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Article: Genetic Modification of T Cells.

Morgan, Richard A / Boyerinas, Benjamin

2016 Volume 4, Issue 2

Abstract: Gene transfer technology and its application to human gene therapy greatly expanded in the last decade. One area of investigation that appears particularly promising is the transfer of new genetic material into T cells for the potential treatment of ... ...

Abstract	Gene transfer technology and its application to human gene therapy greatly expanded in the last decade. One area of investigation that appears particularly promising is the transfer of new genetic material into T cells for the potential treatment of cancer. Herein, we describe several core technologies that now yield high-efficiency gene transfer into primary human T cells. These gene transfer techniques include viral-based gene transfer methods based on modified
Language	English
Publishing date	2016-04-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines4020009
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Article ; Online: Metabolic reprogramming via an engineered PGC-1α improves human chimeric antigen receptor T-cell therapy against solid tumors.

Lontos, Konstantinos / Wang, Yiyang / Joshi, Supriya K / Frisch, Andrew T / Watson, McLane J / Kumar, Alok / Menk, Ashley V / Wang, Yupeng / Cumberland, Rachel / Lohmueller, Jason / Carrizosa, Esteban / Boyerinas, Benjamin / Delgoffe, Greg M

Journal for immunotherapy of cancer

2023 Volume 11, Issue 3

Abstract: Background: Cellular immunotherapies for cancer represent a means by which a patient's immune system can be augmented with high numbers of tumor-specific T cells. Chimeric antigen receptor (CAR) therapy involves genetic engineering to 'redirect' ... ...

Abstract	Background: Cellular immunotherapies for cancer represent a means by which a patient's immune system can be augmented with high numbers of tumor-specific T cells. Chimeric antigen receptor (CAR) therapy involves genetic engineering to 'redirect' peripheral T cells to tumor targets, showing remarkable potency in blood cancers. However, due to several resistance mechanisms, CAR-T cell therapies remain ineffective in solid tumors. We and others have shown the tumor microenvironment harbors a distinct metabolic landscape that produces a barrier to immune cell function. Further, altered differentiation of T cells within tumors induces defects in mitochondrial biogenesis, resulting in severe cell-intrinsic metabolic deficiencies. While we and others have shown murine T cell receptor (TCR)-transgenic cells can be improved through enhanced mitochondrial biogenesis, we sought to determine whether human CAR-T cells could be enabled through a metabolic reprogramming approach. Materials and methods: Anti-EGFR CAR-T cells were infused in NSG mice which bore A549 tumors. The tumor infiltrating lymphocytes were analyzed for exhaustion and metabolic deficiencies. Lentiviruses carrying PPAR-gamma coactivator 1α (PGC-1α), PGC-1α Results: Here, in this study, we show that an inhibition resistant, engineered version of PGC-1α, can metabolically reprogram human CAR-T cells. Transcriptomic profiling of PGC-1α-transduced CAR-T cells showed this approach effectively induced mitochondrial biogenesis, but also upregulated programs associated with effector functions. Treatment of immunodeficient animals bearing human solid tumors with these cells resulted in substantially improved in vivo efficacy. In contrast, a truncated version of PGC-1α, NT-PGC-1α, did not improve the in vivo outcomes. Conclusions: Our data further support a role for metabolic reprogramming in immunomodulatory treatments and highlight the utility of genes like PGC-1α as attractive candidates to include in cargo along with chimeric receptors or TCRs for cell therapy of solid tumors.
MeSH term(s)	Humans ; Animals ; Mice ; Receptors, Chimeric Antigen ; Immunotherapy, Adoptive/methods ; Neoplasms ; Receptors, Antigen, T-Cell ; T-Lymphocytes ; Tumor Microenvironment
Chemical Substances	Receptors, Chimeric Antigen ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2023-03-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2022-006522
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Article ; Online: Genetic Modification of T Cells

Richard A. Morgan / Benjamin Boyerinas

Biomedicines, Vol 4, Iss 2, p

2016 Volume 9

Abstract	Gene transfer technology and its application to human gene therapy greatly expanded in the last decade. One area of investigation that appears particularly promising is the transfer of new genetic material into T cells for the potential treatment of cancer. Herein, we describe several core technologies that now yield high-efficiency gene transfer into primary human T cells. These gene transfer techniques include viral-based gene transfer methods based on modified Retroviridae and non-viral methods such as DNA-based transposons and direct transfer of mRNA by electroporation. Where specific examples are cited, we emphasize the transfer of chimeric antigen receptors (CARs) to T cells, which permits engineered T cells to recognize potential tumor antigens.
Keywords	CAR (chimeric antigen receptor) T cells ; immunotherapy ; retroviral vector ; lentiviral vector ; CD19 CAR ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2016-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: HSPCs in the balance: The vascular niche.

Boyerinas, Benjamin / Sipkins, Dorothy A

Cell stem cell

2010 Volume 7, Issue 6, Page(s) 645–646

Language	English
Publishing date	2010-12-03
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2010.11.021
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Article ; Online: Adhesion to osteopontin in the bone marrow niche regulates lymphoblastic leukemia cell dormancy.

Boyerinas, Benjamin / Zafrir, Maya / Yesilkanal, Ali E / Price, Trevor T / Hyjek, Elizabeth M / Sipkins, Dorothy A

Blood

2013 Volume 121, Issue 24, Page(s) 4821–4831

Abstract: Malignant cells may evade death from cytotoxic agents if they are in a dormant state. The host microenvironment plays important roles in cancer progression, but how niches might control cancer cell dormancy is little understood. Here we show that ... ...

Abstract	Malignant cells may evade death from cytotoxic agents if they are in a dormant state. The host microenvironment plays important roles in cancer progression, but how niches might control cancer cell dormancy is little understood. Here we show that osteopontin (OPN), an extracellular matrix molecule secreted by osteoblasts, can function to anchor leukemic blasts in anatomic locations supporting tumor dormancy. We demonstrate that acute lymphoblastic leukemia (ALL) cells specifically adhere to OPN in vitro and secrete OPN when localized to the endosteal niche in vivo. Using intravital microscopy to perform imaging studies of the calvarial bone marrow (BM) of xenografted mice, we show that OPN is highly expressed adjacent to dormant tumor cells within the marrow. Inhibition of the OPN-signaling axis significantly increases the leukemic cell Ki-67 proliferative index and leads to a twofold increase in tumor burden in treated mice. Moreover, using cell-cycle-dependent Ara-C chemotherapy to produce minimal residual disease (MRD) in leukemic mice, we show that OPN neutralization synergizes with Ara-C to reduce detectable BM MRD. Taken together, these data suggest that ALL interacts with extracellular OPN within the malignant BM, and that this interaction induces cell cycle exit in leukemic blasts, protecting them from cytotoxic chemotherapy.
MeSH term(s)	Adult ; Animals ; Antibodies, Neutralizing/pharmacology ; Antimetabolites, Antineoplastic/pharmacology ; Blast Crisis/drug therapy ; Blast Crisis/genetics ; Blast Crisis/metabolism ; Blast Crisis/pathology ; Bone Marrow/metabolism ; Bone Marrow/pathology ; Cell Adhesion/drug effects ; Cell Adhesion/genetics ; Child ; Child, Preschool ; Cytarabine/pharmacology ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Female ; Humans ; Ki-67 Antigen/genetics ; Ki-67 Antigen/metabolism ; Male ; Mice ; Mice, SCID ; Neoplasm Transplantation ; Neoplasm, Residual/genetics ; Neoplasm, Residual/metabolism ; Neoplasm, Residual/pathology ; Osteoblasts/metabolism ; Osteoblasts/pathology ; Osteopontin/antagonists & inhibitors ; Osteopontin/genetics ; Osteopontin/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Signal Transduction ; Transplantation, Heterologous ; Tumor Microenvironment
Chemical Substances	Antibodies, Neutralizing ; Antimetabolites, Antineoplastic ; Ki-67 Antigen ; Cytarabine (04079A1RDZ) ; Osteopontin (106441-73-0)
Language	English
Publishing date	2013-04-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2012-12-475483
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Article ; Online: Antibody-Dependent Cellular Cytotoxicity Activity of a Novel Anti-PD-L1 Antibody Avelumab (MSB0010718C) on Human Tumor Cells.

Boyerinas, Benjamin / Jochems, Caroline / Fantini, Massimo / Heery, Christopher R / Gulley, James L / Tsang, Kwong Yok / Schlom, Jeffrey

Cancer immunology research

2015 Volume 3, Issue 10, Page(s) 1148–1157

Abstract: Several anti-PD-1/PD-L1 monoclonal antibodies (mAb) are currently providing evidence of clinical benefit in subsets of cancer patients. The mode of action of these mAbs is to inhibit PD-1 on immune cells interacting with PD-L1 on tumor cells. These mAbs ... ...

Abstract	Several anti-PD-1/PD-L1 monoclonal antibodies (mAb) are currently providing evidence of clinical benefit in subsets of cancer patients. The mode of action of these mAbs is to inhibit PD-1 on immune cells interacting with PD-L1 on tumor cells. These mAbs are either designed or engineered to eliminate antibody-dependent cell-mediated cytotoxicity (ADCC), which, however, has been implicated as an important mechanism in several highly effective mAb-mediated cancer therapies. A fully human anti-PD-L1 mAb would potentially be able to block PD-1/PD-L1 interactions and also mediate the ADCC lysis of tumor cells. MSB0010718C (designated avelumab) is a fully human IgG1 anti-PD-L1 mAb. The studies reported here demonstrate (i) the ability of avelumab to lyse a range of human tumor cells in the presence of PBMC or NK effectors; (ii) IFNγ can enhance tumor cell PD-L1 expression and, in some cases, enhance ADCC tumor cell lysis; (iii) purified NK cells are potent effectors for avelumab; (iv) similar levels of avelumab-mediated ADCC lysis of tumor cells are seen using purified NK as effectors from either healthy donors or cancer patients; (v) very low levels of avelumab-mediated lysis are seen using whole PBMCs as targets; this finding complements results seen in analyses of PBMC subsets of patients receiving avelumab; and (vi) the addition of IL12 to NK cells greatly enhances avelumab-mediated ADCC. These studies thus provide an additional mode of action for an anti-PD-L1 mAb and support the rationale for further studies to enhance avelumab-mediated ADCC activity.
MeSH term(s)	Antibodies, Monoclonal/pharmacology ; Antibody-Dependent Cell Cytotoxicity/drug effects ; Antibody-Dependent Cell Cytotoxicity/genetics ; Antibody-Dependent Cell Cytotoxicity/immunology ; Antineoplastic Agents/pharmacology ; B7-H1 Antigen/antagonists & inhibitors ; B7-H1 Antigen/genetics ; B7-H1 Antigen/metabolism ; Biomarkers, Tumor ; Cell Line, Tumor ; Cell Membrane/metabolism ; Gene Expression ; Genotype ; Humans ; Interferon-gamma/metabolism ; Interferon-gamma/pharmacology ; Interleukin-12/pharmacology ; Killer Cells, Natural/drug effects ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/metabolism ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/metabolism ; Receptors, IgG/genetics ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/metabolism
Chemical Substances	Antibodies, Monoclonal ; Antineoplastic Agents ; B7-H1 Antigen ; Biomarkers, Tumor ; FCGR3A protein, human ; Receptors, IgG ; Interleukin-12 (187348-17-0) ; Interferon-gamma (82115-62-6) ; avelumab (KXG2PJ551I)
Language	English
Publishing date	2015-05-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-15-0059
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Article ; Online: Identification and characterization of a cytotoxic T-lymphocyte agonist epitope of brachyury, a transcription factor involved in epithelial to mesenchymal transition and metastasis.

Tucker, Jo A / Jochems, Caroline / Boyerinas, Benjamin / Fallon, Jonathan / Greiner, John W / Palena, Claudia / Rodell, Timothy C / Schlom, Jeffrey / Tsang, Kwong-Yok

Cancer immunology, immunotherapy : CII

2014 Volume 63, Issue 12, Page(s) 1307–1317

Abstract: The transcription factor brachyury is a major driver of epithelial to mesenchymal transition in human carcinoma cells. It is overexpressed in several human tumor types versus normal adult tissues, except for testes and thyroid. Overexpression is ... ...

Abstract	The transcription factor brachyury is a major driver of epithelial to mesenchymal transition in human carcinoma cells. It is overexpressed in several human tumor types versus normal adult tissues, except for testes and thyroid. Overexpression is associated with drug resistance and poor prognosis. Previous studies identified a brachyury HLA-A2 cytotoxic T-lymphocyte epitope. The studies reported here describe an enhancer epitope of brachyury. Compared to the native epitope, the agonist epitope: (a) has enhanced binding to MHC class I, (b) increased the IFN-γ production from brachyury-specific T cells, (c) generated brachyury-specific T cells with greater levels of perforin and increased proliferation, (d) generated T cells more proficient at lysing human carcinoma cells endogenously expressing the native epitope, and (e) achieved greater brachyury-specific T-cell responses in vivo in HLA-A2 transgenic mice. These studies also report the generation of a heat-killed recombinant Saccharomyces cerevisiae (yeast) vector expressing the full-length brachyury gene encoding the agonist epitope. Compared to yeast-brachyury (native) devoid of the agonist epitope, the yeast-brachyury (agonist) enhanced the activation of brachyury-specific T cells, which efficiently lysed human carcinoma cells. In addition to providing the rationale for the recombinant yeast-brachyury (agonist) as a potential vaccine in cancer therapy, these studies also provide the rationale for the use of the agonist in (a) dendritic cell (DC) vaccines, (b) adjuvant or liposomal vaccines, (c) recombinant viral and/or bacterial vaccines, (d) protein/polypeptide vaccines, (e) activation of T cells ex vivo in adoptive therapy protocols, and (f) generation of genetically engineered targeted T cells.
MeSH term(s)	Animals ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition/immunology ; Epitopes, T-Lymphocyte/immunology ; Female ; Fetal Proteins/immunology ; Humans ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; T-Box Domain Proteins/immunology ; T-Lymphocytes, Cytotoxic/immunology
Chemical Substances	Epitopes, T-Lymphocyte ; Fetal Proteins ; T-Box Domain Proteins ; Brachyury protein (EQ43SC3GDB)
Language	English
Publishing date	2014-09-04
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-014-1603-2
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Article ; Online: The role of let-7 in cell differentiation and cancer.

Boyerinas, Benjamin / Park, Sun-Mi / Hau, Annika / Murmann, Andrea E / Peter, Marcus E

Endocrine-related cancer

2010 Volume 17, Issue 1, Page(s) F19–36

Abstract: MicroRNAs (miRNAs or miRs) are small noncoding RNAs capable of regulating gene expression at the translational level. Current evidence suggests that a significant portion of the human genome is regulated by microRNAs, and many reports have demonstrated ... ...

Abstract	MicroRNAs (miRNAs or miRs) are small noncoding RNAs capable of regulating gene expression at the translational level. Current evidence suggests that a significant portion of the human genome is regulated by microRNAs, and many reports have demonstrated that microRNA expression is deregulated in human cancer. The let-7 family of microRNAs, first discovered in Caenorhabditis elegans, is functionally conserved from worms to humans. The human let-7 family contains 13 members located on nine different chromosomes, and many human cancers have deregulated let-7 expression. A growing body of evidence suggests that restoration of let-7 expression may be a useful therapeutic option in cancers, where its expression has been lost. In this review, we discuss the role of let-7 in normal development and differentiation, and provide an overview of the relationship between deregulated let-7 expression and tumorigenesis. The regulation of let-7 expression, cancer-relevant let-7 targets, and the relationship between let-7 and drug sensitivity are highlighted.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacokinetics ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/growth & development ; Caenorhabditis elegans/physiology ; Cell Differentiation/physiology ; Cell Transformation, Neoplastic/genetics ; Drosophila melanogaster/genetics ; Drosophila melanogaster/growth & development ; Drug Resistance, Neoplasm/genetics ; Evolution, Molecular ; Female ; Gene Expression Regulation, Developmental ; Gene Expression Regulation, Neoplastic ; Humans ; Larva ; Male ; MicroRNAs/genetics ; MicroRNAs/physiology ; MicroRNAs/therapeutic use ; Multigene Family ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplasms/therapy ; RNA, Neoplasm/genetics ; Species Specificity
Chemical Substances	Antineoplastic Agents ; Let-7 microRNA, Drosophila ; MicroRNAs ; RNA, Neoplasm ; let-7 microRNA, C elegans ; mirnlet7 microRNA, human
Language	English
Publishing date	2010-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1218450-0
ISSN	1479-6821 ; 1351-0088
ISSN (online)	1479-6821
ISSN	1351-0088
DOI	10.1677/ERC-09-0184
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Article ; Online: Identification and characterization of agonist epitopes of the MUC1-C oncoprotein.

Jochems, Caroline / Tucker, Jo A / Vergati, Matteo / Boyerinas, Benjamin / Gulley, James L / Schlom, Jeffrey / Tsang, Kwong-Yok

Cancer immunology, immunotherapy : CII

2013 Volume 63, Issue 2, Page(s) 161–174

Abstract: The MUC1 tumor-associated antigen is overexpressed in the majority of human carcinomas and several hematologic malignancies. Much attention has been paid to the hypoglycosylated variable number of tandem repeats (VNTR) region of the N-terminus of MUC1 as ...

Abstract	The MUC1 tumor-associated antigen is overexpressed in the majority of human carcinomas and several hematologic malignancies. Much attention has been paid to the hypoglycosylated variable number of tandem repeats (VNTR) region of the N-terminus of MUC1 as a vaccine target, and recombinant viral vector vaccines are also being evaluated that express the entire MUC1 transgene. While previous studies have described MUC1 as a tumor-associated tissue differentiation antigen, studies have now determined that the C-terminus of MUC1 (MUC1-C) is an oncoprotein, and its expression is an indication of poor prognosis in numerous tumor types. We report here the identification of nine potential CD8⁺ cytotoxic T lymphocyte epitopes of MUC1, seven in the C-terminus and two in the VNTR region, and have identified enhancer agonist peptides for each of these epitopes. These epitopes span HLA-A2, HLA-A3, and HLA-A24 major histocompatibility complex (MHC) class I alleles, which encompass the majority of the population. The agonist peptides, compared to the native peptides, more efficiently (a) generate T-cell lines from the peripheral blood mononuclear cells of cancer patients, (b) enhance the production of IFN-γ by peptide-activated human T cells, and (c) lyse human tumor cell targets in an MHC-restricted manner. The agonist epitopes described here can be incorporated into various vaccine platforms and for the ex vivo generation of human T cells. These studies provide the rationale for the T-cell-mediated targeting of the oncogenic MUC1-C, which has been shown to be an important factor in both drug resistance and poor prognosis for numerous tumor types.
MeSH term(s)	CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; Epitopes, T-Lymphocyte/immunology ; HLA-A2 Antigen/immunology ; HLA-A24 Antigen/immunology ; HLA-A3 Antigen/immunology ; Humans ; Interferon-gamma/biosynthesis ; Minisatellite Repeats ; Mucin-1/immunology ; Neoplasms/immunology ; Peptide Fragments/immunology
Chemical Substances	Epitopes, T-Lymphocyte ; HLA-A2 Antigen ; HLA-A24 Antigen ; HLA-A3 Antigen ; Mucin-1 ; Peptide Fragments ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2013-11-15
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-013-1494-7
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Article ; Online: Let-7 modulates acquired resistance of ovarian cancer to Taxanes via IMP-1-mediated stabilization of multidrug resistance 1.

Boyerinas, Benjamin / Park, Sun-Mi / Murmann, Andrea E / Gwin, Katja / Montag, Anton G / Zillhardt, Marion / Hua, You-Jia / Lengyel, Ernst / Peter, Marcus E

International journal of cancer

2011 Volume 130, Issue 8, Page(s) 1787–1797

Abstract: Ovarian cancer patients frequently develop resistance to chemotherapy regiments using Taxol and carboplatin. One of the resistance factors that protects cancer cells from Taxol-based therapy is multidrug resistance 1 (MDR1). micro(mi)RNAs are small ... ...

Abstract	Ovarian cancer patients frequently develop resistance to chemotherapy regiments using Taxol and carboplatin. One of the resistance factors that protects cancer cells from Taxol-based therapy is multidrug resistance 1 (MDR1). micro(mi)RNAs are small noncoding RNAs that negatively regulate protein expression. Members of the let-7 family of miRNAs are downregulated in many human cancers, and low let-7 expression has been correlated with resistance to microtubule targeting drugs (Taxanes), although little is known that would explain this activity. We now provide evidence that, although let-7 is not a universal sensitizer of cancer cells to Taxanes, it affects acquired resistance of cells to this class of drugs by targeting IMP-1, resulting in destabilization of the mRNA of MDR1. Introducing let-7g into ADR-RES cells expressing both IMP-1 and MDR1 reduced expression of both proteins rendering the cells more sensitive to treatment with either Taxol or vinblastine without affecting the sensitivity of the cells to carboplatin, a non-MDR1 substrate. This effect could be reversed by reintroducing IMP-1 into let-7g high/MDR1 low cells causing MDR1 to again become stabilized. Consistently, many relapsed ovarian cancer patients tested before and after chemotherapy were found to downregulate let-7 and to co-upregulate IMP-1 and MDR1, and the increase in the expression levels of both proteins after chemotherapy negatively correlated with disease-free time before recurrence. Our data point at IMP-1 and MDR1 as indicators for response to therapy, and at IMP-1 as a novel therapeutic target for overcoming multidrug resistance of ovarian cancer.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B, Member 1/genetics ; ATP Binding Cassette Transporter, Subfamily B, Member 1/metabolism ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Blotting, Western ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Disease-Free Survival ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; HEK293 Cells ; HeLa Cells ; Humans ; Immunohistochemistry ; In Situ Hybridization ; MicroRNAs/genetics ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; RNA Interference ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Taxoids/pharmacology ; Taxoids/therapeutic use
Chemical Substances	ATP Binding Cassette Transporter, Subfamily B, Member 1 ; Antineoplastic Agents ; DNA-Binding Proteins ; IGF2BP1 protein, human ; LIN28B protein, human ; MicroRNAs ; RNA, Messenger ; RNA-Binding Proteins ; Taxoids ; mirnlet7 microRNA, human
Language	English
Publishing date	2011-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.26190
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