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1. Full Text No small surprise – small cell carcinoma of the ovary, hypercalcaemic type, is a malignant rhabdoid tumour
by Foulkes, William D and Clarke, Blaise A and Hasselblatt, Martin and Majewski, Jacek and Albrecht, Steffen and McCluggage, W Glenn
The Journal of pathology, ISSN 0022-3417, 07/2014, Volume 233, Issue 3, pp. 209 - 214
SMARCB1 | rhabdoid tumour | small cell carcinoma of the ovary | hypercalcaemic type | Pathology | Oncology | Life Sciences & Biomedicine | Science & Technology | Immunohistochemistry | Carcinoma, Small Cell - genetics | Humans | Ovarian Neoplasms - pathology | Rhabdoid Tumor - pathology | Exome | Ovarian Neoplasms - genetics | SMARCB1 Protein | Carcinoma, Small Cell - chemistry | Female | Nuclear Proteins - genetics | DNA Helicases - genetics | Hypercalcemia - genetics | Genetic Predisposition to Disease | Ovarian Neoplasms - chemistry | Hypercalcemia - pathology | Genetic Association Studies | Biomarkers, Tumor - analysis | Rhabdoid Tumor - chemistry | Hypercalcemia - metabolism | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Sequence Analysis, DNA | Chromosomal Proteins, Non-Histone - genetics | Phenotype | Rhabdoid Tumor - genetics | Biomarkers, Tumor - genetics | Mutation | Carcinoma, Small Cell - pathology | Carcinoma | Ovarian cancer | Cancer | Index Medicus
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2. Full Text INI1-deficient tumors: Diagnostic features and molecular genetics
by Hollmann, Travis J and Hornick, Jason L
The American journal of surgical pathology, ISSN 0147-5185, 10/2011, Volume 35, Issue 10, pp. e47 - e63
malignant rhabdoid tumor | SMARCB1 | epithelioid sarcoma | schwannomatosis | SNF5 | soft tissue tumors | renal medullarycarcinoma | INI1 | Pathology | Life Sciences & Biomedicine | Surgery | Science & Technology | Myoepithelioma - metabolism | Kidney Neoplasms - genetics | Soft Tissue Neoplasms - diagnosis | Humans | Transcription Factors - deficiency | Carcinoma, Medullary - diagnosis | Carcinoma, Medullary - metabolism | Kidney Neoplasms - metabolism | DNA-Binding Proteins - deficiency | Kidney Neoplasms - diagnosis | DNA-Binding Proteins - metabolism | SMARCB1 Protein | Biomarkers, Tumor - metabolism | Sarcoma - diagnosis | Cytogenetic Analysis | Rhabdoid Tumor - metabolism | Sarcoma - genetics | Soft Tissue Neoplasms - genetics | Epithelioid Cells - pathology | Myoepithelioma - diagnosis | Chondrosarcoma - diagnosis | Chromosomal Proteins, Non-Histone - metabolism | Carcinoma, Medullary - genetics | Nerve Sheath Neoplasms - diagnosis | Soft Tissue Neoplasms - metabolism | Nerve Sheath Neoplasms - metabolism | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Chromosomal Proteins, Non-Histone - deficiency | Chromosomal Proteins, Non-Histone - genetics | Epithelioid Cells - metabolism | Immunohistochemistry - methods | Sarcoma - metabolism | Transcription Factors - metabolism | Rhabdoid Tumor - genetics | Rhabdoid Tumor - diagnosis | Index Medicus
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3. Full Text Inhibition of MYC attenuates tumor cell self‐renewal and promotes senescence in SMARCB1‐deficient Group 2 atypical teratoid rhabdoid tumors to suppress tumor growth in vivo
by Alimova, Irina and Pierce, Angela and Danis, Etienne and Donson, Andrew and Birks, Diane K and Griesinger, Andrea and Foreman, Nicholas K and Santi, Mariarita and Soucek, Laura and Venkataraman, Sujatha and Vibhakar, Rajeev
International journal of cancer, ISSN 0020-7136, 04/2019, Volume 144, Issue 8, pp. 1983 - 1995
rhabdoid tumor | SMARCB1 | ATRT | MYC | SWI/SNF complex | Life Sciences & Biomedicine | Oncology | Science & Technology | Chromatin - metabolism | Humans | Cellular Senescence - drug effects | SMARCB1 Protein - genetics | Rhabdoid Tumor - pathology | Cell Self Renewal - drug effects | Cell Self Renewal - genetics | Bone Morphogenetic Proteins - metabolism | Cell Transformation, Neoplastic - genetics | Female | Gene Expression Regulation, Neoplastic - drug effects | Bone Morphogenetic Proteins - genetics | Gene Expression Regulation, Neoplastic - genetics | Cellular Senescence - genetics | Proto-Oncogene Proteins c-myc - metabolism | Azepines - pharmacology | Triazoles - pharmacology | Xenograft Model Antitumor Assays | Teratoma - pathology | Animals | Rhabdoid Tumor - genetics | Mice, Nude | Cell Line, Tumor | Teratoma - genetics | Mice | Proto-Oncogene Proteins c-myc - genetics | Chromatin - genetics | Cell culture | Brain | Senescence | Brain tumors | Xenotransplantation | Transgenic | Myc protein | Subgroups | Chromatin remodeling | Organic chemistry | Molecular modelling | Depletion | Clonal deletion | Xenografts | Tumorigenesis | Inhibition | Children | Pluripotency | Tumors | Index Medicus
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4. Full Text Cancer surveillance in Gorlin syndrome and rhabdoid tumor predisposition syndrome
by Foulkes, William D and Kamihara, Junne and Evans, D. Gareth R and Brugières, Laurence and Bourdeaut, Franck and Molenaar, Jan J and Walsh, Michael F and Brodeur, Garrett M and Diller, Lisa
Clinical cancer research, ISSN 1078-0432, 06/2017, Volume 23, Issue 12, pp. e62 - e67
Life Sciences & Biomedicine | Oncology | Science & Technology | Kidney Neoplasms - genetics | Basal Cell Nevus Syndrome - diagnosis | Brain Neoplasms - diagnosis | Humans | Brain Neoplasms - pathology | Brain Neoplasms - genetics | Child, Preschool | Repressor Proteins - genetics | SMARCB1 Protein - genetics | Chromatin Assembly and Disassembly - genetics | Infant | Rhabdoid Tumor - pathology | Transcription Factors - genetics | Patched-1 Receptor - genetics | Kidney Neoplasms - diagnosis | Basal Cell Nevus Syndrome - pathology | Rhabdoid Tumor - genetics | Germ-Line Mutation | Kidney Neoplasms - pathology | Rhabdoid Tumor - diagnosis | Basal Cell Nevus Syndrome - genetics | Nuclear Proteins - genetics | DNA Helicases - genetics | Brain | Carcinoma | Kidneys | Brain tumors | Abnormalities | Risk | Chromatin remodeling | Hypercalcemia | Cranium | Magnetic resonance imaging | Surveillance | Gorlin syndrome | Hedgehog protein | Medulloblastoma | Carrier lifetime | Mutation | Children | Age | Cancer | Tumors | Index Medicus
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5. Full Text Familial rhabdoid tumour 'avant la lettre'—from pathology review to exome sequencing and back again
by Witkowski, Leora and Lalonde, Emilie and Zhang, Jian and Albrecht, Steffen and Hamel, Nancy and Cavallone, Luca and May, Sandra Thompson and Nicholson, James C and Coleman, Nicholas and Murray, Matthew J and Tauber, Peter F and Huntsman, David G and Schönberger, Stefan and Yandell, David and Hasselblatt, Martin and Tischkowitz, Marc D and Majewski, Jacek and Foulkes, William D
The Journal of pathology, ISSN 0022-3417, 09/2013, Volume 231, Issue 1, pp. 35 - 43
exome sequencing | ovarian | chromatin remodelling | cancer | rhabdoid tumour | germ cell tumour | SMARCA4 | Chromatin remodelling | Exome sequencing | Rhabdoid tumour | Germ cell tumour | Ovarian | Cancer | Humans | Teratoma - diagnosis | Male | Ovarian Neoplasms - genetics | DNA Mutational Analysis | Diagnostic Errors | Biomarkers, Tumor - metabolism | Female | Ovarian Neoplasms - metabolism | Rhabdoid Tumor - metabolism | Tumor Cells, Cultured | Nuclear Proteins - genetics | DNA Helicases - genetics | Genetic Predisposition to Disease | Ovarian Neoplasms - diagnosis | Nuclear Proteins - metabolism | Transcription Factors - genetics | Transcription Factors - metabolism | DNA Helicases - metabolism | Exome - genetics | Rhabdoid Tumor - genetics | Pedigree | Chromosome Aberrations | Biomarkers, Tumor - genetics | Rhabdoid Tumor - diagnosis | DNA, Neoplasm - genetics | Mutation | Genes, Dominant - genetics | Sequence Analysis, DNA - methods | Genetic aspects | Tumors | Index Medicus
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6. Full Text Rhabdoid Tumor Predisposition Syndrome
by Sredni, Simone T and Tomita, Tadanori
Pediatric and developmental pathology, ISSN 1093-5266, 1/2015, Volume 18, Issue 1, pp. 49 - 58
Malignant rhabdoid tumors | Schwannomatosis | SMARCB1 | AT/RT | Rhab-doid tumor predisposition syndrome | SMARCA4 | Pathology | Pediatrics | Life Sciences & Biomedicine | Science & Technology | Immunohistochemistry | Age Factors | Humans | Child, Preschool | Family Health | Infant | Male | Neurofibromatoses - genetics | SMARCB1 Protein | Neurilemmoma - genetics | Germ-Line Mutation | Female | Nuclear Proteins - genetics | Child | DNA Helicases - genetics | Infant, Newborn | Diagnosis, Differential | Genetic Predisposition to Disease | Rhabdoid Tumor - classification | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Chromosomal Proteins, Non-Histone - genetics | Rhabdoid Tumor - genetics | Skin Neoplasms - genetics | Rhabdoid Tumor - diagnosis | Index Medicus
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7. Full Text SMARCB1 is required for widespread BAF complex-mediated activation of enhancers and bivalent promoters
by Nakayama, Robert T and Pulice, John L and Valencia, Alfredo M and McBride, Matthew J and McKenzie, Zachary M and Gillespie, Mark A and Ku, Wai Lim and Teng, Mingxiang and Cui, Kairong and Williams, Robert T and Cassel, Seth H and Qing, He and Widmer, Christian J and Demetri, George D and Irizarry, Rafael A and Zhao, Keji and Ranish, Jeffrey A and Kadoch, Cigall
Nature genetics, ISSN 1061-4036, 11/2017, Volume 49, Issue 11, pp. 1613 - 1623
Life Sciences & Biomedicine | Genetics & Heredity | Science & Technology | Chromatin - metabolism | Humans | Gene Expression Regulation, Neoplastic | SMARCB1 Protein - genetics | Polycomb-Group Proteins - metabolism | Rhabdoid Tumor - pathology | Carcinogenesis - metabolism | Genetic Complementation Test | Rhabdoid Tumor - metabolism | SMARCB1 Protein - deficiency | Sarcoma - genetics | Chromatin - chemistry | Promoter Regions, Genetic | Chromosomal Proteins, Non-Histone - metabolism | Carcinogenesis - genetics | Chromatin Assembly and Disassembly | Transcription Factors - genetics | Sarcoma - pathology | Chromosomal Proteins, Non-Histone - genetics | Carcinogenesis - pathology | Sarcoma - metabolism | Transcription Factors - metabolism | Rhabdoid Tumor - genetics | Enhancer Elements, Genetic | Polycomb-Group Proteins - genetics | Cell Line, Tumor | Cellular proteins | Genetic aspects | Gene expression | Health aspects | Carcinogenesis | Malignant rhabdoid tumor | Pediatrics | Chromatin | Deactivation | Sarcoma | Ontology | Activation | Genomes | Tumor cell lines | Mammals | Inactivation | Promoters | Proteins | Consortia | Polycomb group proteins | Enhancers | Collaboration | Stem cells | Epigenetics | Tumorigenesis | Bioinformatics | Cancer | Index Medicus
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