This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
, No Gclids
Disease Info Card
Neoplasms, Hormone-dependent
Information about Neoplasms, Hormone-dependent: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Neoplasms, Hormone-dependent
Most recent studies have shown that Neoplasms, Hormone-dependent shares some biological mechanisms with adenocarcinoma, carcinogenesis, carcinoma, cell-transformation-neoplastic, endometrial-carcinoma, endometrial-polyp, hormone-refractory-prostate-cancer, hyperplasia, lymphatic-metastasis, malignant-neoplasm-of-breast, malignant-neoplasm-of-prostate, malignant-neoplasms, malignant-paraganglionic-neoplasm, mammary-neoplasms, mammary-neoplasms-experimental, neoplasm-metastasis, neoplasm-recurrence-local, neoplasms, prostatic-neoplasms.
Among the many pathways, these few ones have gauged particular interests from scientists studying Neoplasms, Hormone-dependent, and have been seen in publications frequently: Aging, Angiogenesis, Cell Cycle, Cell Cycle Arrest, Cell Death, Cell Growth, Cell Proliferation, Dna Repair, Drug Resistance, Hypersensitivity, Induction Of Apoptosis, Localization, Menopause, Methylation, Pathogenesis, Programmed Cell Death, Rna Interference, S Phase, Secretion, Translation
Quite a number of genes have been found to play important roles in Neoplasms, Hormone-dependent, such as AKR1B1, AR, AREG, CDKN1A, CYP19A1, DBT, EGF, EGFR, ERBB2, ESR1, FDXR, KLK3, NPEPPS, PGR, PLAG1, PROS1, PSAT1, TMEM37, TP53. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.