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Article ; Online: Comprehensive Profiling of DNA Repair Defects in Breast Cancer Identifies a Novel Class of Endocrine Therapy Resistance Drivers.

Anurag, Meenakshi / Punturi, Nindo / Hoog, Jeremy / Bainbridge, Matthew N / Ellis, Matthew J / Haricharan, Svasti

Clinical cancer research : an official journal of the American Association for Cancer Research

2018 Volume 24, Issue 19, Page(s) 4887–4899

Abstract: Purpose: ...

Abstract	Purpose:
MeSH term(s)	Animals ; Antineoplastic Agents, Hormonal/administration & dosage ; Aromatase Inhibitors/administration & dosage ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Calcium-Binding Proteins/genetics ; Cell Cycle Proteins/genetics ; DNA Glycosylases/genetics ; DNA Repair/drug effects ; DNA-(Apurinic or Apyrimidinic Site) Lyase/genetics ; DNA-Binding Proteins/genetics ; Drug Resistance, Neoplasm/genetics ; Endonucleases/genetics ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/drug effects ; Heterografts ; Humans ; MCF-7 Cells ; Mice ; Middle Aged ; Receptors, Estrogen/genetics ; Tamoxifen/administration & dosage
Chemical Substances	Antineoplastic Agents, Hormonal ; Aromatase Inhibitors ; CETN2 protein, human ; Calcium-Binding Proteins ; Cell Cycle Proteins ; DNA-Binding Proteins ; Receptors, Estrogen ; Tamoxifen (094ZI81Y45) ; ERCC1 protein, human (EC 3.1.-) ; Endonucleases (EC 3.1.-) ; DNA Glycosylases (EC 3.2.2.-) ; DNA-(Apurinic or Apyrimidinic Site) Lyase (EC 4.2.99.18) ; NEIL2 protein, human (EC 4.2.99.18)
Language	English
Publishing date	2018-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-17-3702
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Article ; Online: Endocrine-Sensitive Disease Rate in Postmenopausal Patients With Estrogen Receptor-Rich/ERBB2-Negative Breast Cancer Receiving Neoadjuvant Anastrozole, Fulvestrant, or Their Combination: A Phase 3 Randomized Clinical Trial.

Ma, Cynthia X / Suman, Vera J / Sanati, Souzan / Vij, Kiran / Anurag, Meenakshi / Leitch, A Marilyn / Unzeitig, Gary W / Hoog, Jeremy / Fernandez-Martinez, Aranzazu / Fan, Cheng / Gibbs, Richard A / Watson, Mark A / Dockter, Travis J / Hahn, Olwen / Guenther, Joseph M / Caudle, Abigail / Crouch, Erika / Tiersten, Amy / Mita, Monica /

Razaq, Wajeeha / Hieken, Tina J / Wang, Yang / Rimawi, Mothaffar F / Weiss, Anna / Winer, Eric P / Hunt, Kelly K / Perou, Charles M / Ellis, Matthew J / Partridge, Ann H / Carey, Lisa A

JAMA oncology

2024 Volume 10, Issue 3, Page(s) 362–371

Abstract: Importance: Adding fulvestrant to anastrozole (A+F) improved survival in postmenopausal women with advanced estrogen receptor (ER)-positive/ERBB2 (formerly HER2)-negative breast cancer. However, the combination has not been tested in early-stage disease. ...

Abstract	Importance: Adding fulvestrant to anastrozole (A+F) improved survival in postmenopausal women with advanced estrogen receptor (ER)-positive/ERBB2 (formerly HER2)-negative breast cancer. However, the combination has not been tested in early-stage disease. Objective: To determine whether neoadjuvant fulvestrant or A+F increases the rate of pathologic complete response or ypT1-2N0/N1mic/Ki67 2.7% or less residual disease (referred to as endocrine-sensitive disease) over anastrozole alone. Design, setting, and participants: A phase 3 randomized clinical trial assessing differences in clinical and correlative outcomes between each of the fulvestrant-containing arms and the anastrozole arm. Postmenopausal women with clinical stage II to III, ER-rich (Allred score 6-8 or >66%)/ERBB2-negative breast cancer were included. All analyses were based on data frozen on March 2, 2023. Interventions: Patients received anastrozole, fulvestrant, or a combination for 6 months preoperatively. Tumor Ki67 was assessed at week 4 and optionally at week 12, and if greater than 10% at either time point, the patient switched to neoadjuvant chemotherapy or immediate surgery. Main outcomes and measures: The primary outcome was the endocrine-sensitive disease rate (ESDR). A secondary outcome was the percentage change in Ki67 after 4 weeks of neoadjuvant endocrine therapy (NET) (week 4 Ki67 suppression). Results: Between February 2014 and November 2018, 1362 female patients (mean [SD] age, 65.0 [8.2] years) were enrolled. Among the 1298 evaluable patients, ESDRs were 18.7% (95% CI, 15.1%-22.7%), 22.8% (95% CI, 18.9%-27.1%), and 20.5% (95% CI, 16.8%-24.6%) with anastrozole, fulvestrant, and A+F, respectively. Compared to anastrozole, neither fulvestrant-containing regimen significantly improved ESDR or week 4 Ki67 suppression. The rate of week 4 or week 12 Ki67 greater than 10% was 25.1%, 24.2%, and 15.7% with anastrozole, fulvestrant, and A+F, respectively. Pathologic complete response/residual cancer burden class I occurred in 8 of 167 patients and 17 of 167 patients, respectively (15.0%; 95% CI, 9.9%-21.3%), after switching to neoadjuvant chemotherapy due to week 4 or week 12 Ki67 greater than 10%. PAM50 subtyping derived from RNA sequencing of baseline biopsies available for 753 patients (58%) identified 394 luminal A, 304 luminal B, and 55 nonluminal tumors. A+F led to a greater week 4 Ki67 suppression than anastrozole alone in luminal B tumors (median [IQR], -90.4% [-95.2 to -81.9%] vs -76.7% [-89.0 to -55.6%]; P < .001), but not luminal A tumors. Thirty-six nonluminal tumors (65.5%) had a week 4 or week 12 Ki67 greater than 10%. Conclusions and relevance: In this randomized clinical trial, neither fulvestrant nor A+F significantly improved the 6-month ESDR over anastrozole in ER-rich/ERBB2-negative breast cancer. Aromatase inhibition remains the standard-of-care NET. Differential NET response by PAM50 subtype in exploratory analyses warrants further investigation. Trial registration: ClinicalTrials.gov Identifier: NCT01953588.
MeSH term(s)	Aged ; Female ; Humans ; Anastrozole/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Breast Neoplasms/pathology ; Fulvestrant ; Ki-67 Antigen ; Neoadjuvant Therapy ; Nitriles/adverse effects ; Postmenopause ; Receptor, ErbB-2 ; Receptors, Estrogen ; Triazoles/adverse effects ; Triple Negative Breast Neoplasms/drug therapy ; Middle Aged
Chemical Substances	Anastrozole (2Z07MYW1AZ) ; ERBB2 protein, human (EC 2.7.10.1) ; Fulvestrant (22X328QOC4) ; Ki-67 Antigen ; Nitriles ; Receptor, ErbB-2 (EC 2.7.10.1) ; Receptors, Estrogen ; Triazoles
Language	English
Publishing date	2024-01-18
Publishing country	United States
Document type	Randomized Controlled Trial ; Clinical Trial, Phase III ; Journal Article
ISSN	2374-2445
ISSN (online)	2374-2445
DOI	10.1001/jamaoncol.2023.6038
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Article ; Online: Cancer-associated exportin-6 upregulation inhibits the transcriptionally repressive and anticancer effects of nuclear profilin-1.

Zhu, Cuige / Kim, Sun-Joong / Mooradian, Arshag / Wang, Faliang / Li, Ziqian / Holohan, Sean / Collins, Patrick L / Wang, Keren / Guo, Zhanfang / Hoog, Jeremy / Ma, Cynthia X / Oltz, Eugene M / Held, Jason M / Shao, Jieya

Cell reports

2021 Volume 34, Issue 7, Page(s) 108749

Abstract: Aberrant expression of nuclear transporters and deregulated subcellular localization of their cargo proteins are emerging as drivers and therapeutic targets of cancer. Here, we present evidence that the nuclear exporter exportin-6 and its cargo profilin- ... ...

Abstract	Aberrant expression of nuclear transporters and deregulated subcellular localization of their cargo proteins are emerging as drivers and therapeutic targets of cancer. Here, we present evidence that the nuclear exporter exportin-6 and its cargo profilin-1 constitute a functionally important and frequently deregulated axis in cancer. Exportin-6 upregulation occurs in numerous cancer types and is associated with poor patient survival. Reducing exportin-6 level in breast cancer cells triggers antitumor effects by accumulating nuclear profilin-1. Mechanistically, nuclear profilin-1 interacts with eleven-nineteen-leukemia protein (ENL) within the super elongation complex (SEC) and inhibits the ability of the SEC to drive transcription of numerous pro-cancer genes including MYC. XPO6 and MYC are positively correlated across diverse cancer types including breast cancer. Therapeutically, exportin-6 loss sensitizes breast cancer cells to the bromodomain and extra-terminal (BET) inhibitor JQ1. Thus, exportin-6 upregulation is a previously unrecognized cancer driver event by spatially inhibiting nuclear profilin-1 as a tumor suppressor.
MeSH term(s)	Animals ; Cell Line, Tumor ; Female ; Heterografts ; Humans ; Karyopherins/genetics ; Karyopherins/metabolism ; MCF-7 Cells ; Mice ; Mice, Nude ; Neoplasms/genetics ; Neoplasms/metabolism ; Profilins/antagonists & inhibitors ; Profilins/genetics ; Profilins/metabolism ; Survival Analysis ; Up-Regulation
Chemical Substances	Karyopherins ; PFN1 protein, human ; Profilins ; XPO6 protein, human
Language	English
Publishing date	2021-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.108749
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Article: A phase II study of palbociclib plus letrozole plus trastuzumab as neoadjuvant treatment for clinical stages II and III ER+ HER2+ breast cancer (PALTAN).

NPJ breast cancer

2023 Volume 9, Issue 1, Page(s) 1

Abstract: Patients with ER+/HER2+ breast cancer (BC) are less likely to achieve pathological complete response (pCR) after chemotherapy with dual HER2 blockade than ER-/HER2+ BC. Endocrine therapy plus trastuzumab is effective in advanced ER+/HER2+ BC. Inhibition ... ...

Abstract	Patients with ER+/HER2+ breast cancer (BC) are less likely to achieve pathological complete response (pCR) after chemotherapy with dual HER2 blockade than ER-/HER2+ BC. Endocrine therapy plus trastuzumab is effective in advanced ER+/HER2+ BC. Inhibition of CDK4/6 and HER2 results in synergistic cell proliferation reduction. We combined palbociclib, letrozole, and trastuzumab (PLT) as a chemotherapy-sparing regimen. We evaluated neoadjuvant PLT in early ER+/HER2+ BC. Primary endpoint was pCR after 16 weeks. Research biopsies were performed for whole exome and RNA sequencing, PAM50 subtyping, and Ki67 assessment for complete cell cycle arrest (CCCA: Ki67 ≤ 2.7%). After 26 patients, accrual stopped due to futility. pCR (residual cancer burden-RCB 0) was 7.7%, RCB 0/I was 38.5%. Grade (G) 3/4 treatment-emergent adverse events occurred in 19. Among these, G3/4 neutropenia was 50%, hypertension 26.9%, and leucopenia 7.7%. Analysis indicated CCCA in 85% at C1 day 15 (C1D15), compared to 27% at surgery after palbociclib was discontinued. Baseline PAM50 subtyping identified 31.2% HER2-E, 43.8% Luminal B, and 25% Luminal A. 161 genes were differentially expressed comparing C1D15 to baseline. MKI67, TK1, CCNB1, AURKB, and PLK1 were among the genes downregulated, consistent with CCCA at C1D15. Molecular Signatures Database gene-sets analyses demonstrated downregulated processes involved in proliferation, ER and mTORC1 signaling, and DNA damage repair at C1D15, consistent with the study drug's mechanisms of action. Neoadjuvant PLT showed a pCR of 7.7% and an RCB 0/I rate of 38.5%. RNA sequencing and Ki67 data indicated potent anti-proliferative effects of study treatments. ClinicalTrials.gov- NCT02907918.
Language	English
Publishing date	2023-01-06
Publishing country	United States
Document type	Journal Article
ISSN	2374-4677
ISSN	2374-4677
DOI	10.1038/s41523-022-00504-z
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Article ; Online: Inhibition of cyclin dependent kinase 9 by dinaciclib suppresses cyclin B1 expression and tumor growth in triple negative breast cancer.

Rajput, Sandeep / Khera, Nimmish / Guo, Zhanfang / Hoog, Jeremy / Li, Shunqiang / Ma, Cynthia X

Oncotarget

2016 Volume 7, Issue 35, Page(s) 56864–56875

Abstract: Cyclin-dependent kinases (CDKs) are potential cancer therapeutic targets because of their critical role in promoting cell growth. Dinaciclib is a novel CDK inhibitor currently under clinical evaluation for the treatment of advanced malignancies. In this ... ...

Abstract	Cyclin-dependent kinases (CDKs) are potential cancer therapeutic targets because of their critical role in promoting cell growth. Dinaciclib is a novel CDK inhibitor currently under clinical evaluation for the treatment of advanced malignancies. In this study, we demonstrated the anti-tumor activity of dinaciclib in triple negative breast cancer (TNBC) patient derived xenograft (PDX) and cell lines in vitro and in vivo. Treatment with dinaciclib induced cell cycle arrest at G2/M phase and marked apoptosis. These changes were accompanied by reduced phosphorylation of CDK1 and retinoblastoma (Rb) protein and decreased protein levels of cyclin B1, cMYC and survivin. We further demonstrated that siRNA knockdown of CDK9, the kinase subunit of positive transcription elongation factor b (P-TEFb), instead of CDK1 or CDK2, reduced the levels of cyclin B1 and MYC in TNBC cell lines. These data support the importance of CDK9, in addition to CDK1, in mediating the growth inhibitory effect of dinaciclib in TNBC. Further investigation of CDK9 as a therapeutic target in TNBC is needed.
Language	English
Publishing date	2016-08-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.10870
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Article: Proteomic Resistance Biomarkers for PI3K Inhibitor in Triple Negative Breast Cancer Patient-Derived Xenograft Models.

Guo, Zhanfang / Primeau, Tina / Luo, Jingqin / Zhang, Cynthia / Sun, Hua / Hoog, Jeremy / Gao, Feng / Huang, Shixia / Edwards, Dean P / Davies, Sherri R / Aft, Rebecca / Ding, Li / Ellis, Matthew J / Li, Shunqiang / Ma, Cynthia X

Cancers

2020 Volume 12, Issue 12

Abstract: PI3K pathway activation is frequently observed in triple negative breast cancer (TNBC). However, single agent PI3K inhibitors have shown limited anti-tumor activity. To investigate biomarkers of response and resistance mechanisms, we tested 17 TNBC ... ...

Abstract	PI3K pathway activation is frequently observed in triple negative breast cancer (TNBC). However, single agent PI3K inhibitors have shown limited anti-tumor activity. To investigate biomarkers of response and resistance mechanisms, we tested 17 TNBC patient-derived xenograft (PDX) models representing diverse genomic backgrounds and varying degrees of PI3K pathway signaling activities for their tumor growth response to the pan-PI3K inhibitor, BKM120. Baseline and post-treatment PDX tumors were subjected to reverse phase protein array (RPPA) to identify protein markers associated with tumor growth response. While BKM120 consistently reduced PI3K pathway activity, as demonstrated by reduced levels of phosphorylated AKT, percentage tumor growth inhibition (%TGI) ranged from 35% in the least sensitive to 84% in the most sensitive model. Several biomarkers showed significant association with resistance, including elevated baseline levels of growth factor receptors (EGFR, pHER3 Y1197), PI3Kp85 regulatory subunit, anti-apoptotic protein BclXL, EMT (Vimentin, MMP9, IntegrinaV), NFKB pathway (IkappaB, RANKL), and intracellular signaling molecules including Caveolin, CBP, and KLF4, as well as treatment-induced increases in the levels of phosphorylated forms of Aurora kinases. Interestingly, increased AKT phosphorylation or PTEN loss at baseline were not significantly correlated to %TGI. These results provide important insights into biomarker development for PI3K inhibitors in TNBC.
Language	English
Publishing date	2020-12-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12123857
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Article ; Online: Immune Checkpoint Profiles in Luminal B Breast Cancer (Alliance).

Anurag, Meenakshi / Zhu, Mayanne / Huang, Chen / Vasaikar, Suhas / Wang, Junkai / Hoog, Jeremy / Burugu, Samantha / Gao, Dongxia / Suman, Vera / Zhang, Xiang H / Zhang, Bing / Nielsen, Torsten / Ellis, Matthew J

Journal of the National Cancer Institute

2019 Volume 112, Issue 7, Page(s) 737–746

Abstract: Background: Unlike estrogen receptor (ER)-negative breast cancer, ER-positive breast cancer outcome is less influenced by lymphocyte content, indicating the presence of immune tolerance mechanisms that may be specific to this disease subset.: Methods!# ...

Abstract	Background: Unlike estrogen receptor (ER)-negative breast cancer, ER-positive breast cancer outcome is less influenced by lymphocyte content, indicating the presence of immune tolerance mechanisms that may be specific to this disease subset. Methods: A supervised analysis of microarray data from the ACOSOG Z1031 (Alliance) neoadjuvant aromatase inhibitor (AI) trial identified upregulated genes in Luminal (Lum) B breast cancers that correlated with AI-resistant tumor proliferation (percentage of Ki67-positive cancer nuclei, Pearson r > 0.4) (33 cases Ki67 > 10% on AI) vs LumB breast cancers that were more AI sensitive (33 cases Ki67 < 10% on AI). Overrepresentation analysis was performed using WebGestalt. All statistical tests were two-sided. Results: Thirty candidate genes positively correlated (r ≥ 0.4) with AI-resistant proliferation in LumB and were upregulated greater than twofold. Gene ontologies identified that the targetable immune checkpoint (IC) components IDO1, LAG3, and PD1 were overrepresented resistance candidates (P ≤ .001). High IDO1 mRNA was associated with poor prognosis in LumB disease (Molecular Taxonomy of Breast Cancer International Consortium, hazard ratio = 1.43, 95% confidence interval = 1.04 to 1.98, P = .03). IDO1 also statistically significantly correlated with STAT1 at protein level in LumB disease (Pearson r = 0.74). As a composite immune tolerance signature, expression of IFN-γ/STAT1 pathway components was associated with higher baseline Ki67, lower estrogen, and progesterone receptor mRNA levels and worse disease-specific survival (P = .002). In a tissue microarray analysis, IDO1 was observed in stromal cells and tumor-associated macrophages, with a higher incidence in LumB cases. Furthermore, IDO1 expression was associated with a macrophage mRNA signature (M1 by CIBERSORT Pearson r = 0.62 ) and by tissue microarray analysis. Conclusions: Targetable IC components are upregulated in the majority of endocrine therapy-resistant LumB cases. Our findings provide rationale for IC inhibition in poor-outcome ER-positive breast cancer.
MeSH term(s)	Antigens, CD/biosynthesis ; Antigens, CD/genetics ; Antigens, CD/immunology ; Antineoplastic Agents, Hormonal/therapeutic use ; Aromatase Inhibitors/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/immunology ; Cell Proliferation/physiology ; Drug Resistance, Neoplasm ; Female ; Humans ; Immune Tolerance ; Indoleamine-Pyrrole 2,3,-Dioxygenase/biosynthesis ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics ; Indoleamine-Pyrrole 2,3,-Dioxygenase/immunology ; Interferon-gamma/metabolism ; Letrozole/therapeutic use ; Prognosis ; Programmed Cell Death 1 Receptor/biosynthesis ; Programmed Cell Death 1 Receptor/genetics ; Programmed Cell Death 1 Receptor/immunology ; STAT1 Transcription Factor/metabolism ; Signal Transduction ; Tissue Array Analysis ; Transcriptome ; Up-Regulation
Chemical Substances	Antigens, CD ; Antineoplastic Agents, Hormonal ; Aromatase Inhibitors ; CD223 antigen ; IDO1 protein, human ; IFNG protein, human ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; PDCD1 protein, human ; Programmed Cell Death 1 Receptor ; STAT1 Transcription Factor ; STAT1 protein, human ; Letrozole (7LKK855W8I) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2019-10-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2992-0
ISSN	1460-2105 ; 0027-8874 ; 0198-0157
ISSN (online)	1460-2105
ISSN	0027-8874 ; 0198-0157
DOI	10.1093/jnci/djz213
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Article ; Online: Cytokine sensitivity screening highlights BMP4 pathway signaling as a therapeutic opportunity in ER

Shee, Kevin / Jiang, Amanda / Varn, Frederick S / Liu, Stephanie / Traphagen, Nicole A / Owens, Philip / Ma, Cynthia X / Hoog, Jeremy / Cheng, Chao / Golub, Todd R / Straussman, Ravid / Miller, Todd W

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2018 Volume 33, Issue 2, Page(s) 1644–1657

Abstract: Despite the success of approved systemic therapies for estrogen receptor α (ER)-positive breast cancer, drug resistance remains common. We hypothesized that secreted factors from the human tumor microenvironment could modulate drug resistance. We ... ...

Abstract	Despite the success of approved systemic therapies for estrogen receptor α (ER)-positive breast cancer, drug resistance remains common. We hypothesized that secreted factors from the human tumor microenvironment could modulate drug resistance. We previously screened a library of 297 recombinant-secreted microenvironmental proteins for the ability to confer resistance to the anti-estrogen fulvestrant in 2 ER
MeSH term(s)	Androgen Antagonists/therapeutic use ; Bone Morphogenetic Protein 4/metabolism ; Bone Morphogenetic Protein Receptors, Type I/genetics ; Bone Morphogenetic Protein Receptors, Type I/metabolism ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cyclin-Dependent Kinase 4/metabolism ; Cyclin-Dependent Kinase 6/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cytokines/metabolism ; Female ; Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Receptors, Estrogen/metabolism ; Signal Transduction ; Survival Analysis ; Transcriptome ; Tumor Microenvironment
Chemical Substances	Androgen Antagonists ; BMP4 protein, human ; Bone Morphogenetic Protein 4 ; CDKN1A protein, human ; Cyclin-Dependent Kinase Inhibitor p21 ; Cytokines ; Receptors, Estrogen ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; CDK4 protein, human (EC 2.7.11.22) ; CDK6 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Cyclin-Dependent Kinase 6 (EC 2.7.11.22) ; BMPR1A protein, human (EC 2.7.11.30) ; Bone Morphogenetic Protein Receptors, Type I (EC 2.7.11.30)
Language	English
Publishing date	2018-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201801241R
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Article ; Online: Preclinical PET imaging of glycoprotein non-metastatic melanoma B in triple negative breast cancer: feasibility of an antibody-based companion diagnostic agent.

Marquez-Nostra, Bernadette V / Lee, Supum / Laforest, Richard / Vitale, Laura / Nie, Xingyu / Hyrc, Krzysztof / Keler, Tibor / Hawthorne, Thomas / Hoog, Jeremy / Li, Shunqiang / Dehdashti, Farrokh / Ma, Cynthia X / Lapi, Suzanne E

Oncotarget

2017 Volume 8, Issue 61, Page(s) 104303–104314

Abstract: High levels of expression of glycoprotein non-metastatic B (gpNMB) in triple negative breast cancer (TNBC) and its association with metastasis and recurrence make it an attractive target for therapy with the antibody drug conjugate, glembatumumab vedotin ...

Abstract	High levels of expression of glycoprotein non-metastatic B (gpNMB) in triple negative breast cancer (TNBC) and its association with metastasis and recurrence make it an attractive target for therapy with the antibody drug conjugate, glembatumumab vedotin (CDX-011). This report describes the development of a companion PET-based diagnostic imaging agent using
Language	English
Publishing date	2017-11-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.22228
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Article ; Online: Development of a Ki-67-based clinical trial assay for neoadjuvant endocrine therapy response monitoring in breast cancer.

Goncalves, Rodrigo / DeSchryver, Katherine / Ma, Cynthia / Tao, Yu / Hoog, Jeremy / Cheang, Maggie / Crouch, Erika / Dahiya, Neha / Sanati, Souzan / Barnes, Michael / Sarian, Luis Otávio Zanatta / Olson, John / Allred, Donald Craig / Ellis, Matthew J

Breast cancer research and treatment

2017 Volume 165, Issue 2, Page(s) 355–364

Abstract: Purpose: The recent publication of the ACOSOG Z1031 trial results demonstrated that Ki-67 proliferation marker-based neoadjuvant endocrine therapy response monitoring could be used for tailoring the use of adjuvant chemotherapy in ER+HER2-negative ... ...

Abstract	Purpose: The recent publication of the ACOSOG Z1031 trial results demonstrated that Ki-67 proliferation marker-based neoadjuvant endocrine therapy response monitoring could be used for tailoring the use of adjuvant chemotherapy in ER+HER2-negative breast cancer patients. In this paper, we describe the development of the Ki-67 clinical trial assay used for this study. Methods: Ki-67 assay assessment focused on reproducing a 2.7% Ki-67 cut-point (CP) required for calculating the Preoperative Endocrine Prognostic Index and a 10% CP for poor endocrine therapy response identification within the first month of neoadjuvant endocrine treatment. Image analysis was assessed to increase the efficiency of the scoring process. Clinical outcome concordance for two independent Ki-67 scores was the primary performance metric. Results: Discordant scores led to a triage approach where cases with complex histological features that software algorithms could not resolve were flagged for visual point counting (17%). The final Ki-67 scoring approach was run on T1/2 N0 cases from the P024 and POL trials (N = 58). The percent positive agreement for the 2.7% CP was 87.5% (95% CI 61.7-98.5%); percent negative agreement 88.9% (95% CI: 65.3-98.6%). Minor discordance did not affect the ability to predict similar relapse-free outcomes (Log-Rank P = 0.044 and P = 0.055). The data for the 10% early triage CP in the POL trial were similar (N = 66), the percentage positive agreement was 100%, and percent negative agreement 93.55% (95% CI: 78.58-99.21%). The independent survival predictions were concordant (Log-rank P = 0.0001 and P = 0.01). Conclusions: We have developed an efficient and reproducible Ki-67 scoring system that was approved by the Clinical Trials Evaluation Program for NCI-supported neoadjuvant endocrine therapy trials. Using the methodology described here, investigators are able to identify a subgroup of patients with ER+HER2-negative breast cancer that can be safely managed without the need of adjuvant chemotherapy.
Language	English
Publishing date	2017-09
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	604563-7
ISSN	1573-7217 ; 0167-6806
ISSN (online)	1573-7217
ISSN	0167-6806
DOI	10.1007/s10549-017-4329-y
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