NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells.


Journal

Journal of ovarian research
ISSN: 1757-2215
Titre abrégé: J Ovarian Res
Pays: England
ID NLM: 101474849

Informations de publication

Date de publication:
04 May 2024
Historique:
received: 30 01 2024
accepted: 20 04 2024
medline: 5 5 2024
pubmed: 5 5 2024
entrez: 4 5 2024
Statut: epublish

Résumé

Genetic studies implicate the oncogenic transcription factor Forkhead Box M1 (FOXM1) as a potential therapeutic target in high-grade serous ovarian cancer (HGSOC). We evaluated the activity of different FOXM1 inhibitors in HGSOC cell models. We treated HGSOC and fallopian tube epithelial (FTE) cells with a panel of previously reported FOXM1 inhibitors. Based on drug potency, efficacy, and selectivity, determined through cell viability assays, we focused on two compounds, NB-73 and NB-115 (NB compounds), for further investigation. NB compounds potently and selectively inhibited FOXM1 with lesser effects on other FOX family members. NB compounds decreased FOXM1 expression via targeting the FOXM1 protein by promoting its proteasome-mediated degradation, and effectively suppressed FOXM1 gene targets at both the protein and mRNA level. At the cellular level, NB compounds promoted apoptotic cell death. Importantly, while inhibition of apoptosis using a pan-caspase inhibitor rescued HGSOC cells from NB compound-induced cell death, it did not rescue FOXM1 protein degradation, supporting that FOXM1 protein loss from NB compound treatment is specific and not a general consequence of cytotoxicity. Drug washout studies indicated that FOXM1 reduction was retained for at least 72 h post-treatment, suggesting that NB compounds exhibit long-lasting effects in HGSOC cells. NB compounds effectively suppressed both two-dimensional and three-dimensional HGSOC cell colony formation at sub-micromolar concentrations. Finally, NB compounds exhibited synergistic activity with carboplatin in HGSOC cells. NB compounds are potent, selective, and efficacious inhibitors of FOXM1 in HGSOC cells and are worthy of further investigation as HGSOC therapeutics.

Sections du résumé

BACKGROUND BACKGROUND
Genetic studies implicate the oncogenic transcription factor Forkhead Box M1 (FOXM1) as a potential therapeutic target in high-grade serous ovarian cancer (HGSOC). We evaluated the activity of different FOXM1 inhibitors in HGSOC cell models.
RESULTS RESULTS
We treated HGSOC and fallopian tube epithelial (FTE) cells with a panel of previously reported FOXM1 inhibitors. Based on drug potency, efficacy, and selectivity, determined through cell viability assays, we focused on two compounds, NB-73 and NB-115 (NB compounds), for further investigation. NB compounds potently and selectively inhibited FOXM1 with lesser effects on other FOX family members. NB compounds decreased FOXM1 expression via targeting the FOXM1 protein by promoting its proteasome-mediated degradation, and effectively suppressed FOXM1 gene targets at both the protein and mRNA level. At the cellular level, NB compounds promoted apoptotic cell death. Importantly, while inhibition of apoptosis using a pan-caspase inhibitor rescued HGSOC cells from NB compound-induced cell death, it did not rescue FOXM1 protein degradation, supporting that FOXM1 protein loss from NB compound treatment is specific and not a general consequence of cytotoxicity. Drug washout studies indicated that FOXM1 reduction was retained for at least 72 h post-treatment, suggesting that NB compounds exhibit long-lasting effects in HGSOC cells. NB compounds effectively suppressed both two-dimensional and three-dimensional HGSOC cell colony formation at sub-micromolar concentrations. Finally, NB compounds exhibited synergistic activity with carboplatin in HGSOC cells.
CONCLUSIONS CONCLUSIONS
NB compounds are potent, selective, and efficacious inhibitors of FOXM1 in HGSOC cells and are worthy of further investigation as HGSOC therapeutics.

Identifiants

pubmed: 38704607
doi: 10.1186/s13048-024-01421-4
pii: 10.1186/s13048-024-01421-4
doi:

Substances chimiques

Forkhead Box Protein M1 0
FOXM1 protein, human 0
Antineoplastic Agents 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

94

Subventions

Organisme : NCI NIH HHS
ID : P30CA036727
Pays : United States
Organisme : NCI NIH HHS
ID : T32CA009476
Pays : United States
Organisme : NCI NIH HHS
ID : T32CA009476
Pays : United States

Informations de copyright

© 2024. The Author(s).

Références

Bowtell DD, Bohm S, Ahmed AA, Aspuria PJ, Bast RC Jr, Beral V, Berek JS, Birrer MJ, Blagden S, Bookman MA, et al. Rethinking ovarian cancer II: reducing mortality from high-grade serous ovarian cancer. Nat Rev Cancer. 2015;15(11):668–79.
pubmed: 26493647 pmcid: 4892184 doi: 10.1038/nrc4019
Laoukili J, Stahl M, Medema RH. FoxM1: at the crossroads of ageing and cancer. Biochem Biophys Acta. 2007;1775(1):92–102.
pubmed: 17014965
Raychaudhuri P, Park HJ. FoxM1: a master regulator of tumor metastasis. Can Res. 2011;71(13):4329–33.
doi: 10.1158/0008-5472.CAN-11-0640
Alvarez-Fernández M, Medema RH. Novel functions of FoxM1: from molecular mechanisms to cancer therapy. Front Oncol. 2013;3:30–30.
pubmed: 23467617 pmcid: 3588610 doi: 10.3389/fonc.2013.00030
Halasi M, Gartel AL. FOX(M1) news–it is cancer. Mol Cancer Ther. 2013;12(3):245–54.
pubmed: 23443798 pmcid: 3596487 doi: 10.1158/1535-7163.MCT-12-0712
Lam EW, Brosens JJ, Gomes AR, Koo CY. Forkhead box proteins: tuning forks for transcriptional harmony. Nat Rev Cancer. 2013;13(7):482–95.
pubmed: 23792361 doi: 10.1038/nrc3539
Liu C, Barger CJ, Karpf AR. FOXM1: A Multifunctional Oncoprotein and Emerging Therapeutic Target in Ovarian Cancer. Cancers. 2021;13(12):3065.
pubmed: 34205406 pmcid: 8235333 doi: 10.3390/cancers13123065
Bell D, Berchuck A, Birrer M, Chien J, Cramer DW, Dao F, Dhir R, DiSaia P, Gabra H, Glenn P, et al. Integrated genomic analyses of ovarian carcinoma. Nature. 2011;474(7353):609–15.
doi: 10.1038/nature10166
Barger CJ, Zhang W, Hillman J, Stablewski AB, Higgins MJ, Vanderhyden BC, Odunsi K, Karpf AR. Genetic determinants of FOXM1 overexpression in epithelial ovarian cancer and functional contribution to cell cycle progression. Oncotarget. 2015;6(29):27613–27.
pubmed: 26243836 pmcid: 4695012 doi: 10.18632/oncotarget.4546
Zhang Q, Zhang R, Liu M, Wu H, Yang B. An integrated model of CDCA5 and FOXM1 expression combined with a residual disease that predicts prognosis in ovarian cancer patients. Cell Mol Biol (Noisy-le-grand). 2023;69(10):143–9.
pubmed: 38279460 doi: 10.14715/cmb/2023.69.10.20
Sousa A, Dugourd A, Memon D, Petursson B, Petsalaki E, Saez-Rodriguez J, Beltrao P. Pan-Cancer landscape of protein activities identifies drivers of signalling dysregulation and patient survival. Mol Syst Biol. 2023;19(3):e10631.
pubmed: 36688815 pmcid: 9996241 doi: 10.15252/msb.202110631
Barger CJ, Branick C, Chee L, Karpf AR. Pan-cancer analyses reveal genomic features of FOXM1 overexpression in cancer. Cancers (Basel). 2019;11(2):251.
pubmed: 30795624 doi: 10.3390/cancers11020251
Raghuwanshi S, Gartel AL. Small-molecule inhibitors targeting FOXM1: Current challenges and future perspectives in cancer treatments. Biochim Biophys Acta Rev Cancer. 2023;1878(6):189015.
pubmed: 37913940 doi: 10.1016/j.bbcan.2023.189015
Kwok JM-M, Myatt SS, Marson CM, Coombes RC, Constantinidou D, Lam EW-F. Thiostrepton selectively targets breast cancer cells through inhibition of forkhead box M1 expression. Mol Cancer Ther. 2008;7(7):2022–32.
pubmed: 18645012 doi: 10.1158/1535-7163.MCT-08-0188
Halasi M, Gartel AL. A novel mode of FoxM1 regulation: Positive auto-regulatory loop. Cell Cycle. 2009;8(12):1966–7.
pubmed: 19411834 doi: 10.4161/cc.8.12.8708
Hegde NS, Sanders DA, Rodriguez R, Balasubramanian S. The transcription factor FOXM1 is a cellular target of the natural product thiostrepton. Nat Chem. 2011;3(9):725–31.
pubmed: 21860463 doi: 10.1038/nchem.1114
Gartel A. Thiazole Antibiotics Siomycin a and Thiostrepton Inhibit the Transcriptional Activity of FOXM1. Front Oncol 2013, 3(150).
Halasi M, Váraljai R, Benevolenskaya E, Gartel AL. A novel function of molecular chaperone HSP70: suppression of oncogenic FOXM1 after proteotoxic stress *. J Biol Chem. 2016;291(1):142–8.
pubmed: 26559972 doi: 10.1074/jbc.M115.678227
Gormally MV, Dexheimer TS, Marsico G, Sanders DA, Lowe C, Matak-Vinković D, Michael S, Jadhav A, Rai G, Maloney DJ, et al. Suppression of the FOXM1 transcriptional programme via novel small molecule inhibition. Nat Commun. 2014;5(1):5165.
pubmed: 25387393 doi: 10.1038/ncomms6165
Chen X, Müller GA, Quaas M, Fischer M, Han N, Stutchbury B, Sharrocks AD, Engeland K. The Forkhead Transcription Factor FOXM1 Controls Cell Cycle-Dependent Gene Expression through an Atypical Chromatin Binding Mechanism. Mol Cell Biol. 2013;33(2):227.
pubmed: 23109430 pmcid: 3554121 doi: 10.1128/MCB.00881-12
Iness AN, Litovchick L. MuvB: A Key to Cell Cycle Control in Ovarian Cancer. Front Oncol. 2018;8:223–223.
pubmed: 29942794 pmcid: 6004728 doi: 10.3389/fonc.2018.00223
Sanders DA, Gormally MV, Marsico G, Beraldi D, Tannahill D, Balasubramanian S. FOXM1 binds directly to non-consensus sequences in the human genome. Genome Biol. 2015;16(1):130.
pubmed: 26100407 pmcid: 4492089 doi: 10.1186/s13059-015-0696-z
Kang K, Choi Y, Kim HH, Yoo KH, Yu S. Predicting FOXM1-Mediated Gene Regulation through the Analysis of Genome-Wide FOXM1 Binding Sites in MCF-7, K562, SK-N-SH, GM12878 and ECC-1 Cell Lines. Int J Mol Sci. 2020;21(17):6141.
pubmed: 32858881 pmcid: 7503762 doi: 10.3390/ijms21176141
Tang Q, Liu C, Zhang S, He L, Liu Y, Wang J, Zhao X, Li X. FOXM1 increases hTERT protein stability and indicates poor prognosis in gastric cancer. Neoplasia. 2023;36:100863.
pubmed: 36528911 doi: 10.1016/j.neo.2022.100863
Zhang N, Wei P, Gong A, Chiu WT, Lee HT, Colman H, Huang H, Xue J, Liu M, Wang Y, et al. FoxM1 promotes beta-catenin nuclear localization and controls Wnt target-gene expression and glioma tumorigenesis. Cancer Cell. 2011;20(4):427–42.
pubmed: 22014570 pmcid: 3199318 doi: 10.1016/j.ccr.2011.08.016
Ketola K, Munuganti RSN, Davies A, Nip KM, Bishop JL, Zoubeidi A. Targeting Prostate Cancer Subtype 1 by Forkhead Box M1 Pathway Inhibition. Clin Cancer Res. 2017;23(22):6923–33.
pubmed: 28899970 doi: 10.1158/1078-0432.CCR-17-0901
Chen Y, Ruben EA, Rajadas J, Teng NNH. In silico investigation of FOXM1 binding and novel inhibitors in epithelial ovarian cancer. Bioorg Med Chem. 2015;23(15):4576–82.
pubmed: 26164623 doi: 10.1016/j.bmc.2015.06.002
Sun L, Ren X, Wang I-C, Pradhan A, Zhang Y, Flood HM, Han B, Whitsett JA, Kalin TV, Kalinichenko VV. The FOXM1 inhibitor RCM-1 suppresses goblet cell metaplasia and prevents IL-13 and STAT6 signaling in allergen-exposed mice. Sci Signaling. 2017;10(475):eaai8583.
doi: 10.1126/scisignal.aai8583
Ziegler Y, Laws MJ, Sanabria Guillen V, Kim SH, Dey P, Smith BP, Gong P, Bindman N, Zhao Y, Carlson K, et al. Suppression of FOXM1 activities and breast cancer growth in vitro and in vivo by a new class of compounds. nbj Breast Cancer. 2019;5(1):45.
doi: 10.1038/s41523-019-0141-7
Koboldt DC, Fulton RS, McLellan MD, Schmidt H, Kalicki-Veizer J, McMichael JF, Fulton LL, Dooling DJ, Ding L, Mardis ER, et al. Comprehensive molecular portraits of human breast tumours. Nature. 2012;490(7418):61–70.
doi: 10.1038/nature11412
Perets R, Drapkin R. It’s totally tubular riding the new wave of ovarian cancer research. Cancer Res. 2016;76(1):10–7.
pubmed: 26669862 doi: 10.1158/0008-5472.CAN-15-1382
Klinkebiel D, Zhang W, Akers SN, Odunsi K, Karpf AR. DNA methylome analyses implicate Fallopian Tube Epithelia as the origin for high-grade serous ovarian cancer. Mol Cancer Res. 2016;14(9):787–94.
pubmed: 27259716 pmcid: 5025356 doi: 10.1158/1541-7786.MCR-16-0097
Karst AM, Jones PM, Vena N, Ligon AH, Liu JF, Hirsch MS, Etemadmoghadam D, Bowtell DDL, Drapkin R. Cyclin E1 Deregulation Occurs Early in Secretory Cell Transformation to Promote Formation of Fallopian Tube-Derived High-Grade Serous Ovarian Cancers. Can Res. 2014;74(4):1141–52.
doi: 10.1158/0008-5472.CAN-13-2247
Barger CJ, Zhang W, Sharma A, Chee L, James SR, Kufel CN, Miller A, Meza J, Drapkin R, Odunsi K, et al. Expression of the POTE gene family in human ovarian cancer. Sci Rep. 2018;8(1):17136.
pubmed: 30459449 pmcid: 6244393 doi: 10.1038/s41598-018-35567-1
Schindelin J, Arganda-Carreras I, Frise E, Kaynig V, Longair M, Pietzsch T, Preibisch S, Rueden C, Saalfeld S, Schmid B, et al. Fiji: an open-source platform for biological-image analysis. Nat Methods. 2012;9(7):676–82.
pubmed: 22743772 doi: 10.1038/nmeth.2019
Brzozowska B, Gałecki M, Tartas A, Ginter J, Kaźmierczak U, Lundholm L. Freeware tool for analysing numbers and sizes of cell colonies. Radiat Environ Biophys. 2019;58(1):109–17.
pubmed: 30673853 pmcid: 6394662 doi: 10.1007/s00411-018-00772-z
Cokol-Cakmak M, Bakan F, Cetiner S, Cokol M. Diagonal Method to Measure Synergy Among Any Number of Drugs. JoVE. 2018;136:e57713.
Domcke S, Sinha R, Levine DA, Sander C, Schultz N. Evaluating cell lines as tumour models by comparison of genomic profiles. Nat Commun. 2013;4:2126.
pubmed: 23839242 doi: 10.1038/ncomms3126
Mitra AK, Davis DA, Tomar S, Roy L, Gurler H, Xie J, Lantvit DD, Cardenas H, Fang F, Liu Y, et al. In vivo tumor growth of high-grade serous ovarian cancer cell lines. Gynecol Oncol. 2015;138(2):372–7.
pubmed: 26050922 pmcid: 4528621 doi: 10.1016/j.ygyno.2015.05.040
Laoukili J, Alvarez M, Meijer LAT, Stahl M, Mohammed S, Kleij L, Heck AJR, Medema RH. Activation of FoxM1 during G2 Requires Cyclin A/Cdk-Dependent Relief of Autorepression by the FoxM1 N-Terminal Domain. Mol Cell Biol. 2008;28(9):3076.
pubmed: 18285455 pmcid: 2293089 doi: 10.1128/MCB.01710-07
Anders L, Ke N, Hydbring P, Choi YJ, Widlund HR, Chick JM, Zhai H, Vidal M, Gygi SP, Braun P, et al. A systematic screen for CDK4/6 substrates links FOXM1 phosphorylation to senescence suppression in cancer cells. Cancer Cell. 2011;20(5):620–34.
pubmed: 22094256 pmcid: 3237683 doi: 10.1016/j.ccr.2011.10.001
Wang X, Quail E, Hung N-J, Tan Y, Ye H, Costa RH. Increased levels of forkhead box M1B transcription factor in transgenic mouse hepatocytes prevent age-related proliferation defects in regenerating liver. Proc Natl Acad Sci. 2001;98(20):11468–73.
pubmed: 11572993 pmcid: 58753 doi: 10.1073/pnas.201360898
Leung TWC, Lin SSW, Tsang ACC, Tong CSW, Ching JCY, Leung WY, Gimlich R, Wong GG, Yao K-M. Over-expression of FoxM1 stimulates cyclin B1 expression. FEBS Lett. 2001;507(1):59–66.
pubmed: 11682060 doi: 10.1016/S0014-5793(01)02915-5
Laoukili J, Kooistra MRH, Brás A, Kauw J, Kerkhoven RM, Morrison A, Clevers H, Medema RH. FoxM1 is required for execution of the mitotic programme and chromosome stability. Nat Cell Biol. 2005;7(2):126–36.
pubmed: 15654331 doi: 10.1038/ncb1217
Bi X, Zheng D, Cai J, Xu D, Chen L, Xu Z, Cao M, Li P, Shen Y, Wang H, et al. Pan-cancer analyses reveal multi-omic signatures and clinical implementations of the forkhead-box gene family. Cancer Med. 2023;12(16):17428–44.
pubmed: 37401400 pmcid: 10501247 doi: 10.1002/cam4.6312
Wang L-L, Xiu Y-L, Chen X, Sun K-X, Chen S, Wu D-D, Liu B-L, Zhao Y. The transcription factor FOXA1 induces epithelial ovarian cancer tumorigenesis and progression. Tumor Biology. 2017;39(5):1010428317706210.
pubmed: 28488543 doi: 10.1177/1010428317706210
Wang K, Guan C, Fang C, Jin X, Yu J, Zhang Y, Zheng L. Clinical significance and prognostic value of Forkhead box A1 expression in human epithelial ovarian cancer. Oncol Lett. 2018;15(4):4457–62.
pubmed: 29541214 pmcid: 5835846
Zhang Y, Wang Y, Zhao G, Tanner EJ, Adli M, Matei D. FOXK2 promotes ovarian cancer stemness by regulating the unfolded protein response pathway. J Clin Invest. 2022;132(10):e151591.
pubmed: 35349489 pmcid: 9106354 doi: 10.1172/JCI151591
Liu Y, Ao X, Ding W, Ponnusamy M, Wu W, Hao X, Yu W, Wang Y, Li P, Wang J. Critical role of FOXO3a in carcinogenesis. Mol Cancer. 2018;17(1):104.
pubmed: 30045773 pmcid: 6060507 doi: 10.1186/s12943-018-0856-3
Tonge PJ. Drug-Target Kinetics in Drug Discovery. ACS Chem Neurosci. 2018;9(1):29–39.
pubmed: 28640596 doi: 10.1021/acschemneuro.7b00185
Peper A. Aspects of the relationship between drug dose and drug effect. Dose Response. 2009;7(2):172–92.
pubmed: 19543483 pmcid: 2695574 doi: 10.2203/dose-response.08-019.Peper
Ward TH, Cummings J, Dean E, Greystoke A, Hou JM, Backen A, Ranson M, Dive C. Biomarkers of apoptosis. Br J Cancer. 2008;99(6):841–6.
pubmed: 19238626 pmcid: 2538762 doi: 10.1038/sj.bjc.6604519
Chaitanya GV, Steven AJ, Babu PP. PARP-1 cleavage fragments: signatures of cell-death proteases in neurodegeneration. Cell Commun Signal. 2010;8:31.
pubmed: 21176168 pmcid: 3022541 doi: 10.1186/1478-811X-8-31
Caserta TM, Smith AN, Gultice AD, Reedy MA, Brown TL. Q-VD-OPh, a broad spectrum caspase inhibitor with potent antiapoptotic properties. Apoptosis. 2003;8(4):345–52.
pubmed: 12815277 doi: 10.1023/A:1024116916932
Widmann C, Gibson S, Johnson GL. Caspase-dependent cleavage of signaling proteins during apoptosis A turn-off mechanism for anti-apoptotic signals. J Biol Chem. 1998;273(12):7141–7.
pubmed: 9507028 doi: 10.1074/jbc.273.12.7141
Sukharev SA, Pleshakova OV, Sadovnikov VB. Role of proteases in activation of apoptosis. Cell Death Differ. 1997;4(6):457–62.
pubmed: 16465266 doi: 10.1038/sj.cdd.4400263
Brix N, Samaga D, Belka C, Zitzelsberger H, Lauber K. Analysis of clonogenic growth in vitro. Nat Protoc. 2021;16(11):4963–91.
pubmed: 34697469 doi: 10.1038/s41596-021-00615-0
Sher G, Masoodi T, Patil K, Akhtar S, Kuttikrishnan S, Ahmad A, Uddin S. Dysregulated FOXM1 signaling in the regulation of cancer stem cells. Semin Cancer Biol. 2022;86(Pt 3):107–21.
pubmed: 35931301 doi: 10.1016/j.semcancer.2022.07.009
Borowicz S, Van Scoyk M, Avasarala S, Karuppusamy Rathinam MK, Tauler J, Bikkavilli RK, Winn RA. The soft agar colony formation assay. J Vis Exp. 2014;92:e51998.
Barger CJ, Chee L, Albahrani M, Munoz-Trujillo C, Boghean L, Branick C, Odunsi K, Drapkin R, Zou L, Karpf AR. Co-regulation and function of FOXM1/RHNO1 bidirectional genes in cancer. eLife. 2021;10:e55070.
pubmed: 33890574 pmcid: 8104967 doi: 10.7554/eLife.55070
Kalathil D, John S, Nair AS. FOXM1 and Cancer: Faulty Cellular Signaling Derails Homeostasis. Front Oncol. 2020;10:626836.
pubmed: 33680951 doi: 10.3389/fonc.2020.626836
Wang LL, Xiu YL, Chen X, Sun KX, Chen S, Wu DD, Liu BL, Zhao Y. The transcription factor FOXA1 induces epithelial ovarian cancer tumorigenesis and progression. Tumour Biol. 2017;39(5):1010428317706210.
pubmed: 28488543 doi: 10.1177/1010428317706210
Doepner M, Lee I, Natale CA, Brathwaite R, Venkat S, Kim SH, Wei Y, Vakoc CR, Capell BC, Katzenellenbogen JA, et al. Endogenous DOPA inhibits melanoma through suppression of CHRM1 signaling. Sci Adv. 2022;8(35):eabn4007.
pubmed: 36054350 pmcid: 10848963 doi: 10.1126/sciadv.abn4007
Cheng Y, Sun F, Thornton K, Jing X, Dong J, Yun G, Pisano M, Zhan F, Kim SH, Katzenellenbogen JA, et al. FOXM1 regulates glycolysis and energy production in multiple myeloma. Oncogene. 2022;41(32):3899–911.
pubmed: 35794249 pmcid: 9355869 doi: 10.1038/s41388-022-02398-4
Nandi I, Smith HW, Sanguin-Gendreau V, Ji L, Pacis A, Papavasiliou V, Zuo D, Nam S, Attalla SS, Kim SH, et al. Coordinated activation of c-Src and FOXM1 drives tumor cell proliferation and breast cancer progression. J Clin Invest. 2023;133(7):e162324.
pubmed: 36795481 pmcid: 10065076 doi: 10.1172/JCI162324
Ziegler Y, Guillen VS, Kim SH, Katzenellenbogen JA, Katzenellenbogen BS. Transcription Regulation and Genome Rewiring Governing Sensitivity and Resistance to FOXM1 Inhibition in Breast Cancer. Cancers (Basel). 2021;13(24):6282.
pubmed: 34944900 doi: 10.3390/cancers13246282

Auteurs

Cassie Liu (C)

Eppley Institute, University of Nebraska Medical Center, Omaha, NE, 68918-6805, USA.
Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, 68918-6805, USA.

Makenzie Vorderbruggen (M)

Eppley Institute, University of Nebraska Medical Center, Omaha, NE, 68918-6805, USA.
Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, 68918-6805, USA.

Catalina Muñoz-Trujillo (C)

Eppley Institute, University of Nebraska Medical Center, Omaha, NE, 68918-6805, USA.
Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, 68918-6805, USA.

Sung Hoon Kim (SH)

Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, IL, 61801, USA.

John A Katzenellenbogen (JA)

Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, IL, 61801, USA.
Cancer Center, University of Illinois at Urbana-Champaign, Urbana, IL, 61801, USA.

Benita S Katzenellenbogen (BS)

Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL, 61801, USA.
Cancer Center, University of Illinois at Urbana-Champaign, Urbana, IL, 61801, USA.

Adam R Karpf (AR)

Eppley Institute, University of Nebraska Medical Center, Omaha, NE, 68918-6805, USA. adam.karpf@unmc.edu.
Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE, 68918-6805, USA. adam.karpf@unmc.edu.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH