Title of Invention: ESTROGEN AND ANTI-ESTROGEN MARKER GENES Abstract: The invention relates to a method for screening compounds with estrogenic or anti-estrogenic activity by providing a cellular system of a sample thereof being capable of expressing at least a single gene of Table 1, incubating at least a portion of the system with compounds to be screened, and comparing an expression of the single gene of Table 1 in the system with the gene expression in a control cellular system. Another object of the invention concerns a method for monitoring physiological and/or pathological conditions, which are caused, mediated and/or propagated by estrogen receptor signaling, by administering an effective amount of at least a single compound to a mammal in need of such treatment and determining an expression of the single gene of Table 1 in a biological sample withdrawn from the mammal. The invention also relates to the use of the genes of Table 1 as well as substances specifically interacting with gene products encoded by the genes of Table 1. Detailed Description: The invention relates to a method for screening compounds with estrogenic or anti-estrogenic activity by providing a cellular system of a sample thereof being capable of expressing at least a single gene of Table 1, incubating at least a portion of the system with compounds to be screened, and comparing an expression of the single gene of Table 1 in the system with the gene expression in a control cellular system. Another object of the invention concerns a method for monitoring physiological and/or pathological conditions, which are caused, mediated and/or propagated by estrogen receptor signaling, by administering an effective amount of at least a single compound to a mammal in need of such treatment and determining an expression of the single gene of Table 1 in a biological sample withdrawn from the mammal. The invention also relates to the use of the genes of Table 1 as well as substances specifically interacting with gene products encoded by the genes of Table 1. An endocrine active compound (EAC) is an exogenous agent of anthropogenous and natural origin that can interfere with or mimic the physiologic function of endogenous hormones by altering hormone synthesis, secretion, transport, binding, action or elimination. EACs may either cause a variety of adverse health effects, which are related to development, reproduction, nervous and immune systems in human and wildlife populations, or have beneficial effects on estrogen-dependent diseases, warranting a thorough analysis regarding their mode of action. Arising from different chemical classes with differing structures, it is not surprising that EAC effects on the endocrine system are mediated by a variety of mechanisms. A major mechanism involves steroid hormone receptors that belong to the nuclear receptor superfamily and regulate gene transcription. Estrogen receptor ERα and ERβ are well-described targets of estrogenic chemicals, including many everyday life products such as pharmaceuticals, pesticides or food ingredients. Although all compounds share a similarity to mediate ER-dependent gene transcription, in the public mind, phytoestrogens, a large family of naturally occurring plant-derived compounds, are mostly considered as beneficial, whereas synthetic EACs are associated with harmful effects. However, scientific investigations do not support this generalized view. Experimental outcomes are dependent on multiple factors, such as the treatment concentration, used species, tissue or cell type, and the intrinsic estrogen status. Only a deeper understanding of mechanisms underlying the biological effects can help to understand this controversy and support the assessment of relevance for humans and the environment. Consequently, endocrine disruption has become an important issue, as many environmental compounds of differing provenance and chemical class may induce hormonal imbalances in many species by binding to the estrogen receptors and stimulating or inhibiting estrogen responsive genes. This may be followed by changing expression levels of many other genes, controlling several essential cellular processes. However, rapid non-genomic effects involving the steroid-induced modulation of mitogen-activated protein kinase, phosphatidylinositol 3-OH kinase, GPCR and growth factor signaling cascades can also cause alterations in the transcriptome. Thus knowledge about variations in global gene expression is more important for reliable evaluation of estrogenicity than investigating initial binding events to the ER. Many of the putative marker genes for estrogenicity found for DES were regulated to a lesser extent by Genistein (GEN), Zearalenone (ZEA), Bisphenol A (BPA), o,p′-Dichlordiphenyltrichlorethane (DDT) and Resveratrol (RESV), which confirms the lower estrogenic potencies reported for these compounds (Mueller et al. 2004 Toxicol Sci 80(1): 14-25). Such lower potencies complicate risk assessment and extrapolation of low dose effects from animal studies to humans, indicating the need of a more sensitive experimental system for the evaluation of estrogenicity and estimation of dose-response-relationships. In particular, results for BPA and DDT give cause for thought, because even at doses 50 to 100 times higher than GEN and ZEA, the marker gene regulations were often weaker than for the phytoestrogens. The importance for new screening tools is also illustrated by REACH (Registration, Evaluation, Authorization and Restriction of Chemicals), the new European Community regulation on chemicals (European Commission 2007). In accordance with REACH, around 30,000 existing chemicals have to be tested and endocrine disruption is one essential issue within the REACH testing program. However, enormous costs and animal welfare issues make it difficult to fulfill REACH requirements using existing, traditional toxicological assays. It has been recently suggested in US 2003/0008309 A1 that the effects of environmental hormones can be detected by evaluating chemical substances having estrogen-like activity. DNA fragments containing portions or wholes of genes and/or ESTs (Expressed Sequence Tags) whose expression is affected by chemical substances having estrogen-like activity are immobilized on the basal plate of the microarray. However, prior art is mainly restricted to expression level changes in the breast cancer-derived MCF-7 cell and lacks the compilation of distinct expression profiles. U.S. Pat. No. 7,371,207 B2 teaches a plurality of genes, each of whom is differentially expressed in kidney cells exposed to estrogen and/or other hormones or combination of hormones and kidney cells without said exposure, which plurality comprises a first group and a second group, wherein each gene in said first group is differentially expressed at a higher level in said kidney cells exposed to estrogen and/or other hormones or combination of hormones than in said kidney cells without said exposure, and wherein each gene in said second group is differentially expressed at a lower level in said kidney cells exposed to estrogen and/or other hormones or combination of hormones than in said kidney cells without said exposure. However, the genes are limited such that said first group comprises the full-length genes NTT73, CYP7B 1 and ABCC3, and said second group comprises the full-length genes BHMT and SAHH, which reduces screening stability, but enhances error rates. Therefore, the technical problem forming the basis of the present invention is to provide a method for screening compounds, which effectively allows the identification and characterization of their estrogenic or anti-estrogenic properties. It is another problem of the invention to provide substances for the detection of estrogenic or anti-estrogenic activity, which makes a simple and fast monitoring of estrogen-dependent diseases possible. The present invention solves the problem by providing a method for screening compounds with estrogenic or anti-estrogenic activity comprising the steps of: (a) providing a cellular system or a sample thereof being capable of expressing at least one gene of Table 1, wherein the system is selected from the group of single cells, cell cultures, tissues, organs and mammals, (b) incubating at least a portion of the system with compounds to be screened, and (c) detecting the activity by comparing an expression of the at least one gene of Table 1 in the system with the gene expression in a control cellular system. It has been surprisingly demonstrated by the inventors that the aforementioned group of 72 genes is correlated with estrogenicity. Consequently, the aforementioned plurality of marker genes represent novel estrogen/estrogen receptor target genes, which themselves and their gene products, respectively, are well suited targets for differentiating the stage of estrogenicity. The underlying genes are selected as result of a differential expression analysis. The identified genes are not inevitably associated by function or location in their entity as presently known, but it is not excluded that such relations appear between a single member or more members of the group. Instead of that, all genes are characterized by a distinct difference to EAC-untreated cells, which is exhibited by either up-regulation or repression. The genes are already described in the state of the art by sequence and other features, but lacking a linkage to estrogenicity. The similar gene regulation reflects the ability of EACs to exert estrogen-like growth stimulatory activity through the up-regulation of proliferation promoting genes and down-regulation of negative proliferation regulators and apoptosis inducing genes. The aforementioned genes may be named in another way, but are easily assigned by the accession number, which is generally accepted and fixed in numerous data bases, such as the GenBank, SwissProt and the like. The linkage of estrogenicity to distinct genes is utilized for the in-vitro detection of endocrine active compounds, which are able to interfere with estrogen receptor signaling, and anti-estrogenic compounds. Building a compound specific gene expression profile, which is based on the plurality of genes according to Table 1, is of unexpected benefit in establishing an estrogenic or anti-estrogenic mechanism of action and, therefore, supports the evaluation of potential hazards or benefits of novel compounds supplementary to the classical screening methods. Either a single marker gene or more than a single marker can be used for the utmost test reliability. That means the inventive principle underlying the present method comprises prospecting for a gene product that can be either detected on the genetic level or on the protein level, wherein the genetic level is preferred. The gene product is chosen in respect of both its absolute and relative amount as well as the specificity for a certain cell type. In general, “a gene” is a region on the genome that is capable of being transcribed to RNA that either has a regulatory function, a catalytic function and/or encodes a protein. A gene typically has introns and exons, which may organize to produce different RNA splice variants that encode alternative versions of a mature protein. “Gene” contemplates fragments of genes that may or may not represent a functional domain. A “plurality of genes” as used herein refers to a group of identified or isolated genes whose levels of expression vary in different tissues, cells or under different conditions or biological states. The different conditions may be caused by exposure to certain agent(s)—whether exogenous or endogenous—which include hormones, receptor ligands, chemical compounds and the like. The expression of a plurality of genes demonstrates certain patterns. That is, each gene in the plurality is expressed differently in different conditions or with or without exposure to a certain endogenous or exogenous agents. The extent or level of differential expression of each gene may vary in the plurality and may be determined qualitatively and/or quantitatively according to this invention. A gene expression profile, as used herein, refers to a plurality of genes that are differentially expressed at different levels, which constitutes a “pattern” or a “profile.” As used herein, the term “expression profile”, “profile”, “expression pattern”, “pattern”, “gene expression profile” and “gene expression pattern” are used interchangeably. The term “gene product” denotes molecules that are formed from the substrate of said genes by biochemical, chemical or physical reactions, such as DNA synthesis, transcription, splicing, translation, fragmentation or methylation. Preferred gene products of the invention are RNA, particularly mRNA and cRNA, cDNA and proteins. As used herein, a “compound with estrogenic activity” is an agent that exerts at least some of the biological effects of estrogen, which refers to any factor, agent, compound whether endogenous or exogenous in origin, which is capable of binding and interacting with estrogen receptors and thereby eliciting certain biological effects of estrogen. The skilled artisan would know that, for instance, one of the biological effects of estrogen is to promote the development of the female reproductive system. Other biological effects of estrogen are well documented and discussed. For instance, estrogen is thought to affect tissues such as brain, liver, muscle, bone cells and stomach, which express the estrogen receptor gene. In the meaning of the invention, a “compound with anti-estrogenic activity” comprises such compounds that are able to reverse the estrogenic effects as described above. “Estrogen” is a general term for hormones that are steroidal chemical substances secreted from ovarian follicles, placenta, and such and that induce the development of female reproductive organs such as follicles and mammary glands or other organs. In the first step (a), a cellular system is provided. The cellular system is defined to be any subject provided that the subject comprises cells. Hence, the cellular system can be selected from the group of single cells, cell cultures, tissues, organs and mammals. The mammal is preferably a laboratory animal and/or a non-human organism. The scope of the cellular system also comprises parts of such biological entities, i.e. samples of tissues, organs and mammals. It shall be understood that each cellular system in the aforementioned order represents a sample of the respective following system. Particularly, the cellular sample is taken in-vivo or in-situ from a mammal to be tested. The withdrawal of the cellular sample follows good medical practice. Biological samples may be taken from any kind of biological species, but the sample is especially taken from a human, rat or a mouse, more preferably a human. Such mammal should produce little or no estrogen if screening compounds with estrogenic activity. For instance, an aromatase knockout animal cannot produce estrogen. Because the major source of circulating estrogen is the ovary, ovariectomy dramatically decreases circulating estrogen levels. Thus, in one embodiment, ovariectomized animals are used. Contrary to that, an estrogen-stimulated cellular system is provided if screening compounds with anti-estrogenic activity. In the present invention, the cellular system may also comprise a biological fluid, wherein the sample of body fluid preferably consists of blood, serum, plasma, saliva or urine. It is also preferred to gather a tissue sample by biopsy, especially taken close to the location of ailment. The biological samples can be originated from any tissue, including the uterus, pituitary gland, liver, brain, colon, breast, adipose tissue, etc. In preferred embodiments, the biological samples are from the kidney, pituitary gland and the uterus. The sample may be purified to remove disturbing substances, such as inhibitors for the formation of hydrogen bonds. The cell sample refers to any type of primary cells or genetically engineered cells, either in the isolated status, in culture or as cell line, provided that they are capable of expressing at least one gene of Table 1. It shall be understood that variants, mutants, parts or homologous gene sequences having the same function, are included in the scope of definition as well as protection. The degree of alteration between the original sequence and its derivatives is inevitably limited by the requirement of altered gene expression by EACs. Preferably, the homology amounts to at least 85%. Possible alterations comprise deletion, insertion, substitution, modification and addition of at least one nucleotide, or the fusion with another nucleic acid. The engineered cells are capable of expressing these genes by transfection with appropriate vectors harboring them or parts thereof. Preferably, the recombinant cells are of eukaryotic origin. In a more preferred embodiment of the present invention, the human Ishikawa cell line is provided in step (a) of the screening method. Ishikawa cells are human endometrial cancers cells of uterus origin. The cell sample is stored, such as frozen, cultivated for a certain period or immediately subjected to step (b). Before incubating it with compounds to be screened, the cell sample is divided into multiple portions. At least two portions are provided; one is used for screening while the other one serves as control. Preferably, the number of portions for screening exceeds the number of control portions. Usually, numerous portions are subjected to a high-throughput screening. The compounds are composed of biological and/or chemical structures capable to interact with a target molecule. Herein, any component of estrogen signaling shall be considered as “target molecule”, which is not limited to the estrogen receptor target, but may also comprise the selected genes themselves, or a regulator protein or a gene product thereof, or a component of a signal transduction pathway comprising said gene or gene products thereof. Consequently, the specific interaction of compounds may involve either the mere targeting or the induction of alterations in cell function, or it may even include both effects simultaneously. The compounds to be screened in the inventive method are not restricted anyway. In particular, the compounds are selected from the group of nucleic acids, peptides, carbohydrates, polymers, small molecules having a molecular weight between 50 and 1.000 Da and proteins. These compounds are often available in libraries. It is preferred to incubate a single compound within a distinct portion of the cell sample. However, it is also possible to investigate the cooperative effect of compounds by incubating at least two compounds within one portion. A further portion of cells is simultaneously incubated in the absence of the compounds. The term “incubation” denotes the contacting of the compounds with the cells for a distinct period, which depends on the kind of compounds and/or target. The incubation process also depends on various other parameters, e.g. the cell type and the sensitivity of detection, which optimization follows routine procedures known to those skilled in the art. The incubation procedure can be realized without a chemical conversion or may involve a biochemical reaction. Adding chemical solutions and/or applying physical procedures, e.g. impact of heat, can improve the accessibility of the target structures in the sample. Specific incubation products are formed as result of the incubation. In step (c), the identification of effective compounds in the meaning of the invention is indirectly performed by determining the expression pattern of at least a single gene of Table 1, which the system is capable of expressing. The determination is performed at a specified moment and correlated to the signal strength at the beginning of the experiment and the positive/negative control. Either the control system is not incubated with the compounds (negative control) or the control system is incubated with a standard compound having no estrogenic/anti-estrogenic activity (negative control) or a standard compound having estrogenic/anti-estrogenic activity (positive control) as set forth at the example of microarray below The activity is revealed by a change in expression. Preferably, the genes expressed or repressed in cells with EAC exposure are compared to the genes expressed or repressed in cells that were not exposed to EAC. Pairwise comparisons are made between each of the treatments. A pairwise comparison is the expression data for a given gene under a given treatment condition compared to the expression data for this gene under a second treatment condition. The comparison is performed using suitable statistical technique with the assistance of known and commercially available programs. Suitable tests for monitoring gene expression, determination and variant analysis of nucleotide sequences are known to those skilled in the art or can be easily designed as a matter of routine. The assay according to the invention may be any assay suitable to detect and/or quantify gene expression. Many different types of assays are known, examples of which are set forth below, including analyses by nucleotide arrays and nucleotide filters. The hybridization conditions (temperature, time, and concentrations) are adjusted according to procedures also well known in the art. It is preferred to apply chip hybridization and/or PCR for the determination of gene expression. In another preferred embodiment, the assay of the invention involves the use of a high density oligonucleotide array. In still another preferred embodiment, the analysis is performed by multiplex qPCR, more preferably low density TaqMan arrays or branched DNA assays. Other solid supports and microarrays are known and commercially available to the skilled artisan. Consequently, this invention relates to a method for predicting the cellular effect of a compound having estrogen-like activity by preparing a nucleic acid sample from a cell to be evaluated, contacting the nucleic acid sample with an microarray, detecting a nucleic acid hybridizing with the microarray, and comparing a result detected in step (c) with a result detected using a nucleic acid sample prepared from a control cell. In a preferred embodiment of the present invention, the gene products RNA, cRNA, cDNA and/or protein are detected, more preferably mRNA, cRNA and/or cDNA. For instance, the total RNA from such cells is prepared by methods known to the skilled artisan such as by Trizol (Invitrogen) followed by subsequent re-purification, e.g. via Rneasy columns (Qiagen). The total RNA is used to generate a labeled target according to methods and using detectable labels well-know in the art. For instance, the RNA may be labeled with biotin to form a cRNA target for use in an assay. Next, with the extracted mRNA as a template, cDNAs are produced using a reverse transcriptase (for example, SuperScript Reverse Transcriptase; GibcoBRL) and labeled dNTP (for example, Cy3-dUTP and Cy5-dUTP; Amersham Pharmacia Biotech), and a cDNA sample that reflects the amount of genes expressed within the cells to be evaluated is prepared. This causes labeled cDNA to be included in the cDNA sample. Here, either fluorescent label or radiolabel may be used as a label. The cDNA sample prepared in this manner is applied to the below-mentioned microarray in its single stranded denatured form, and cDNAs included in the cDNA sample are hybridized with the genes immobilized on the basal plate. “In-situ hybridization” is a methodology for determining the presence of or the copy number of a gene in a sample, for example, fluorescence in-situ hybridization (FISH). Generally, in-situ hybridization comprises the following major steps: (1) fixation of tissue or biological structure to be analyzed; (2) pre-hybridization treatment of the biological structure to increase accessibility of target nucleic acid, and to reduce non-specific binding; (3) hybridization of the mixture of nucleic acids to the nucleic acid in the biological structure or tissue; (4) post-hybridization washes to remove nucleic acid fragments not bound in the hybridization; and (5) detection of the hybridized nucleic acid fragments. The probes used in such applications are typically labeled, for example, with radioisotopes or fluorescent reporters. Preferred probes are sufficiently long, for example, from about 50, 100 or 200 nucleotides (nt) to about 1000 or more nucleotides, to enable specific hybridization with the target nucleic acid(s) under stringent conditions. Here, hybridization with cDNA can be accomplished, for example, by incubating at 65° C. for 10 to 20 hours. As used herein, the term “microarray” refers to nucleotide arrays that can be used to detect biomolecules, for instance to measure gene expression. “Array”, “slide” and “(DNA) chip” are used interchangeably in this disclosure. A microarray usually comprises a basal plate, e.g. made of slide glass, silicone, or the like, and DNA fragments immobilized as an array on this basal plate. With this microarray, DNAs contained in a sample can be detected by hybridizing them with the DNA fragments immobilized on the basal plate. Since the DNA within the sample is radiolabeled or fluorescently labeled, detection with radio imaging scanner, fluorescence imaging scanner, or the like is possible. Various kinds of arrays are made in research and manufacturing facilities worldwide, some of which are available commercially. There are, for example, two main kinds of nucleotide arrays that differ in the manner in which the nucleic acid materials are placed onto the array substrate: spotted arrays and in-situ synthesized arrays. One of the most widely used oligonucleotide arrays is GeneChip made by Affymetrix, Inc. The oligonucleotide probes have a length of 10 to 50 nucleotides (nt), preferably 15 to 30 nt, more preferably 20 to 25 nt. They are synthesized in-silico on the array substrate. These arrays tend to achieve high densities, e.g. more than 40,000 genes per cm2. The spotted arrays, on the other hand, tend to have lower densities, but the probes, typically partial cDNA molecules, usually are much longer than 25 nucleotides. A representative type of spotted cDNA array is LifeArray made by Incyte Genomics. Pre-synthesized and amplified cDNA sequences are attached to the substrate of these kinds of arrays. In one embodiment, the array is a matrix, in which each position represents a discrete binding site for a product encoded by a gene, e.g. a protein or RNA, and in which binding sites are present for products of most or almost all of the genes according to Table 1 and optionally Table 4. In one embodiment, the “binding site” (hereinafter “site”) is a nucleic acid or nucleic acid analogue to which a particular cognate cDNA can specifically hybridize. The nucleic acid or analogue of the binding site can be, e.g. a synthetic oligomer, a full-length cDNA, a less-than full length cDNA or a gene fragment. Preferably, the microarray has binding sites for genes relevant to the action of the gene expression modulating agent of interest or in a biological pathway of interest. It is preferably that more than one DNA fragment, which is capable of hybridizing under stringent conditions to a gene or parts thereof as selected from the group of genes according to Table 1 and optionally Table 4, is immobilized on the basal plate. The DNA fragment to be immobilized on the basal plate may contain the whole or a part of the genes. The term “parts of a gene” used herein means a portion of the gene and a nucleotide sequence equivalent to at least 10 nt, preferably at least 25 nt, more preferably 50 nt, most preferably 300 nt, highly preferably 500 nt. It is additionally preferable that genes constitutively expressing regardless of the presence or absence of chemical substances having estrogen-like activity (hereinafter referred to as negative control genes and the like) are immobilized on the basal plates of the microarray. The expression level of the genes according to the invention can be corrected by immobilizing negative control genes on the basal plate and correcting the expression level of the negative control genes to a constant value. Thus, the changes in the expression level of genes according to Table 1 and optionally Table 4 can be detected with certainty. Accuracy can be further enhanced by choosing several negative control genes and/or such that have different expression levels. The nucleic acid or analogue are attached to a solid support or basal plate, which terms are used interchangeably herein, and which may be made from glass, plastic (e.g. polypropylene or nylon), polyacrylamide, nitrocellulose or other materials. When the DNA fragments and negative control genes are immobilized on the basal plate, a conventionally known technique can be used. For example, the surface of the basal plate can be treated with polycations such as polylysines to electrostatically bind the DNA fragments through their charges on the surface of the basal plate. Furthermore, techniques to covalently bind the 5′-end of the DNA fragments to the basal plate may be used. Alternatively, a basal plate having linkers on its surface can be produced, and functional groups that can form covalent bonds with the linkers are introduced at the end of the DNA fragments. The DNA fragments are immobilized by forming a covalent bond between the linker and the functional group. A preferred method for attaching the nucleic acids to a surface is by printing on glass plates. Finally, cDNAs that hybridized with the DNA fragments on the microarray are detected. In cases where the hybridized cDNAs are fluorescently labeled, the fluorescence is detected with, for example, a fluorescence laser microscope and a CCD camera, and the fluorescence intensity is analyzed with a computer. Similarly, in cases where the hybridized cDNAs are radiolabeled, detection can be carried out using an RI image scanner and such, and the intensity of the radiation can be analyzed with a computer. In another embodiment of the screening method, the detection of estrogenic or anti-estrogenic activity can be additionally refined in step (c). For this purpose, the gene expression is determined by detecting at least one gene product encoded by the gene(s) of Table 1 and correlating an amount of signal or change in signal with the gene expression in the system. The cellular system of the invention is incubated with various concentrations of an identified endocrine active compound. The amount of emitted signal or change in signal observed in the presence of the EAC is indicative of the change in gene expression experienced by the compound. The change can be then related to the concentration of the EAC in the sample, i.e. the calibration curve enables the meter-reading of a matching concentration. Preferably, the calibration curve is based on the Lambert-Beer equation if using UV/VIS coloring or luminescence. Estrogenicity of compounds is diagnosed by comparing the concentration of the gene product in the sample with known gene product concentration levels of either non-estrogenic cells and/or estrogenic cells. It shall be understood that the known concentrations are statistically proven, therefore representing a certain level or range, respectively. The direction and strength of gene expression have also been figured out by the differential expression analysis of the target genes of the invention such that either a distinct up-regulation or down-regulation with a certain factor has been recognized as set forth below, which forms the basis of biomarker selection. Any measured concentration, which differs from the gene product concentration level of EAC-unstimulated cells, indicates an abnormality of the tested cell sample, whereas a compound cannot be classified as EAC at a gene product concentration which is comparable to the concentration level of EAC-unstimulated cells. It is preferred to measure concentration, which are higher than the gene product concentration level of unstimulated cells, for detecting estrogenicity. Using this method, the inventors demonstrated sensitivity to submicromolar or even nanomolar concentrations. The calibration plot reveals that the method can be applied in a dynamic range that spans over a couple of magnitude. According to a preferred embodiment of the invention, the “Polymerase Chain Reaction” or “PCR” is an amplification-based assay used to measure the copy number of the gene. In such assays, the corresponding nucleic acid sequences act as a template in an amplification reaction. In a quantitative amplification, the amount of amplification product will be proportional to the amount of template in the original sample. Comparison to appropriate controls provides a measure of the copy number of the gene, corresponding to the specific probe used, according to the principle discussed above. Detailed protocols for real-time quantitative PCR are provided, for example, for RNA. The “level of mRNA” in a biological sample refers to the amount of mRNA transcribed from a given gene that is present in a cell or a biological sample. One aspect of the biological state of a biological sample (e.g. a cell or cell culture) usefully measured in the present invention is its transcriptional state. The transcriptional state of a biological sample includes the identities and abundances of the constituent RNA species, especially mRNAs, in the cell under a given set of conditions. Preferably, a substantial fraction of all constituent RNA species in the biological sample are measured, but at least a sufficient fraction is measured to characterize the action of a compound of interest. The primers are designed based on the nucleotide sequence information of the region flanking the site to be amplified. The primers may be designed so as to amplify a region of 100 to 200 base pairs in length. The nucleic acid amplification method includes, but is not particularly limited to, a PCR, preferably a real-time PCR. The level of mRNA may also be quantified by other methods described herein. After performing an amplification reaction of a nucleic acid using the biological sample to be analyzed and primers as described above, it is checked whether the nucleic acid is amplified or not. In order to facilitate the detection of an amplified nucleic acid, a primer may be labeled in advance. Examples of applicable fluorescent labels include FAM™, TET™, HEX™, TAMRA™ and ROX™ manufactured by Applied Biosystems. In these cases, either the 5′-end or the 3′-end of a primer may be labeled, preferably the 5′-end. Alternatively, the nucleic acid may be labeled during PCR by using labeled nucleotides, or even after PCR is completed. Light emission is measured by a general-purpose luminescence determination device. Methods of “real-time quantitative PCR” using TaqMan probes are also well-known in the art. Hence, a TaqMan-based assay can be applied to quantify polynucleotides. TaqMan based assays use a fluorogenic oligonucleotide probe that contains a 5′-fluorescent dye and a 3′-quenching agent. The probe hybridizes to a PCR product, but cannot itself be extended due to a blocking agent at the 3′-end. When the PCR product is amplified in subsequent cycles, the 5′-nuclease activity of the polymerase, for example, AmpliTaq, results in the cleavage of the TaqMan probe. This cleavage separates the 5′-fluorescent dye and the 3′-quenching agent, thereby resulting in an increase in fluorescence as a function of amplification. Other suitable amplification methods include, but are not limited to, ligase chain reaction (LCR), transcription amplification, self-sustained sequence replication, dot PCR and linker adapter PCR. When mass spectroscopy is used, primers may be designed so as to allow the amplification of nucleic acid fragments having a length that varies with the expression pattern. The presence or absence of an amplified nucleic acid fragment can also be checked by subjecting a reaction solution to electrophoresis, such as for single-strand conformation polymorphism (SSCP) analysis, which may be performed by capillary electrophoresis. However, other electrophoresis methods, for instance gel electrophoresis, are also applicable and well known to those skilled in the art. Therefore, the present invention relates to the assessment or measurement of modulations of gene expression by the assays as set forth above. Such modulation refers to the induction or inhibition of expression of a gene. Typically, modulation of gene expression may be caused by endogenous or exogenous factors or agents. The effect of a given compound can be measured by any means known to those skilled in the art. For example, expression levels may be measured by PCR, Northern blotting, Primer Extension, Differential Display techniques, etc. The induction of expression (i.e. up-regulation) refers to any observable or measurable increase in the levels of expression of a particular gene, either qualitatively or quantitatively. Contrary to that, the inhibition of expression (i.e. down-regulation) refers to any observable or measurable decrease in the levels of expression of a particular gene, either qualitatively or quantitatively. The measurement of levels of expression may be carried out using any techniques that are capable of measuring RNA transcripts in a biological sample. Examples of these techniques include, as discussed above, PCR, TaqMan, Primer Extension, Differential display and nucleotide arrays, among other things. It is another embodiment of the present invention that in the case of modulation the gene product concentration either exceeds or under-run, respectively, at least twice the gene product concentration in the control system, preferably at least 10 times, more preferably at least 25 times, most preferably at least 40 times In a preferred embodiment of the invention, the estrogenic activity of a compound is positively detected in step (c) if the expression involves an up-regulation of genes selected from the group of genes according to Table 2 and/or a down-regulation of genes selected from the group of genes according to Table 3. The term “positive detection” denotes to the fact that the respective activity is actually proven as inherent feature of a certain compound. Several novel genes, not characterized in conjunction with estrogen receptor activity, but involved in positive regulation of cell growth and development, were identified as being markedly up-regulated by estrogenic compounds (Table 2) but inhibited by ICI. PIM1, a proto-oncogene having intrinsic serine-threonine kinase activity, can enhance cell cycle progression by altering the activity of several cell cycle regulators including p21 (Waf), Cdc25A and C-TAK1. G0/G1 switch 2 (G0S2) was found to be involved in adipocyte differentiation and drives cell cycle progression in blood mononuclear cells. Aminopeptidase N (ANPEP) and the structural molecule Laminin beta 3 (LAMB3) play an important role in cell migration during tumor invasion and tissue remodeling. Amino acid transporters, for example L-type amino acid transporter LAT1 (SCL7A5) and its subunit 42F heavy chain 42F hc (SCL3A2), function in supplying essential amino acids to cells which are required for protein synthesis and as energy sources. High expression of both of these genes was found in tumor cells and promoted tumor growth progression. Furthermore, SLC3A2 can specifically associate with beta 1 integrins on the surface of human tumor cells and therefore contributes to malignant transformation, by allowing anchorage and serum-independent-growth. Among marker genes which were down-regulated in response to estrogenic chemicals (Table 3), most were found to be related to cell growth inhibition (spermidine/spermine N1-acetyltransferase, SAT, and retinol binding protein 1 cellular, RBP1) and apoptosis induction (proline dehydrogenase oxidase 1, PRODH and tumor necrosis factor receptor superfamily member 25, TNFRSF25). Contrary to that, the anti-estrogenic activity of a compound is positively detected in step (c) if the expression involves a down-regulation of genes of Table 2 and/or an up-regulation of genes of Table 3. Although each biomarker gene of the invention exhibits a sensitivity that allows the use of a single marker gene in the scope of the screening method, it is preferred to apply more than one marker gene for detecting estrogenicity. In an embodiment of the invention, the cellular system provided in step (a) is therefore capable of expressing at least two genes of Table 1, preferably at least 10 genes, more preferably at least 25 genes, most preferably at least 40 genes, highly preferably the entire panel of 72 genes. Accordingly, the expression of at least two genes of Table 1 is compared with the gene expression in the control system in step (c), preferably at least 10 genes, more preferably at least 25 genes, most preferably at least 40 genes, highly preferably the entire panel of 72 genes. The inventors have illustrated that analyzing multiple estrogen-responsive genes increases screening stability and reduces error rates by covering a broader spectrum of estrogenic responses than single-gene reporter assays. The prior teaching concerning multiple genes is valid and applicable without restrictions to the Tables 2 and 3, which represents subsets of Table 1, provided that the respective preferred plurality of genes is re-calculated by the rule of three. In addition to the expression of genes, which are selected from the group according to Table 1, the cellular system or the sample thereof is preferably capable of expressing at least a single gene of Table 4 in step (a) of the inventive screening method. Furthermore, in step (c) the expression of the single gene of Table 4 is compared with the gene expression in the control system. Several estrogen/estrogen receptor-regulated genes were identified, such as alkaline phosphatase placental-like 2 (ALPPL2), progesterone receptor (PGR), seven in absentia homolog 2 (Drosophila) (SIAH2), transforming growth factor alpha (TGFA) and genes modulating estrogen receptor activity, such as nuclear receptor interacting protein 1 (NRIP1). Moreover, a pathway of note, WNT/β-catenin signaling, was up-regulated by most estrogenic compound treatments but not after ICI treatment. WNT/β-catenin signaling is involved in a variety of developmental processes including regulation of cell growth and differentiation. WNT2B encodes a member of the wingless-type MMTV integration site family of highly conserved, secreted signaling molecules. Up-regulation of WNT2B by estrogen might play an important role in human breast cancer. The HMG box transcription factor, SOX17, can interact with β-catenin and potentiates the transcriptional activation of target genes similar to Tcf/Lef. Four and a half LIM domains 2 (FHL2) protein exerts co-activator properties enhancing β-catenin/TCF-mediated transcription and was found to be over-expressed in ovarian cancer. In a preferred embodiment of the invention, the estrogenic activity of a compound is positively detected in step (c) if the expression involves an up-regulation of genes selected from the group of genes according to Table 5 and/or a down-regulation of genes selected from the group of genes according to Table 6. Contrary to that, the anti-estrogenic activity of a compound is positively detected in step (c) if the expression involves a down-regulation of genes of Table 5 and/or an up-regulation of genes of Table 6. In another preferred embodiment of the invention, multiple genes of Table 4 are applied in both steps (a) and (c), more preferably at least 2 genes, most preferably at least 10 genes, highly preferably the entire panel of 15 genes. Once more, the prior teaching concerning multiple genes is valid and applicable without restrictions to the Tables 5 and 6, which represents subsets of Table 4, provided that the respective preferred plurality of genes is re-calculated by the rule of three. In a more preferred embodiment of the invention, the expression of the selected estrogenic marker genes ALPP2, CEBPD, FOXD1, GOS2, NRIP1, PGR and PIM1 is compared with the gene expression in the control system. In a most preferred embodiment of the invention, the expression of all genes of Table 1 and Table 4 is compared with the gene expression in the control system. The identified 87 genes showed similar expression patterns in response to all EAC treatments in Ishikawa plus, whereas ICI lowered the magnitude or reversed the expression of these genes, indicating ER dependent regulation. Apart from estrogenic gene regulation Bisphenol A, o,p′-DDT, Resveratrol, Zearalenone and Genistein displayed similarities to ICI in their expression patterns. In another preferred embodiment of the invention, the cellular system provided in step (a) is capable of expressing at least one gene that is selected from the group of the particular preferred genes according to Table 7. Accordingly, the expression of the at least one gene of Table 7 is compared with the gene expression in the control system in step (c). It is also preferred to apply a plurality of genes according to Table 7 in both steps (a) and (c), more preferably at least 2 genes, most preferably at least 10 genes, highly preferably the entire panel of 49 genes. In a more preferred embodiment of the invention, the estrogenic activity of a compound is positively detected in step (c) if the expression involves an up-regulation of genes selected from the group of genes according to Table 8 and/or a down-regulation of genes selected from the group of genes according to Table 9. Contrary to that, the anti-estrogenic activity of a compound is positively detected in step (c) if the expression involves a down-regulation of genes of Table 8 and/or an up-regulation of genes of Table 9. The prior teaching concerning multiple genes is valid and applicable without restrictions to the Tables 8 and 9, which represents subsets of Table 7, provided that the respective preferred plurality of genes is re-calculated by the rule of three. In addition to the expression of genes of Table 7, the cellular system of step (a) is preferably capable of expressing at least a single gene, which is selected from the group of genes according of Table 10, whose expression is compared with the gene expression in the control system in step (c). It is also preferred to apply a plurality of genes according to Table 10 in both steps (a) and (c), more preferably at least 2 genes, most preferably at least 10 genes, highly preferably the entire panel of 34 genes. In a preferred embodiment of the invention, the estrogenic activity of a compound is positively detected in step (c) if the expression involves an up-regulation of genes selected from the group of genes according to Table 11 and/or a down-regulation of genes selected from the group of genes according to Table 12. Contrary to that, the anti-estrogenic activity of a compound is positively detected in step (c) if the expression involves a down-regulation of genes of Table 11 and/or an up-regulation of genes of Table 12. The prior teaching concerning multiple genes is valid and applicable without restrictions to the Tables 11 and 12, which represents subsets of Table 10, provided that the respective preferred plurality of genes is re-calculated by the rule of three. If in step (a) the cellular system or the sample thereof is capable of expressing multiple genes of Table 1 and/or additionally capable of expressing multiple genes of Table 4, and furthermore in step (c) an expression pattern of multiple genes of Table 1 and/or Table 4 is compared with the expression pattern in the control system, the estrogenicity can be characterized compound-specifically. Particularly, the expression pattern is determined by a correlation of the multiple genes and/or a magnitude of altered regulation. The screening method of this invention not only evaluates the effect of chemical substances having estrogen-like or anti-estrogenic activity on cells to be evaluated, but can also indicate the details of this effect. By individually evaluating the expression level of categorized genes, it is possible to distinguish how chemical substances having estrogen-like or anti-estrogenic activity that affect the cells to be evaluated. The invention also teaches an embodiment of the screening method, wherein in step (a) a mammal, preferably a laboratory mammal, is provided, in step (b) the compound to be screened is administered to the mammal, and in step (c) a therapeutic effect is detected via a level of estrogenic or anti-estrogenic activity in a biological sample withdrawn from the mammal in comparison with a mammal showing non-endocrine disrupting and/or endocrine disrupting effects. With the therapeutic effect, the qualitative level is incorporated into step (c). A “therapeutically relevant effect” relieves to some extent one or more symptoms of a disease or returns to normality, either partially or completely, one or more physiological or biochemical parameters associated with or causative of the disease or pathological conditions. In addition, the expression “therapeutically effective amount” denotes an amount which, compared with a corresponding subject who has not received this amount, has the following consequence: improved treatment, healing, prevention or elimination of a disease, syndrome, condition, complaint, disorder or side-effects or also the reduction in the advance of a disease, complaint or disorder. The expression “therapeutically effective amount” also encompasses the amounts which are effective for increasing normal physiological function. Testing of several compounds makes the selection of that compound possible that is best suited for the treatment of the mammal subject. The in-vivo dose rate of the chosen compound is advantageously pre-adjusted to the estrogenicity of the specific cells with regard to their in-vitro data. Therefore, the therapeutic efficacy is remarkably enhanced. A compound identified by the screening method is another object of the invention. The prior teaching of the present specification concerning the screening method is valid and applicable without restrictions to the compound itself if expedient. The identification of compounds that induce or repress the expression of a gene associated with a given disorder or condition can lead to the development of pharmaceuticals that can be administered to a patient at therapeutically effective doses to prevent, treat or control such disorder or condition. Hence, the invention furthermore relates to a medicament comprising at least one compound according to the invention, and optionally excipients and/or adjuvants. In the meaning of the invention, an “adjuvant” denotes every substance that enables, intensifies or modifies a specific response against the active ingredient of the invention if administered simultaneously, contemporarily or sequentially. Known adjuvants for injection solutions are, for example, aluminum compositions, such as aluminum hydroxide or aluminum phosphate, saponins, such as QS21, muramyldipeptide or muramyltripeptide, proteins, such as gamma-interferon or TNF, M59, squalen or polyols. Consequently, the invention also relates to a pharmaceutical composition comprising as active ingredient an effective amount of at least one compound as screened according to the invention and/or physiologically acceptable salts thereof together with pharmaceutically tolerable adjuvants. A “medicament”, “pharmaceutical composition” or “pharmaceutical formulation” in the meaning of the invention is any agent in the field of medicine, which comprises one or more EAC of the invention or preparations thereof and can be used in prophylaxis, therapy, follow-up or aftercare of patients who suffer from diseases, which are associated with estrogen receptor signaling, in such a way that a pathogenic modification of their overall condition or of the condition of particular regions of the organism could establish at least temporarily. Furthermore, the active ingredient may be administered alone or in combination with other treatments. A synergistic effect may be achieved by using more than one compound in the pharmaceutical composition, i.e. the EAC of the invention is combined with at least another agent as active ingredient. The active ingredients can be used either simultaneously or sequentially. Pharmaceutical formulations can be adapted for administration via any desired suitable method, for example by oral (including buccal or sublingual), rectal, nasal, topical (including buccal, sublingual or transdermal), vaginal or parenteral (including subcutaneous, intramuscular, intravenous or intradermal) methods. Such formulations can be prepared using all processes known in the pharmaceutical art by, for example, combining the active ingredient with the excipient(s) or adjuvant(s). The pharmaceutical composition of the invention is produced in a known way using common solid or liquid carriers, diluents and/or additives and usual adjuvants for pharmaceutical engineering and with an appropriate dosage. The amount of excipient material that is combined with the active ingredient to produce a single dosage form varies depending upon the host treated
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