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Journal Article
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 3613 - 14
Journal Article
Gastroenterology, ISSN 0016-5085, 2014, Volume 146, Issue 2, pp. 453 - 460.e5
Journal Article
Nature, ISSN 0028-0836, 08/2012, Volume 488, Issue 7411, pp. 337 - 342
Inactivation of tumour-suppressor genes by homozygous deletion is a prototypic event in the cancer genome, yet such deletions often encompass neighbouring... 
ENOLASE DEFICIENCY | CELLS | INHIBITION | MULTIDISCIPLINARY SCIENCES | REGIONS | Neoplasm Transplantation | RNA, Small Interfering - genetics | Enzyme Inhibitors | Phosphopyruvate Hydratase - deficiency | Cell Proliferation | Biomarkers, Tumor - deficiency | Humans | Brain Neoplasms - pathology | Gene Expression Regulation, Neoplastic | Phosphonoacetic Acid - analogs & derivatives | Phosphopyruvate Hydratase - metabolism | Antineoplastic Agents - therapeutic use | DNA-Binding Proteins - deficiency | Gene Knockdown Techniques | Glioblastoma - genetics | Phosphopyruvate Hydratase - genetics | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Antineoplastic Agents - pharmacology | Chromosomes, Human, Pair 1 - genetics | Genes, Tumor Suppressor | Hydroxamic Acids - pharmacology | Molecular Targeted Therapy - methods | Genes, Essential - genetics | Brain Neoplasms - genetics | Phosphopyruvate Hydratase - antagonists & inhibitors | Brain Neoplasms - drug therapy | DNA-Binding Proteins - genetics | Phosphonoacetic Acid - therapeutic use | Phosphonoacetic Acid - pharmacology | Homozygote | Animals | Glioblastoma - pathology | Cell Line, Tumor | Hydroxamic Acids - therapeutic use | Biomarkers, Tumor - genetics | Mice | Glioblastoma - drug therapy | Sequence Deletion - genetics | Gene mutations | Physiological aspects | Tumor suppressor genes | Genetic aspects | Research | Health aspects | Risk factors | Cancer | Proteins | Genetics | Kinases | Genes | Index Medicus
Journal Article
The American Journal of Surgical Pathology, ISSN 0147-5185, 11/2014, Volume 38, Issue 11, pp. 1501 - 1509
Lynch syndrome (LS) is an autosomal dominant inherited disorder caused by germline mutations in DNA mismatch repair (MMR) genes. Mutation carriers are at... 
Microsatellite instability | Endometrial adenocarcinoma | Lynch syndrome | Mismatch-repair deficiency | SURGERY | mismatch-repair deficiency | microsatellite instability | NONPOLYPOSIS COLORECTAL-CANCER | REPAIR PROTEIN IMMUNOHISTOCHEMISTRY | RISK | GENE MUTATION | endometrial adenocarcinoma | PATHOLOGY | CLINICAL-CRITERIA | ACADEMIC-MEDICAL-CENTER | TUMOR MORPHOLOGY | GERMLINE MUTATIONS | GYNECOLOGIC CANCERS | Immunohistochemistry | MutL Protein Homolog 1 | Predictive Value of Tests | Microsatellite Instability | Biomarkers, Tumor - deficiency | Colorectal Neoplasms, Hereditary Nonpolyposis - pathology | Humans | Middle Aged | DNA Mismatch Repair - genetics | Mass Screening - methods | DNA-Binding Proteins - deficiency | Neoplasm Grading | Endometrial Neoplasms - genetics | DNA Mutational Analysis | MutS Homolog 2 Protein - deficiency | Nuclear Proteins - deficiency | Aged, 80 and over | Adult | Female | Mismatch Repair Endonuclease PMS2 | DNA Repair Enzymes - deficiency | Adenosine Triphosphatases - deficiency | Endometrial Neoplasms - chemistry | Risk Assessment | Colorectal Neoplasms, Hereditary Nonpolyposis - genetics | Risk Factors | California | Biopsy | Adaptor Proteins, Signal Transducing - deficiency | Endometrial Neoplasms - pathology | Aged | Biomarkers, Tumor - genetics | Colorectal Neoplasms, Hereditary Nonpolyposis - chemistry | Index Medicus
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 06/2015, Volume 372, Issue 26, pp. 2509 - 2520
Persons with mismatch repair–deficient tumors are more likely than persons with mismatch repair–proficient tumors to benefit from pembrolizumab — which... 
MEDICINE, GENERAL & INTERNAL | COLORECTAL CARCINOMAS | ANTI-PD-L1 ANTIBODY | SAFETY | MICROSATELLITE INSTABILITY | DNA | GERMLINE MUTATIONS | PREDISPOSE | CLINICAL ACTIVITY | CANCER | LYMPHOCYTES | Antibodies, Monoclonal, Humanized - adverse effects | Antibodies, Monoclonal, Humanized - therapeutic use | Colorectal Neoplasms - genetics | Humans | Middle Aged | Kaplan-Meier Estimate | Male | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Adenocarcinoma - drug therapy | Adenocarcinoma - secondary | Disease-Free Survival | Neoplasm Metastasis - genetics | Neoplasm Metastasis - drug therapy | Antineoplastic Agents - adverse effects | Colorectal Neoplasms - drug therapy | DNA Mismatch Repair | Adult | Female | Adenocarcinoma - genetics | Aged | Colorectal Neoplasms - pathology | Antibody diversity | Carcinoma | Genetic disorders | Analysis | Research | Risk factors | Cancer | Tumors | Antigens | Yeast | PD-1 protein | Colorectal carcinoma | Body weight | Colorectal cancer | Autoantigens | DNA repair | Survival | Metastases | Pembrolizumab | Immune checkpoint | Immunogenicity | Mismatch repair | Death | Mutation | Genetic recombination | Cancer therapies | Drug dosages | Immune system | Medical research | Melanoma | Patients | Studies | Hypotheses | Pancreatic cancer | Epigenetics | Biomarkers | Ligands
Journal Article
Molecular Cell, ISSN 1097-2765, 02/2016, Volume 61, Issue 3, pp. 449 - 460
G-quadruplex (G4)-forming genomic sequences, including telomeres, represent natural replication fork barriers. Stalled replication forks can be stabilized and... 
HUMAN GENOME | REPLICATION | MAMMALIAN TELOMERES | SMALL-MOLECULE | HUMAN-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | HOMOLOGOUS RECOMBINATION | CANCER | TUMORS | LIGAND RHPS4 | CELL BIOLOGY | Neoplasms - metabolism | G-Quadruplexes - drug effects | Mad2 Proteins - metabolism | Biomarkers, Tumor - deficiency | Humans | Drug Resistance, Neoplasm | Male | Intracellular Signaling Peptides and Proteins - metabolism | Telomere - drug effects | Molecular Targeted Therapy | DNA Breaks, Double-Stranded | Dose-Response Relationship, Drug | G2 Phase Cell Cycle Checkpoints - drug effects | Transfection | Neoplasms - genetics | RNA Interference | Time Factors | HEK293 Cells | Antineoplastic Agents - pharmacology | Telomere - metabolism | BRCA1 Protein - deficiency | Aminoquinolines - pharmacology | Intracellular Signaling Peptides and Proteins - genetics | Telomere - genetics | Picolinic Acids - pharmacology | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Animals | Tumor Burden - drug effects | Mice, Nude | Mad2 Proteins - genetics | BRCA2 Protein - deficiency | Biomarkers, Tumor - genetics | Cell Proliferation - drug effects | Tumor Suppressor p53-Binding Protein 1 | Neoplasms - pathology | BRCA2 Protein - genetics | Purines | Lung cancer | DNA damage | Genomics | Radiation | Chromosomes | DNA repair | Telomeres | Cells
Journal Article
Thorax, ISSN 0040-6376, 2012, Volume 67, Issue 9, pp. 796 - 803
Journal Article
American Journal of Surgical Pathology, ISSN 0147-5185, 07/2012, Volume 36, Issue 7, pp. 964 - 972
Journal Article