Features:· Introduction of the alphabetical scheme of the programs;· Addition of freeware CD-ROM, flash disks and other files to Index, search and download folders;· Cutting out of graphic images;· Scrolling of large amount of files;· Auto indexing (a new index in the 5 minutes);· Auto search from selected folders for various search engines (Google, Bing and Yahoo);· Controlling of the end of the Index (a new format);· Allowing the user to set the default program for the index and the archiving;· Full support for USB.Breast cancer due to alterations in genes associated with the estrogen pathway, including ERα and ERβ, have unique risk factors, and are generally treated with a combination of chemotherapy and endocrine therapy. The endocrine therapy tends to be based on modulation of the estradiol-ERα or progesterone-ERβ pathway, rather than the estrogen-ERα-independent pathway. Whereas the efficacy of aromatase inhibitor-based endocrine therapy has been demonstrated, recent clinical observations have shown that cyclin-dependent kinase inhibitors, which could have a potential to interfere with the estrogen-signaling, are effective in a subset of ER-positive breast cancers that are ER-α negative \[[@CR29]\]. This suggests that new strategies to target estrogen-independent signaling pathways may be necessary. Here we have shown that a potential therapeutic target in breast cancer is the growth receptor, insulin-like growth factor-1 (IGF-1). In the previous studies, we showed that IGF-1 affects MPA-driven breast cancer growth in vitro and in vivo \[[@CR30]\]. We showed that IGF-1 contributes to MPA-induced cell proliferation, migration, and invasion in vitro, and, importantly, that IGF-1 can reverse the anti-proliferative, anti-migratory, and anti-invasive effect of anti-estrogen therapy in ER-positive breast cancer cells. Similar to previous studies, we demonstrated that IGF-1 inhibits chemosensitivity to the TOP-2 inhibitor, etoposide, and, as a result of reversing the anti-proliferative effect of anti-estrogen therapy, the anti-proliferative effect was associated with the alterations in gene expression associated with apoptosis and autophagy. However, in this study, we additionally showed that the MAPK signaling pathway plays 08929e5ed8