The presence of the transgenes was determined by genomic PCR using gene specific primers for K-ras, AhCre and Rosa26R-LacZ. Homozygous mice were identified by crossing with wild type mice and genotyping the progeny. Animals were anaesthetized using halothane inhalation (induction dose at 2-4%, followed by maintenance dose at 0.5-2% (Merial Animal health, United Kingdom) during all the surgical procedures. As an analgesic, Temgesic (GenusXpress, 0.03mg per animal) was also administered intra-muscularly in the end of the surgery. Murine Endometriosis Model Female K-ras vl2+/' /AhCre +/+ /ROSA26R-LacZ +/+ transgenic mice were used as donor animals. They were ovariectomised and allowed to recover for at least seven days and then treated sequentially with steroid hormones as previously described [24, 25] . On days 1 and 2, animals were injected subcutaneously with lOOng of 17β- oestradial (E2) dissolved in 0.1ml arachis oil (Sigma, Poole, Dorset, United Kingdom) . There was no hormone treatment on days 3, 4 and 5. On days 6, 7 and 8, IOng of 17β-oestradial and 500ng of progesterone (Sigma), dissolved in 0.1ml arachis oil, were administered subcutaneously. The time of hormone injection on day 8 was set as time point 0, and a laparotomy was performed under general anaesthetic between 4-6 h after time point 0. In order to induce decidualization and also the Cre expression via the Ah promoter, 20μl of 16 mg/kg β-NF (Sigma) dissolved in warm maize oil was injected into each horn of the uterus. Tissue degeneration that mimics menstruation was induced by hormone withdrawal, and the menstruating endometrial tissues were collected from these donor mice at 60 hours after time point 0. Table 1 summarizes the schedule of the hormone treatment and tissue collection. The collected menstruating endometrial tissue was re-suspended in matrigel (BD biosciences, Oxford, United Kingdom) . Adult female C57BL/6 mice were used as recipients. These mice were given a long-lasting estradiol pellet (Innovative Research of America, FL, USA) subcutaneously the day before tissue implantation. Immediately after the endometrial tissue was collected and re-suspended, lOOμl of the menstruating tissue suspension was carefully injected subcutaneously to the abdominal side of the recipient and the incision was sealed with superglue and followed by spray plaster (Boots, London, UK) . Histological Analysis Uterine tissues and endometriosis lesions were collected and stained for LacZ positive cells. After the whole-mount X-gal histochemistry, tissues were post-fixed in either formalin solution (Sigma) for 4 hours or Zinc fixative (BD Biosciences) for 8 hours, then embedded in paraffin wax and 5μm sections cut for routine H&E staining or immunohistochemistry. The following antibodies were used for immunohistochemistry: anti-cytokeratin (epithelial cells, wide spectrum, DAKO, Ely, United Kingdom) ; anti-human-smooth muscle actin (clone 1A4, DAKO); anti-mouse-CD31 (endothelial cells, clone MBC 13.3, BD Biosciences) ; anti-mouse-CD45 (leukocytes, clone 30-F11, BD Biosciences) . A mouse on mouse (M.0. M.) kit (Vector Laboratories, Peterborough, United Kingdom) was used for staining using the monoclonal anti-smooth actin antibody. All the other anti-mouse primary antibodies were detected by a biotin conjugated goat polyclonal antibody against rat IgG (Zymed, San Francisco, CA) . Streptavidin (Vector Laboratories) and DAB (Sigma) were used for secondary antibody detection and final visualization, and the cell nuclei were counter-stained with haematoxylin. Results K-ras promotes the formation of endometriosis lesions The recipient animals were sacrificed at Day 7, 14, 21 and 28 after tissue implantation, and lesions developed around implantation site were collected. All the lesions were visible macroscopically, with a few small vessels nearby appearing to grow into it, providing indication that these lesions might -be viable with blood supply. The size of the lesions varied from 1x3 mm to 6x3mm. No lesions were found elsewhere other than around the implantation site. The same experiments have been carried out using wild type C57B6 mice as donors, however the lesions were not only much smaller but also survive no longer than 14 days. These lesions had much less well organised structure with many dying cells and no glandular structures present (Figure 1) . In contrast, intact glands are visible within the K-ras induced endometriosis-like lesions. Vessels are also found within these lesions, corresponding to the macroscopically observation of blood vessels grown into the lesions. Characterization of K-ras induced endometriosis lesions The recombination of the K~rasV12 transgene and R0SA26R-LacZ reporter gene in the K-rasV12+/-/AhCre+/+/ROSA26R-LacZ+/+ transgenic mice are both mediated by inducible Cre protein regulated by the Ah promoter. Therefore the recombination of ROSA26R-LacZ reporter gene was used as an indicator of Cre activity and K-rasV12 transgene recombination. Whole-mount beta- galactosidase staining was performed to examine the recombination of ROSA26R-LacZ reporter gene, and blue stained epithelial cells were detectable in the lesions although some non-epithelial-like cells were also positively stained. Figure 2 shows an example of uterus section after Cre protein expression is induced. All the endometrial glands are positively stained (shown as dark), and some of the stromal cells are also positively stained. Clinically an endometriotic lesion contains both the stromal and some glandular cells [1, 4] . Therefore endometriosis lesions collected at different time-points were stained for glandular epithelial cells and stromal cells. As shown in Figure 2, both glandular epithelial cells and stromal cells were detectable in all lesions (positive staining shown as dark) . Many of the positive stained glandular epithelial cells were also positively stained with LacZ staining and were surrounded by stroma. The presence of both gland epithelial cells and stroma cells coheres with the definition of endometriosis. To identify the blood supply within the endometriosis lesion, lesions collected at different time-points were immunohistochemical stained for endothelial cells . As shown in Figure 4, endothelial cells were visible in the endometriotic lesions. We observed macroscopically that a few small vessels were visible around the lesion and seemed to be growing into it, and the presence of endothelial cells within the lesions was in concord with our observation. Lesions collected at different time-points were also stained for leukocytes. As shown in figure 5, many leukocytes were found to be present in endometriosis lesions. Fibrous material was found around the endometriotic lesion as is observed in human lesions. The lesions were stained with Van Gieson's stain to identify the fibrous structure and compared with human endometriosis and lesions collected from Nude mice model. As shown in Figure 6, Ras-induced murine endometriosis shows similar collagen deposition when compared with human endometriosis and nude mouse model. In addition to the examples described above, it was found that implantation of the donor material into the recipient mice can be performed without the addition of matrigel. Lesions resulting from implantations in the absence of matrigel are shown in Figures 7 to 9, 1OB and 11 to 13. These figures also illustrate the close similarity of these lesions to human endometriosis lesions. This is particularly evident from Figures 1OA and B which show the collagen and fibrous structure of lesions from the induced murine endometriosis model disclosed herein and those from human endometriosis. Furthermore it was found that lesions can also form in mouse recipients which have intact ovaries and which are not treated with exogenous estradiol. This is advantageous as human endometriosis patients typically have intact ovaries and are not treated with estradiol. In fact, one of the modalities of treatment is to ablate estradiol production and thus reduce lesion growth in humans . It was also shown that treatment of recipient mice using a specific oestrogen receptor antagonist (ICI 182,780, also know as Fulvestrant) markedly reduced lesion growth, irrespective of whether the lesions were generated in the presence or absence of matrigel. The above results indicate that the endometriosis model disclosed herein behaves in a highly similar manner to endometriosis in humans. Table 1 References 1. Rubin, E.et al (2004) The Female Reproductive System- Endometriosis in Rubin's Pathology: Clinicopathologic Foundations of Medicine pp. 981-984, Lippincott Williams & Wilkins, Philadelphia. 2. Giudice, L. C. & Kao, L. C. (2004) Lancet. 364, 1789-99. 3. Grummer, R. (2006) Hum Reprod Update. 12, 641-9. 4. Nap, A. W. et al (2004) Best Practice & Research Clinical Obstetrics & Gynaecology. 18, 233. 5. Halme, J.et al (1984) Obstet Gynecol. 64, 151-4. 6. D'Hooghe, T. M. (1997) Fertility and Sterility. 68, 613. 7. Hastings, J. M. & Fazleabas, A. T. (2003) Semin Reprod Med. 21, 255-62. 8. Fazleabas, A. T. et al (2002) Ann NY Acad Sci. 955, 308- 317. 9. Sharpe-Timms, K. L. (2002) Ann N Y Acad Sci. 955, 318-27; discussion 340-2, 396-406. 10. Uchiide, I. et al. (2002) Fertil Steril. 78, 782-6. 11. Vernon, M. W. & Wilson, E. A. (1985) Fertil Steril. 44, 684-94. 12. Cummings, A. M. & Metcalf, J. L. (1995) Reprod Toxicol. 9, 233-8. 13. Dunselman, G. A. et al (1989) Gynecol Obstet Invest. 27, 29-33. 14. Somigliana, E. et al (1999) Hum Reprod. 14, 2944-50. 15. Dabrosin, C. et al (2002) Am J Pathol. 161, 909-18. 16. Somigliana, E. et al (2001) Fertil Steril. 75, 203-6. 17. Zamah, N. M. et al (1984) Am J Obstet Gynecol. 149, 591-7. 18. Bruner-Tran, K. L. et al. (2002) Ann N Y Acad Sci. 955, 328-39; discussion 340-2, 396-406. 19. Bergqvist, A. et al (1985) Am J Pathol. 121, 337-41. 20. Nisolle, M. et al (2000), Fertil Steril. 74, 306-12. 21. Aoki, D. et al (1994) Obstet Gynecol. 83, 220-8. 22. Awwad, J. T. et al (1999) Hum Reprod. 14, 3107-11. 23. Grummer, R. et al (2001) Hum Reprod. 16, 1736-43. 24. Finn, C. A. & Pope, M. (1984) J Endocrinol. 100, 295-300. 25. Cheng, C. W. et al (2007) Biol Reprod. 76 871-883 26. Dinulescu, D. M. et al. (2005) Nat Med. 11, 63-70. 27. Amemiya, S. et al (2004) Int J Gynaecol Obstet. 86, 371-6. 28. Otsuka, J. et al (2004) Med Electron Microsc. 31, 188-92. 29. Sekizawa, A. et al (2004) Med Electron Microsc. 37, 97-100. 30. Vigano, P. et al (2006) Hum Reprod Update. 12, 77-89. 31. Gryfe, R. et al (1997) Curr Probl Cancer. 21, 233-300. 32. Okudela, K. et al (2004) Am J Pathol. 164, 91-100. 33. Tammela, J. & Odunsi, K. (2004) Minerva Ginecol. 56, 495- 502. 34. Varras, M. N. et al (1999) Oncology. 56, 89-96. 35. Berkkanoglu, M. et al (2003) Am J Reprod Immunol. 50, 48- 59. 36. Braun, D. P. et al (1998) Curr Opin Obstet Gynecol. 10, 365-9. 37. Lebovic, D. I. et al (2001) Fertil Steril. 75, 1-10. 38. Matarese, G. et al (2003) Trends MoI Med. 9, 223-8. 39. Sidell, N. et al (2002) Ann N Y Acad Sci. 955, 159-73; discussion 199-200, 396-406. 40. Wu, M. Y. & Ho, H. N. 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