The present invention relates to novel substituted 6,7-dihydro-5H-benzo[7]annulene compounds, the processes for their preparation, as well as the therapeutic uses thereof, in particular as anticancer agents via selective antagonism and degradation of estrogen receptors. The Estrogen Receptors (ER) belong to the steroid/nuclear receptor superfamily involved in the regulation of eukaryotic gene expression, cellular proliferation and differentiation in target tissues. ERs are in two forms: the estrogen receptor alpha (ERa) and the estrogen receptor beta (ERP) respectively encoded by the ESR1 and the ESR2 genes. ERa and ERβ are ligand-activated transcription factors which are activated by the hormone estrogen (the most potent estrogen produced in the body is "^-estradiol). In the absence of hormone, ERs are largely located in the cytosol of the cell. When the hormone estrogen binds to ERs, ERs migrate from the cytosol to the nucleus of the cell, form dimers and then bind to specific genomic sequences called Estrogen Response Elements (ERE). The DNA/ER complex interacts with co-regulators to modulate the transcription of target genes. ERa is mainly expressed in reproductive tissues such as uterus, ovary, breast, bone and white adipose tissue. Abnormal ERa signaling leads to development of a variety of diseases, such as cancers, metabolic and cardiovascular diseases, neurodegenerative diseases, inflammation diseases and osteoporosis. ERa is expressed in not more than 10% of normal breast epithelium but approximately 50-80% of breast tumors. Such breast tumors with high level of ERa are classified as ERa-positive breast tumors. The etiological role of estrogen in breast cancer is well established and modulation of ERa signaling remains the mainstay of breast cancer treatment for the majority ERa-positive breast tumors. Currently, several strategies for inhibiting the estrogen axis in breast cancer exist, including: 1- blocking estrogen synthesis by aromatase inhibitors that are used to treat early and advanced ERa-positive breast cancer patients; 2- antagonizing estrogen ligand binding to ERa by tamoxifen which is used to treat ERa-positive breast cancer patients in both pre- and postmenopausal setting; 3- antagonizing and downregulating ERa levels by fulvestrant, which is used to treat breast cancer in patients that have progressed despite endocrine therapies such as tamoxifen or aromatase inhibitors. Although these endocrine therapies have contributed enormously to reduction in breast cancer development, about more than one-third of ERa-positive patients display de-novo resistance or develop resistance over time to such existing therapies. Several mechanisms have been described to explain resistance to such hormone therapies. For example, hypersensitivity of ERa to low estrogen level in treatment with aromatase inhibitors, the switch of tamoxifen effects from antagonist to agonist effects in tamoxifen treatments or multiple growth factor receptor signaling pathways. More recently, acquired mutations in ERa occurring after initiation of hormone therapies may play a role in treatment failure and cancer progression. Certain mutations in ERa, particularly those identified in the Ligand Binding Domain (LBD), result in the ability to bind to DNA in the absence of ligand and confer hormone independence in cells harboring such mutant receptors. Most of the endocrine therapy resistance mechanisms identified rely on ERa-dependent activity. One of the new strategies to counterforce such resistance is to shut down the ERa signaling by removing ERa from the tumor cells using Selective Estrogen Receptors degraders (SERDs). Clinical and preclinical data showed that a significant number of the resistance pathways can be circumvented by the use SERDs. There is still a need to provide SERDs with good degradation efficacy. G.M. Anstead et al. have described 2,3-diarylindenes and 2,3-diarylindenones as binders of estrogen receptors (Journal of Medicinal Chemistry, 1988, Vol. 31 , No. 7, p. 1316-1326). R. McCague et al. have described analogues of (Z)- and (E)~4-hydroxytamoxifen and have tested their binding affinities to estrogen receptors (Journal of Medicinal Chemistry, 1998, Vol. 31 , No. 7, p. 1285-1290). The objective of the present invention is to provide novel compounds able to selectively antagonize and degrade the estrogen receptors (SERDs compounds), for use in cancer treatment. The present invention relates to the compounds of the formula (I): wherein: - R1 and R2 represent independently a hydrogen atom or a deuterium atom; - R3 represents a hydrogen atom, a -COOH group, a -OH group or a -OPO(OH)2 group; - R4 represents a hydrogen atom or a fluorine atom; R5 represents a hydrogen atom or a -OH group; - wherein: o at least one of R3 or R5 is different from a hydrogen atom; o when R3 represents a -COOH group, a -OH group or a -OPO(OH)2 group, then R5 represents a hydrogen atom; o when R5 represents a -OH group, then R3 and R4 represent hydrogen atoms; - R6 is selected from: ■ a phenyl group or a heteroaryl group comprising 3 to 9 carbon atoms and comprising from 1 to 3 heteroatoms independently selected from oxygen, nitrogen and sulphur, said phenyl and heteroaryl groups being unsubstituted or substituted with 1 to 3 substituents independently selected from: a (C-,-C6)-alkyl group unsubstituted or substituted with one or more (such as , 2 or 3) fluorine atoms; a halogen atom; a -OH group; a (Ci-C6)-alkoxy group unsubstituted or substituted with one or more (such as 1 , 2 or 3) fluorine atoms; a cyano group; a sulphur group substituted with 5 fluorine atoms or (C-|-C6)-alkyl groups substituted with two or more (such as 2 or 3) fluorine atoms; a sulfonyl-(C C6)-alkyl group wherein said (C C6)-alkyl group are unsubstitued or substituted with two or more (such as 2 or 3) fluorine atoms; a silane group substituted with 3 (CrC6)-alkyl groups; an amine group unsubstituted or substituted with one or more (such as 1 or 2) (C-|-C6)-alkyl groups; an amide group unsubstituted or substituted with one or more (such as 1 or 2) (d-CeJ-alkyl groups; a heterocycloalkyi group saturated or partially saturated, comprising 3 to 5 carbon atoms and comprising 1 or 2 heteroatoms independently selected from oxygen, nitrogen or sulphur; or a heteroaryl group comprising 2 to 4 carbon atoms and comprising 1 to 3 heteroatoms selected from oxygen, nitrogen or sulphur and being unsubstituted or substituted with an oxo group; ■ a cycloalkyl group or a heterocycloalkyi group comprising 4 to 9 carbon atoms and comprising 1 or 2 heteroatoms independently selected from oxygen, nitrogen or sulphur, said cycloalkyl or heterocycloalkyi groups being saturated or partially saturated and being unsubstituted or substituted with 1 to 4 substituents independently selected from: a fluorine atom; a -OH group; a (C CeJ-alkyl group; a -COOR7 group wherein R7 is a (C C6)-all