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index medicus (19) 19
animals (17) 17
mice (13) 13
oncology (12) 12
female (11) 11
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drug resistance, neoplasm - genetics (7) 7
expression (7) 7
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article (6) 6
brca1 (6) 6
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cell biology (5) 5
drug resistance (5) 5
drug-resistance (5) 5
mammary neoplasms, animal - drug therapy (5) 5
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poly polymerase inhibitors (5) 5
tumors (5) 5
antineoplastic agents - therapeutic use (4) 4
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breast-cancer (4) 4
conditional mouse model (4) 4
disease models, animal (4) 4
gene (4) 4
genes, brca1 (4) 4
genes, p53 (4) 4
genetic aspects (4) 4
in-vivo (4) 4
mammary neoplasms, animal - genetics (4) 4
mammary neoplasms, animal - pathology (4) 4
mammary neoplasms, experimental - drug therapy (4) 4
multidisciplinary sciences (4) 4
poly polymerase (4) 4
rodents (4) 4
adenocarcinoma (3) 3
brca1 protein - deficiency (3) 3
breast neoplasms - metabolism (3) 3
deoxyribonucleic acid--dna (3) 3
dna damage (3) 3
dna repair (3) 3
gene expression (3) 3
health aspects (3) 3
homologous recombination (3) 3
identification (3) 3
mammary neoplasms, experimental - genetics (3) 3
mutation (3) 3
phthalazines - therapeutic use (3) 3
piperazines - therapeutic use (3) 3
proteins (3) 3
resistance (3) 3
sensitivity (3) 3
stem-cells (3) 3
53bp1 (2) 2
analysis (2) 2
antibiotics, antineoplastic - pharmacology (2) 2
antigens (2) 2
antineoplastic agents - administration & dosage (2) 2
atp binding cassette transporter, sub-family b - genetics (2) 2
atp binding cassette transporter, subfamily b (2) 2
atp binding cassette transporter, subfamily g, member 2 (2) 2
atp-binding cassette, sub-family b, member 1 - biosynthesis (2) 2
atp-binding cassette, sub-family b, member 1 - deficiency (2) 2
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biological sciences (2) 2
biology (2) 2
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cell line, tumor (2) 2
cell lung-cancer (2) 2
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deletion (2) 2
dna-binding proteins - metabolism (2) 2
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doxorubicin - pharmacology (2) 2
doxorubicin - therapeutic use (2) 2
drug resistance, neoplasm (2) 2
enzyme inhibitors - administration & dosage (2) 2
enzyme inhibitors - therapeutic use (2) 2
epithelium (2) 2
gene deletion (2) 2
gene expression profiling (2) 2
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1. Full Text REV7 counteracts DNA double-strand break resection and affects PARP inhibition
by Xu, Guotai and Chapman, J. Ross and Brandsma, Inger and Yuan, Jingsong and Mistrik, Martin and Bouwman, Peter and Bartkova, Jirina and Gogola, Ewa and Warmerdam, Daniël and Barazas, Marco and Jaspers, Janneke E and Watanabe, Kenji and Pieterse, Mark and Kersbergen, Ariena and Sol, Wendy and Celie, Patrick H. N and Schouten, Philip C and van den Broek, Bram and Salman, Ahmed and Nieuwland, Marja and de Rink, Iris and de Ronde, Jorma and Jalink, Kees and Boulton, Simon J and Chen, Junjie and van Gent, Dik C and Bartek, Jiri and Jonkers, Jos and Borst, Piet and Rottenberg, Sven
Nature, ISSN 0028-0836, 2015, Volume 521, Issue 7553, pp. 541 - U308
Error-free repair of DNA double-strand breaks (DSBs) is achieved by homologous recombination (HR), and BRCA1 is an important factor for this repair pathway(1).... 
CELLS | REPAIR | COMPLEX | CLASS SWITCH RECOMBINATION | POL-ZETA | 53BP1 | MULTIDISCIPLINARY SCIENCES | RESISTANCE | DAMAGE | POLYMERASE-ZETA | Chromatin - metabolism | Mad2 Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins - metabolism | Humans | Intracellular Signaling Peptides and Proteins - metabolism | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | BRCA1 Protein - metabolism | Ataxia Telangiectasia Mutated Proteins - antagonists & inhibitors | Mad2 Proteins - deficiency | BRCA1 Protein - deficiency | Cell Line | Recombinational DNA Repair | Chromosomal Proteins, Non-Histone - metabolism | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Poly(ADP-ribose) Polymerase Inhibitors | BRCA1 Protein - genetics | Drug Resistance, Neoplasm - genetics | Animals | Mad2 Proteins - genetics | Trans-Activators - metabolism | Mice | Histones - metabolism | Tumor Suppressor p53-Binding Protein 1 | Immunoglobulin Class Switching - genetics | Ionizing radiation | Automated teller machines | Drug resistance | Analysis | DNA damage | Proteins | Rodents | Gene expression | DNA repair | Deoxyribonucleic acid--DNA | Tumors | Defects | Index Medicus
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2. Full Text High Sensitivity of BRCA1-Deficient Mammary Tumors to the PARP Inhibitor AZD2281 Alone and in Combination with Platinum Drugs
by Sven Rottenberg and Janneke E. Jaspers and Ariena Kersbergen and Eline van der Burg and Anders O. H. Nygren and Serge A. L. Zander and Patrick W. B. Derksen and Michiel de Bruin and John Zevenhoven and Alan Lau and Robert Boulter and Aaron Cranston and Mark J. O'Connor and Niall M. B. Martin and Piet Borst and Jos Jonkers
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 11/2008, Volume 105, Issue 44, pp. 17079 - 17084
Whereas target-specific drugs are available for treating ERBB2-overexpressing and hormone receptor-positive breast cancers, no tailored therapy exists for... 
Tumor burden | Relapse | Platinum | Medical treatment | Antineoplastics | Antibodies | Breast cancer | Genetic mutation | Tumors | Cancer | P-glycoprotein | Drug resistance | DNA repair | GEMM | POLY(ADP-RIBOSE) POLYMERASE | MULTIDISCIPLINARY SCIENCES | breast cancer | CONDITIONAL MOUSE MODEL | BRCA1 MUTATIONS | BREAST-CANCER | GENOMIC STABILITY | THERAPY | GENE | drug resistance | DNA-REPAIR | MULTIDRUG-RESISTANCE | Neoplasm Transplantation | DNA Repair - drug effects | Mice, Transgenic | Antineoplastic Agents - therapeutic use | Piperazines - therapeutic use | Poly(ADP-ribose) Polymerase Inhibitors | Platinum Compounds - therapeutic use | BRCA1 Protein - genetics | Drug Resistance, Neoplasm - genetics | Mammary Neoplasms, Animal - pathology | Phthalazines - therapeutic use | Animals | Poly(ADP-ribose) Polymerases - genetics | Cisplatin - therapeutic use | Female | Mammary Neoplasms, Animal - drug therapy | Mice | DNA Damage | Aromatase Inhibitors - therapeutic use | Mammary Neoplasms, Animal - genetics | Genetic aspects | Glycoproteins | Research | Drug therapy | Properties | Health aspects | Index Medicus | Biological Sciences
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3. Full Text FGFR3-TACC3 is an oncogenic fusion protein in respiratory epithelium
by Best, Sarah A and Harapas, Cassandra R and Kersbergen, Ariena and Rathi, Vivek and Asselin-Labat, Marie-Liesse and Sutherland, Kate D
Oncogene, ISSN 0950-9232, 11/2018, Volume 37, Issue 46, pp. 6096 - 6104
Structural rearrangements of the genome can drive lung tumorigenesis through the generation of fusion genes with oncogenic properties. Advanced genomic... 
OF-ORIGIN | STEM-CELLS | ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | MEDIATED GENE-TRANSFER | IDENTIFICATION | CELL BIOLOGY | CELL LUNG-CANCER | ONCOLOGY | MOUSE MODEL | IN-VIVO | GENETICS & HEREDITY | TUMOR-SUPPRESSOR | CARCINOMA | Care and treatment | Development and progression | Genetic aspects | Gene expression | Lung cancer, Non-small cell | Health aspects | Fibroblast growth factor receptors | Fibroblast growth factor | Transformation | Recombination | Epithelial cells | p53 Protein | Transgenic mice | Non-small cell lung carcinoma | Genomes | Epithelium | Cre recombinase | Respiratory tract | Lungs | Nose | Rodents | Tumor suppressor genes | Tumorigenesis | Olfactory epithelium | Fusion protein | Fibroblast growth factor receptor 3
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4. Full Text Selected alkylating agents can overcome drug tolerance of G0-like tumor cells and eradicate BRCA1-deficient mammary tumors in mice
by Pajic, Marina and Blatter, Sohvi and Guyader, Charlotte and Gonggrijp, Maaike and Kersbergen, Ariena and Küçükosmanoğlu, Aslı and Sol, Wendy and Drost, Rinske and Jonkers, Jos and Borst, Piet and Rottenberg, Sven
Clinical Cancer Research, ISSN 1078-0432, 11/2017, Volume 23, Issue 22, pp. 7020 - 7033
Purpose: We aimed to characterize and target drug-tolerant BRCA1-deficient tumor cells that cause residual disease and subsequent tumor relapse.Experimental... 
Drugs | BRCA1 protein | Tumor cells | p53 Protein | Alkylating agents | Fluorescence | Crosslinking | Breast cancer | Gene deletion | Cisplatin | Alkylation | Ubiquitination | Clonal deletion | Restoration | Experimental design | Platinum | Drug tolerance | Deletion | Genetic engineering | Deoxyribonucleic acid--DNA | Tumors | Cancer
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5. Full Text MVA.85A boosting of BCG and an attenuated, phoP deficient M. tuberculosis vaccine both show protective efficacy against tuberculosis in rhesus macaques
by Verreck, Frank A.W and Vervenne, Richard A.W and Kondova, Ivanela and van Kralingen, Klaas W and Remarque, Edmond J and Braskamp, Gerco and van der Werff, Nicole M and Kersbergen, Ariena and Ottenhoff, Tom H.M and Heidt, Peter J and Gilbert, Sarah C and Gicquel, Brigitte and Hill, Adrian V.S and Martin, Carlos and McShane, Helen and Thomas, Alan W
PLoS ONE, ISSN 1932-6203, 04/2009, Volume 4, Issue 4, pp. e5264 - e5264
Background: Continuous high global tuberculosis (TB) mortality rates and variable vaccine efficacy of Mycobacterium bovis Bacille Calmette-Guerin (BCG)... 
MYCOBACTERIUM-TUBERCULOSIS | ENHANCED IMMUNOGENICITY | IMMUNITY | RESPONSES | NONHUMAN PRIMATE MODEL | MVA85A | RECOMBINANT BCG | MULTIDISCIPLINARY SCIENCES | INFECTION | RESEMBLES | SUBUNIT VACCINE | Antigens | Tuberculosis vaccines | Tuberculosis | Health aspects | Vaccination | C-reactive protein | Disease | Identification methods | Zoology | Body weight | Medical services | Clinical trials | Viruses | Biosynthesis | Genomes | Monkeys | Infections | Body weight loss | Vaccines | Phylogeny | Sulfur dioxide | Bacteria | Attenuation | Parasitology | Effectiveness | Secretion | BCG | Animal sciences | Inflammation | Monkeys & apes | Animals | Immunogenicity | Lungs | γ-Interferon | Weight reduction
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6. Full Text Distinct initiating events underpin the immune and metabolic heterogeneity of KRAS-mutant lung adenocarcinoma
by Best, SA and Ding, S and Kersbergen, A and Dong, XY and Song, JY and Xie, Y and Reljic, B and Li, KM and Vince, JE and Rathi, V and Wright, GM and Ritchie, ME and Sutherland, KD
NATURE COMMUNICATIONS, ISSN 2041-1723, 09/2019, Volume 10, Issue 1, pp. 4190 - 14
The KRAS oncoprotein, a critical driver in 33% of lung adenocarcinoma (LUAD), has remained an elusive clinical target due to its perceived undruggable nature.... 
P-31 NMR | SERINE BIOSYNTHESIS | CELLS-OF-ORIGIN | NRF2 | MULTIDISCIPLINARY SCIENCES | 6-AMINONICOTINAMIDE | KEAP1 | DRIVEN | IDENTIFICATION | CANCER | EXPRESSION | Antioxidants | Adenocarcinoma | Heterogeneity | Pentose phosphate | Lung cancer | Pentose | Pentose phosphate pathway | Mutation | Macrophages | Alveoli | Tumors
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7. Full Text Combining cell type-restricted adenoviral targeting with immunostaining and flow cytometry to identify cells-of-origin of lung cancer
by Best, Sarah A and Kersbergen, Ariena and Asselin-Labat, Marie-Liesse and Sutherland, Kate D
Methods in Molecular Biology, ISSN 1064-3745, 2018, Volume 1725, pp. 15 - 29
Lung cancers display considerable intertumoral heterogeneity, leading to the classification of distinct tumor subtypes. Our understanding of the genetic... 
Flow cytometry | Recombinant adenovirus | Cells-of-origin | Immunohistochemical staining | Intra-tracheal injection | Tissue dissociation | Lung Neoplasms - genetics | Genetic Therapy | Flow Cytometry - methods | Transduction, Genetic | Genetic Vectors - administration & dosage | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Tumor Suppressor Protein p53 - genetics | Mice, Knockout | Immunohistochemistry - methods | Adenocarcinoma - diagnosis | Animals | Adenoviridae - genetics | Integrases - metabolism | Adenocarcinoma - genetics | Mice | Mutation | Tumor Cells, Cultured | Lung Neoplasms - diagnosis | Integrases - genetics | Disease Models, Animal
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8. Full Text Loss of 53BP1 causes PARP inhibitor resistance in Brca1-mutated mouse mammary tumors
by Jaspers, Janneke E and Kersbergen, Ariena and Boon, Ute and Sol, Wendy and van Deemter, Liesbeth and Zander, Serge A and st, Rinske and Wientjens, Ellen and Ji, Jiuping and Aly, Amal and Doroshow, James H and Cranston, Aaron and Martin, Niall M. B and Lau, Alan and O'Connor, Mark J and Ganesan, Shridar and Borst, Piet and Jonkers, Jos and Rottenberg, Sven
Cancer discovery, ISSN 2159-8290, 2013, Volume 3, Issue 1, pp. 68 - 81
Inhibition of PARP is a promising therapeutic strategy for homologous recombination-deficient tumors, such as BRCA1-associated cancers. We previously reported... 
POLY(ADP-RIBOSE) POLYMERASE | ONCOLOGY | STRAND-BREAK REPAIR | SENSITIVITY | CELL-CYCLE | HOMOLOGOUS RECOMBINATION | OVARIAN CARCINOMAS | BRCA1 | DNA-END RESECTION | CHEMOTHERAPY RESISTANCE | BRCA2-DEFICIENT TUMORS | Drug Resistance, Neoplasm | Antineoplastic Agents - therapeutic use | Piperazines - therapeutic use | DNA-Binding Proteins - genetics | Enzyme Inhibitors - therapeutic use | Poly(ADP-ribose) Polymerase Inhibitors | Chromosomal Proteins, Non-Histone - genetics | BRCA1 Protein - genetics | Phthalazines - therapeutic use | Animals | Piperidines - therapeutic use | Cell Line, Tumor | ATP-Binding Cassette, Sub-Family B, Member 1 - deficiency | Female | Mammary Neoplasms, Animal - drug therapy | Mice | DNA Damage | Mutation | Tumor Suppressor p53-Binding Protein 1
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9. Full Text Synergy between the KEAP1/NRF2 and PI3K Pathways Drives Non-Small-Cell Lung Cancer with an Altered Immune Microenvironment
by Best, Sarah A and De Souza, David P and Kersbergen, Ariena and Policheni, Antonia N and Dayalan, Saravanan and Tull, Dedreia and Rathi, Vivek and Gray, Daniel H and Ritchie, Matthew E and McConville, Malcolm J and Sutherland, Kate D
Cell Metabolism, ISSN 1550-4131, 04/2018, Volume 27, Issue 4, pp. 935 - 943.e4
The lung presents a highly oxidative environment, which is tolerated through engagement of tightly controlled stress response pathways. A critical stress... 
Keap1 | PD-L1 | Pten | Nrf2 | Taldo1 | non-small-cell lung cancer | STEM-CELLS | ORIGIN | NRF2 | LANDSCAPE | ADENOCARCINOMA | INFLAMMATION | ENDOCRINOLOGY & METABOLISM | BLOCKADE | CARCINOMA | EXPRESSION | DELETION | CELL BIOLOGY | Phosphates | Respiratory agents | Metabolites | Lung cancer, Non-small cell | Stem cells
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10. Full Text Selected Alkylating Agents Can Overcome Drug Tolerance of G 0 -like Tumor Cells and Eradicate BRCA1-Deficient Mammary Tumors in Mice
by Pajic, Marina and Blatter, Sohvi and Guyader, Charlotte and Gonggrijp, Maaike and Kersbergen, Ariena and Küçükosmanoğlu, Aslι and Sol, Wendy and Drost, Rinske and Jonkers, Jos and Borst, Piet and Rottenberg, Sven
Clinical cancer research : an official journal of the American Association for Cancer Research, ISSN 1078-0432, 11/2017, Volume 23, Issue 22, p. 7020
We aimed to characterize and target drug-tolerant BRCA1-deficient tumor cells that cause residual disease and subsequent tumor relapse. We studied responses to... 
Humans | Antineoplastic Agents, Alkylating - pharmacology | Cisplatin - pharmacology | Breast Neoplasms - drug therapy | Mice, Knockout | Dose-Response Relationship, Drug | Nimustine - pharmacology | Drug Resistance, Neoplasm - genetics | Genes, p53 | Animals | Breast Neoplasms - genetics | Resting Phase, Cell Cycle - genetics | Breast Neoplasms - pathology | Breast Neoplasms - mortality | Female | Resting Phase, Cell Cycle - drug effects | Mice | Genes, BRCA1 | Disease Models, Animal
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11. Full Text Tumor-initiating cells are not enriched in cisplatin-surviving BRCA1;p53-deficient mammary tumor cells in vivo
by Pajic, Marina and Kersbergen, Ariena and van Diepen, Frank and Pfauth, Anita and Jonkers, Jos and Borst, Piet and Rottenberg, Sven
Cell Cycle, ISSN 1538-4101, 09/2010, Volume 9, Issue 18, pp. 3780 - 3791
Although many breast cancers respond to chemotherapy or hormonal therapy, lack of tumor eradication is a central clinical problem preceding the development of... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Tumor-initiating cells | Breast cancer | Genetically-engineered mouse model | BRCA1 | Cisplatin | CHEMOSENSITIVITY | DNA-DAMAGE RESPONSE | tumor-initiating cells | breast cancer | CONDITIONAL MOUSE MODEL | IDENTIFICATION | CHEMOTHERAPY | CANCER STEM-CELLS | P53 | CELL BIOLOGY | BREAST-CANCER | genetically-engineered mouse model | RESISTANCE | MUTATIONS | cisplatin | CD24 Antigen - metabolism | Drug Resistance, Neoplasm | Antineoplastic Agents - therapeutic use | Mice, Knockout | Integrin alpha6 - metabolism | Genes, p53 | Maximum Tolerated Dose | Animals | Cisplatin - therapeutic use | Neoplastic Stem Cells - classification | Gene Deletion | Female | Mice | Genes, BRCA1 | Mammary Neoplasms, Experimental - drug therapy | Report
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12. Full Text Radiosensitivity is an acquired vulnerability of PARPI-resistant BRCA1-deficient tumors
by Barazas, Marco and Gasparini, Alessia and Huang, Yike and Küçükosmanoglu, Asli and Annunziato, Stefano and Bouwman, Peter and Sol, Wendy and Kersbergen, Ariena and Proost, Natalie and de Korte-Grimmerink, Renske and van de Ven, Marieke and Jonkers, Jos and Borst, Gerben R and Rottenberg, Sven
Cancer Research, ISSN 0008-5472, 2019, Volume 79, Issue 3, pp. 452 - 460
The defect in homologous recombination (HR) found in BRCA1-associated cancers can be therapeutically exploited by treatment with DNA-damaging agents and PARP... 
SENSITIVITY | MAMMARY-TUMORS | BRCA1 | ONCOLOGY | RESECTION | 53BP1
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13. Full Text Selective Loss of PARG Restores PARylation and Counteracts PARP Inhibitor-Mediated Synthetic Lethality
by Gogola, Ewa and Duarte, Alexandra A and de Ruiter, Julian R and Wiegant, Wouter W and Schmid, Jonas A and de Bruijn, Roebi and James, Dominic I and Guerrero Llobet, Sergi and Vis, Daniel J and Annunziato, Stefano and van den Broek, Bram and Barazas, Marco and Kersbergen, Ariena and van de Ven, Marieke and Tarsounas, Madalena and Ogilvie, Donald J and van Vugt, Marcel and Wessels, Lodewyk F.A and Bartkova, Jirina and Gromova, Irina and Andújar-Sánchez, Miguel and Bartek, Jiri and Lopes, Massimo and van Attikum, Haico and Borst, Piet and Jonkers, Jos and Rottenberg, Sven
Cancer Cell, ISSN 1535-6108, 06/2018, Volume 33, Issue 6, pp. 1078 - 1093.e12
Inhibitors of poly(ADP-ribose) (PAR) polymerase (PARPi) have recently entered the clinic for the treatment of homologous recombination (HR)-deficient cancers.... 
PARG | PARP1 | homologous recombination | PARP inhibitor | replication fork | BRCA1 | drug resistance | BRCA2 | PARylation | BREAST-CANCER | POLY(ADP-RIBOSE) POLYMERASE | REPAIR | MAMMARY-TUMORS | COMBINATION THERAPY | CONDITIONAL MOUSE MODEL | HOMOLOGOUS RECOMBINATION | REPLICATION FORK REVERSAL | DNA-DAMAGE-RESPONSE | DEFICIENT CELLS | ONCOLOGY | CELL BIOLOGY | Homologous Recombination - drug effects | Glycoside Hydrolases - genetics | Humans | Synthetic Lethal Mutations | Mice, 129 Strain | Breast Neoplasms - metabolism | Ovarian Neoplasms - genetics | BRCA1 Protein - metabolism | Female | Ovarian Neoplasms - metabolism | Ovarian Neoplasms - drug therapy | Glycoside Hydrolases - antagonists & inhibitors | Poly ADP Ribosylation - drug effects | Poly (ADP-Ribose) Polymerase-1 - metabolism | Breast Neoplasms - drug therapy | Poly (ADP-Ribose) Polymerase-1 - antagonists & inhibitors | Mice, Knockout | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Animals | Breast Neoplasms - genetics | Cell Line, Tumor | Homologous Recombination - genetics | Glycoside Hydrolases - metabolism | Poly (ADP-Ribose) Polymerase-1 - genetics | Drug resistance | Analysis | Sugars | Monosaccharides
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14. Full Text Lung morphogenesis is orchestrated through Grainyhead-like 2 (Grhl2) transcriptional programs
by Kersbergen, Ariena and Best, Sarah A and Dworkin, Sebastian and Ah-Cann, Casey and de Vries, Michael E and Asselin-Labat, Marie-Liesse and Ritchie, Matthew E and Jane, Stephen M and Sutherland, Kate D
Developmental Biology, ISSN 0012-1606, 11/2018, Volume 443, Issue 1, pp. 1 - 9
The highly conserved transcription factor Grainyhead-like 2 (Grhl2) exhibits a dynamic expression pattern in lung epithelium throughout embryonic development.... 
Lung morphogenesis | Progenitor cells | Elf5 | Grhl2 | HEAD | STEM-CELLS | BRANCHING MORPHOGENESIS | DEVELOPMENTAL BIOLOGY | MULTIPLE ROLES | BRONCHOPULMONARY DYSPLASIA | EPITHELIUM | GENE | GROWTH | CELL DIFFERENTIATION | EXPRESSION | Transcription Factors - physiology | Epithelium - metabolism | Saccule and Utricle - metabolism | Down-Regulation | Respiratory Function Tests - methods | Alveolar Epithelial Cells - metabolism | Gene Expression Profiling | Lung - physiology | Mice - embryology | DNA-Binding Proteins - metabolism | Transcription Factors - metabolism | Animals | Lung - embryology | Cell Differentiation | Lung - metabolism | SOX9 Transcription Factor | Alveolar Epithelial Cells - physiology | Stem cell research | Embryonic development | Microbiology | Genes | Stem cells | Genetic aspects | Genetic transcription | Cell differentiation
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15. Full Text BRCA2-deficient sarcomatoid mammary tumors exhibit multidrug resistance
by Jaspers, Janneke E and Sol, Wendy and Kersbergen, Ariena and Schlicker, Andreas and Guyader, Charlotte and Xu, Guotai and Wessels, Lodewyk and Borst, Piet and Jonkers, Jos and Rottenberg, Sven
Cancer Research, ISSN 0008-5472, 02/2015, Volume 75, Issue 4, pp. 732 - 741
Pan or multidrug resistance is a central problem in clinical oncology. Here, we use a genetically engineered mouse model of BRCA2-associated hereditary breast... 
EPITHELIAL-MESENCHYMAL TRANSITION | GENE | ONCOLOGY | CHEMOTHERAPY RESPONSE | IN-VIVO | SENSITIVITY | BRCA2-MUTATED BREAST CANCERS | CONDITIONAL MOUSE MODEL | INDUCTION | EXPRESSION | BRCA2 MUTATION | ATP Binding Cassette Transporter, Subfamily B - biosynthesis | Drug Resistance, Multiple - genetics | Humans | Antineoplastic Agents - administration & dosage | Breast Neoplasms - drug therapy | Poly(ADP-ribose) Polymerase Inhibitors | Enzyme Inhibitors - administration & dosage | Drug Resistance, Neoplasm - genetics | Mammary Neoplasms, Animal - pathology | Animals | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Female | ATP Binding Cassette Transporter, Subfamily B - genetics | BRCA2 Protein - deficiency | Mammary Neoplasms, Animal - drug therapy | Mice | Gene Expression Regulation, Neoplastic - drug effects | BRCA2 Protein - genetics | Doxorubicin - administration & dosage | Mammary Neoplasms, Animal - genetics | Index Medicus
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