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1. Full Text Hereditary Cancer Predisposition Syndromes
by Judy E. Garber and Kenneth Offit
Journal of Clinical Oncology, ISSN 0732-183X, 01/2005, Volume 23, Issue 2, pp. 276 - 292
Cancer genetics is increasingly becoming integrated into the practice of modern medical oncology. The ability to distinguish a growing proportion of the 5% to... 
CELL CARCINOMA SYNDROME | CUTANEOUS MALIGNANT-MELANOMA | GENOTYPE-PHENOTYPE CORRELATIONS | GERM-LINE MUTATIONS | FOLLOW-UP CARE | ONCOLOGY | NONPOLYPOSIS COLORECTAL-CANCER | VITAMIN-D-RECEPTOR | FAMILIAL ADENOMATOUS POLYPOSIS | SHARED GENETIC SUSCEPTIBILITY | DIFFUSE GASTRIC-CANCER | Genetic Predisposition to Disease | Neoplasms - therapy | Breast Neoplasms - genetics | Gastrointestinal Neoplasms - genetics | Genetic Testing | Neoplasms - genetics | Retinoblastoma - genetics | Humans | Neoplasms - diagnosis | Neoplastic Syndromes, Hereditary - genetics | Mutation
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2. Full Text Pediatric non–Down syndrome acute megakaryoblastic leukemia is characterized by distinct genomic subsets with varying outcomes
by Rooij, Johan and Branstetter, C and Ma, J and Li, Y and Walsh, M.P and Cheng, J and Obulkasim, Askar and Dang, J and Easton, J and Verboon, Peter and Mulder, H.L and Zimmermann, Martin and Koss, C and Gupta, P and Edmonson, M and Rusch, M and Lim, J.Y.S and Reinhardt, Katarina and Pigazzi, M and Song, G and Yeoh, Allen E. J and Shih, L.-Y and Liang, Der and Halene, S and Krause, D.S and Zhang, J and Downing, James and Locatelli, Franco and Reinhardt, Dirk and Heuvel-Eibrink, Marry and Zwaan, Michel and Fornerod, Maarten and Gruber, T.A
Nature Genetics, ISSN 1061-4036, 01/2017, Volume 49, Issue 3, pp. 451 - 456
textabstractAcute megakaryoblastic leukemia (AMKL) is a subtype of acute myeloid leukemia (AML) in which cells morphologically resemble abnormal... 
AML | CELLS | HOXA9 | FUSION | GENE | LANDSCAPE | GENETICS & HEREDITY | PROLIFERATION | EXPERIENCE | CHILDHOOD | SOMATIC MUTATIONS | Humans | Mice, Inbred C57BL | Repressor Proteins - genetics | RNA - genetics | Exome - genetics | Retinoblastoma-Binding Protein 2 - genetics | Animals | Tumor Suppressor Proteins - genetics | Down Syndrome - genetics | Polymorphism, Single Nucleotide - genetics | Female | Mice | Gene Rearrangement - genetics | Leukemia, Megakaryoblastic, Acute - genetics | Genomics - methods | Cellular signal transduction | Genetic aspects | Health aspects | Phosphotransferases | Proteins | Pediatrics | Laboratories | Leukemia | Epigenetics | Mutation | Down syndrome | Kinases | Gene expression | Clinical outcomes | Children & youth | Cancer
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3. Full Text Molecular pathogenesis of osteosarcoma
by Kansara, Maya and Thomas, David M
DNA and Cell Biology, ISSN 1044-5498, 01/2007, Volume 26, Issue 1, pp. 1 - 18
Osteosarcoma is a devastating but rare disease, whose study has illuminated both the basic biology and clinical management of cancer over the past 30 years.... 
SOFT-TISSUE SARCOMAS | BIOCHEMISTRY & MOLECULAR BIOLOGY | SYNDROME ADULT PROGERIA | TUMOR-SUPPRESSOR GENE | FACTOR TH-POK | MESENCHYMAL STEM-CELLS | CELL BIOLOGY | BLOOMS-SYNDROME GENE | LI-FRAUMENI-SYNDROME | GENETICS & HEREDITY | HIGH-GRADE OSTEOSARCOMA | COMPARATIVE GENOMIC HYBRIDIZATION | WERNER-SYNDROME HELICASE | Matrix Metalloproteinases - genetics | Neurofibromin 2 - genetics | Cytoskeletal Proteins - genetics | RecQ Helicases - metabolism | Humans | RecQ Helicases - genetics | Bone Neoplasms - pathology | Osteitis Deformans - genetics | Tumor Suppressor Protein p53 - genetics | Bone Neoplasms - metabolism | Neoplasm Metastasis | Werner Syndrome - genetics | Cytoskeletal Proteins - metabolism | Bone Neoplasms - genetics | Neurofibromin 2 - metabolism | Osteosarcoma - metabolism | Bloom Syndrome - pathology | Genetic Predisposition to Disease | Neoplasm Invasiveness | Retinoblastoma Protein - metabolism | Tumor Suppressor Protein p53 - metabolism | Bloom Syndrome - genetics | Werner Syndrome - pathology | Rothmund-Thomson Syndrome - genetics | Osteitis Deformans - pathology | Animals | Retinoblastoma Protein - genetics | Chromosome Aberrations | Mice | Matrix Metalloproteinases - metabolism | Mutation | Osteosarcoma - genetics | Rothmund-Thomson Syndrome - pathology | Osteosarcoma - pathology
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4. Full Text Treatment of Growing Teratoma Syndrome
by Vaughn, David J and Wilner, Keith and Schwartz, Gary and Flaherty, Keith and Chen, Isan and Lal, Priti and Gallagher, Maryann and O'Dwyer, Peter
The New England Journal of Medicine, ISSN 0028-4793, 01/2009, Volume 360, Issue 4, pp. 423 - 424
To the Editor: Growing teratoma syndrome consists of an enlarging mature teratoma arising during or after chemotherapy for a nonseminomatous germ-cell tumor,... 
MEDICINE, GENERAL & INTERNAL | Humans | Retinoblastoma Protein - metabolism | Male | Antineoplastic Agents - therapeutic use | Piperazines - therapeutic use | Disease Progression | Teratoma - metabolism | Young Adult | Neoplasms, Second Primary - metabolism | Teratoma - drug therapy | Adult | Neoplasms, Germ Cell and Embryonal - drug therapy | Cyclin-Dependent Kinases - antagonists & inhibitors | Neoplasms, Second Primary - drug therapy | Neoplasms, Germ Cell and Embryonal - pathology | Pyridines - therapeutic use | Clinical trials | Monoclonal antibodies | Chemotherapy | Patients | Cells | Tumors | Index Medicus | Abridged Index Medicus
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5. Full Text Hutchinson–Gilford progeria syndrome through the lens of transcription
by Prokocimer, Miron and Barkan, Rachel and Gruenbaum, Yosef
Aging Cell, ISSN 1474-9718, 08/2013, Volume 12, Issue 4, pp. 533 - 543
Summary Lamins are nuclear intermediate filaments. In addition to their structural roles, they are implicated in basic nuclear functions such as chromatin... 
progerin | transcription | lamin A | Hutchinson–Gilford progeria syndrome | lamin B1 | LMNA | nuclear lamina | aging | Nuclear lamina | Lamin B1 | Transcription | Progerin | Aging | Hutchinson-Gilford progeria syndrome | Lamin A | DEFECTIVE MATURATION | STEM-CELLS | OSTEOBLAST DIFFERENTIATION | A-TYPE LAMINS | DNA-DAMAGE | CELLULAR SENESCENCE | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | GROWTH-FACTOR-BETA | RETINOBLASTOMA PROTEIN | ADIPOCYTE DIFFERENTIATION | NUCLEAR-MEMBRANE PROTEIN | Protein Precursors - genetics | Lamin Type B - genetics | Humans | Gene Silencing | Chromatin Assembly and Disassembly | Nuclear Proteins - metabolism | Lamin Type A - metabolism | Progeria - genetics | Progeria - metabolism | Lamin Type B - metabolism | Protein Precursors - metabolism | Mechanotransduction, Cellular | Adult Stem Cells - metabolism | Phenotype | Cell Nucleus - metabolism | Cell Nucleus - genetics | DNA Repair | Progeria - pathology | Lamin Type A - genetics | Transcription, Genetic | Telomere - metabolism | Adult Stem Cells - pathology | Nuclear Proteins - genetics | Telomere - genetics | DNA replication | Genetic transcription | Intermediate filament proteins | Progeria
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6. Full Text Imprinting disorders and assisted reproductive technology
by Manipalviratn, Somjate, M.D and DeCherney, Alan, M.D and Segars, James, M.D
Fertility and Sterility, ISSN 0015-0282, 2009, Volume 91, Issue 2, pp. 305 - 315
Objective To review currently available literature on the association between imprinting disorders (Beckwith-Wiedemann syndrome [BWS], Angelman syndrome [AS]... 
Internal Medicine | Obstetrics and Gynecology | Imprinting disorders | Beckwith-Wiedemann syndrome | Angelman syndrome | assisted reproductive technology | ICSI | epigenetic | retinoblastoma | IVF | HUMAN OOCYTES | MOUSE EMBRYOS | ANGELMAN-SYNDROME | INTRACYTOPLASMIC SPERM INJECTION | OBSTETRICS & GYNECOLOGY | EPIGENETIC INHERITANCE | REPRODUCTIVE BIOLOGY | BECKWITH-WIEDEMANN-SYNDROME | GERM-CELLS | ABERRANT DNA METHYLATION | CHILDREN BORN | IN-VITRO FERTILIZATION | Genomic Imprinting | Retinoblastoma - genetics | Risk Assessment | Humans | Risk Factors | Evidence-Based Medicine | Beckwith-Wiedemann Syndrome - genetics | Pregnancy | DNA Methylation | Reproductive Techniques, Assisted - adverse effects | Animals | Gene Expression Regulation, Developmental | Angelman Syndrome - genetics | Female | Reproductive technology | Angleman syndrome
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7. Full Text Blue Toe Syndrome—Reply
by Sarici, Ahmet and Kizilkilic, Osman and Celkan, Tiraje
JAMA Ophthalmology, ISSN 2168-6165, 05/2014, Volume 132, Issue 5, pp. 654 - 655
Retinal Neoplasms - drug therapy | Melphalan - administration & dosage | Humans | Retinoblastoma - drug therapy | Male | Antineoplastic Agents, Alkylating - administration & dosage | Blue Toe Syndrome - etiology | Catheterization, Peripheral - adverse effects
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8. Full Text Genome-wide methylation analysis in Silver–Russell syndrome patients
by Prickett, A R and Ishida, M and Böhm, S and Frost, J M and Puszyk, W and Abu-Amero, S and Stanier, P and Schulz, R and Moore, G E and Oakey, R J
Human Genetics, ISSN 0340-6717, 3/2015, Volume 134, Issue 3, pp. 317 - 332
Silver–Russell syndrome (SRS) is a clinically heterogeneous disorder characterised by severe in utero growth restriction and poor postnatal growth, body... 
Human Genetics | Gene Function | Molecular Medicine | Biomedicine | Metabolic Diseases | MOLECULAR SUBTYPES | PROGENITOR CELLS | DNA METHYLATION | HUMAN RETINOBLASTOMA GENE | QUANTILE NORMALIZATION | GENETICS & HEREDITY | PATERNAL ISODISOMY | IMPRINTED LOCI | CHROMOSOME-7 | RESTRICTION | EXPRESSION | Genomic Imprinting | Promoter Regions, Genetic | Genome-Wide Association Study | Oligonucleotide Array Sequence Analysis | Humans | Child, Preschool | Repressor Proteins - genetics | Infant | Male | RNA, Long Noncoding - genetics | Sequence Analysis, DNA | Case-Control Studies | Young Adult | Silver-Russell Syndrome - genetics | DNA Methylation | Retinoblastoma Protein - genetics | Adolescent | CpG Islands | Female | Genome, Human | Child | Genetic research | Genomes | DNA microarrays | Methylation | Analysis | Genomics | genomic imprinting | global DNA methylation | Silver-Russell syndrome | CpG islands
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9. Full Text Progeria syndromes and ageing: what is the connection?
by Burtner, Christopher R and Kennedy, Brian K
Nature Reviews Molecular Cell Biology, ISSN 1471-0072, 08/2010, Volume 11, Issue 8, pp. 567 - 578
One of the many debated topics in ageing research is whether progeroid syndromes are really accelerated forms of human ageing. The answer requires a better... 
LIFE-SPAN EXTENSION | ACTIVATED PROTEIN-KINASE | CAENORHABDITIS-ELEGANS | A-TYPE LAMINS | HUTCHINSON-GILFORD-PROGERIA | CALORIC RESTRICTION | RETINOBLASTOMA GENE-PRODUCT | PRELAMIN-A | DIETARY RESTRICTION | MESENCHYMAL STEM-CELLS | CELL BIOLOGY | Signal Transduction | Longevity - drug effects | Humans | Longevity - genetics | Progeria - genetics | Sirolimus - pharmacology | Syndrome | Biological Evolution | Animals | Aging - genetics | Aging - physiology | Progeria - physiopathology | Models, Biological | DNA Repair | Lamin Type A - genetics | DNA Damage | Mesenchymal Stromal Cells - pathology | Longevity - physiology | Mesenchymal Stromal Cells - physiology | Progeria - therapy | Progeria - etiology | Complications and side effects | Progeria | DNA damage | Aging | Physiological aspects | Development and progression | Genetic aspects | Risk factors
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