Breast cancer is cancer that starts in the tissues of the breast. There are two main types of breast cancer:
~Ductal carcinoma starts in the tubes (ducts) that carry milk from the breast to the nipple. Most breast cancers are of this type.
~Lobular carcinoma starts in the parts of the breast, called lobules, which produce milk.
In rare cases, other kids of breast cancer can start in other areas of the breast.
Breast cancer risk factors are things that increase the chance that you could develop breast cancer:
~Some risk factors you can control, such as drinking alcohol. Others, such as family history, you cannot control.
~The more risk factors you have, the more your risk increases. But, it does not mean you will develop cancer. Many women who develop breast cancer do not have any known risk factors or a family history.
~Understanding your risk factors can help you take steps to lower your risk.
Some women are at higher risk for breast cancer because of certain genetic markers or variants that may be passed down from their parents.
~Genes known as BRCA1 or BRCA2 are responsible for most cases of inherited breast cancers.
~A screening tool with questions about your family’s history as well as yours can help your health care provider whether you are at risk for carrying these genes.
~If you are at high risk, a blood test to see if you carry the genes.
`Certain other genes may lead to an increased risk of breast cancer.
Breast implants, using antiperspirants, and wearing underwire bras do not increase the risk for breast cancer. There is also no evidence of a direct link between breast cancer and pesticides.
|Cat. No.||Product Name||CAS No.||Information|
A potent γ-secretase inhibitor that shows dose-dependent reduction of Aβ40 with an IC50 of 5 nM in human SH-SY5Y cells; Notch signaling inhibitor.
A potent, specific P-gp inhibitor with Kd of 5.1 nM; potentiates the cytotoxicity of several drugs including doxorubicin, paclitaxel, etoposide, and vincristine in a panel of human MDR cell lines at 25-80 nM; exhibits potent i.v. and p.o. activity without apparently enhancing the plasma pharmacokinetics of paclitaxel or the toxicity of coadministered drugs.
GDC-0077 (RG-6114) is a potent, highly isoform selective inhibitor of PI3Kα, with IC50 of 0.038 nM, >300-fold selective over β, δ, and γ isoforms, as well as PIKK-family proteins such as mTOR, DNA-PK and VPS34; induces depletion of mutant PI3K alpha protein resulting in reduction of PI3K pathway biomarkers such as pAkt and pPRAS40, inhibition of cell proliferation and increased apoptosis in human PIK3CA mutant breast cancer cell lines to a greater extent when compared to PIK3CA wild-type cells; causes tumor regressions in cell-culture-derived and patient derived PIK3CA mutant breast cancer xenograft models.
A novel, potent and selective inhibitor of CDK4/6 with biochemical IC50 of 1 nM and 4 nM for CDK4/cyclin D1 and CDK6/cyclin D3, respectively; displays >30-fold selectivity for CDK4/cyclin D1 over CDK2/cyclin A, CDK2/cyclin E, CDK5/p25, CDK5/p35, and CDK7/cyclin H/Mat1, 50-fold over CDK9/cyclin T; reversibly pauses the cell cycle in the G1 phase in CDK4/6-dependent cell lines, protects CDK4/6-dependent cells from chemotherapy-induced damage in vitro; induces a reversible cell-cycle arrest in murine and canine HSPCs; attenuates chemotherapy-induced myelosuppression in vivo.
ARV-825 is a hetero-bifunctional PROTAC (Proteolysis Targeting Chimera) that recruits BRD4 to the E3 ubiquitin ligase cereblon, leading to fast, efficient, and prolonged degradation of BRD4 via the proteasome; shows more significant and longer lasting c-MYC suppression than small molecule inhibitors (JQ1, OTX015); leads to a superior effect on BL cells proliferation suppression.
A potent, selective estrogen receptor downregulator (SERD) with ER downregulation pIC50 of 9.68; shows pM equipotent binding to both ERα and ERβ isoforms, highly selective binding compared with progesterone (∼650-fold), glucocorticoid (∼11,223-fold), and androgen (∼36,375-fold) receptor LBDs; downregulator of ERα in vitro and in vivo in ER-positive models of breast cancer and orally available.
CC-671 is a potent, selective, dual TTK (Mps1)/CLK2 inhibitor with IC50 of 5/3 nM, respectively; weakly inhibits DYRK3, DYRK1A, PHKG, DYRK1B, and CLK1 with IC50 of 0.1-0.3 uM, and displays excellent kinase selectivity (7/235 kinases > 80% inhibition at 3 uM); inhibits autophosphorylation of TTK at T686 or phosphorylation of SR protein 75 with IC50 of 0.057 and 0.549 uM in Cal-51 cells; demonstrates strong single agent in vivo efficacy in multiple TNBC xenograft models without significant body weight loss.
A novel, orally active quinoline compound that can reverse P-glycoprotein (P-gp)-mediated MDR; completely reverses resistance against vincristine in vitro in multidrug-resistant variants of mouse leukemia P388 cells and human leukemia K562 cells at 1-10 uM; greatly reduces the SP-derived tumor growth in vivo combined with CPT-11.
A potent, highly selective, irreversible inhibitor of mutant EGFR with Ki of 21.5 nM for EGFR L858R/T790M; shows 22-fold selective over WT EGFR; EGFR del19, T790M, L858R/T790M and L858R mutant kinases demonstrates the highest degree of inhibition at 0.1 uM; orally bioavailable.
Mivebresib (ABBV-075) is a potent and orally available BET bromodomain inhibitor with Ki of 1.0, 12.2, 1.5, and 2.2 nM for BRD2, BRD3, BRD4 and BRDT, respectively; displays 54-fold selectivity over EP300, has potential weak activity against SMARCA4 (70% inhibition at 1 uM), Kd >1 uM for 18 other bromodomains; exhibits inhibition of c-Myc expression and displacing BRD4 from the Myc promoter; dose-dependently inhibits IL-6 concentration in a murine model of LPS-induced endotoxic shock, shows vivo antitumor efficacy in a Kasumi-1 AML mouse xenograft model.
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