Lee et al., 2018 - Google Patents
Synthetic lethal and convergent biological effects of cancer-associated spliceosomal gene mutationsLee et al., 2018
View HTML- Document ID
- 12316009228278738899
- Author
- Lee S
- North K
- Kim E
- Jang E
- Obeng E
- Lu S
- Liu B
- Inoue D
- Yoshimi A
- Ki M
- Yeo M
- Zhang X
- Kim M
- Cho H
- Chung Y
- Taylor J
- Durham B
- Kim Y
- Pastore A
- Monette S
- Palacino J
- Seiler M
- Buonamici S
- Smith P
- Ebert B
- Bradley R
- Abdel-Wahab O
- Publication year
- Publication venue
- Cancer cell
External Links
Snippet
Mutations affecting RNA splicing factors are the most common genetic alterations in myelodysplastic syndrome (MDS) patients and occur in a mutually exclusive manner. The basis for the mutual exclusivity of these mutations and how they contribute to MDS is not well …
- 231100000518 lethal 0 title abstract description 9
Classifications
-
- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12Q—MEASURING OR TESTING PROCESSES INVOLVING ENZYMES OR MICRO-ORGANISMS; COMPOSITIONS OR TEST PAPERS THEREFOR; PROCESSES OF PREPARING SUCH COMPOSITIONS; CONDITION RESPONSIVE CONTROL IN MICROBIOLOGICAL OR ENZYMOLOGICAL PROCESSES
- C12Q1/00—Measuring or testing processes involving enzymes, nucleic acids or micro-organisms; Compositions therefor; Processes of preparing such compositions
- C12Q1/68—Measuring or testing processes involving enzymes, nucleic acids or micro-organisms; Compositions therefor; Processes of preparing such compositions involving nucleic acids
- C12Q1/6876—Hybridisation probes
- C12Q1/6883—Hybridisation probes for diseases caused by alterations of genetic material
- C12Q1/6886—Hybridisation probes for diseases caused by alterations of genetic material for cancer
-
- G—PHYSICS
- G01—MEASURING; TESTING
- G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
- G01N33/00—Investigating or analysing materials by specific methods not covered by the preceding groups
- G01N33/48—Investigating or analysing materials by specific methods not covered by the preceding groups biological material, e.g. blood, urine; Haemocytometers
- G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
- G01N33/5005—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells
- G01N33/5008—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells for testing or evaluating the effect of chemical or biological compounds, e.g. drugs, cosmetics
- G01N33/502—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells for testing or evaluating the effect of chemical or biological compounds, e.g. drugs, cosmetics for testing non-proliferative effects
-
- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12Q—MEASURING OR TESTING PROCESSES INVOLVING ENZYMES OR MICRO-ORGANISMS; COMPOSITIONS OR TEST PAPERS THEREFOR; PROCESSES OF PREPARING SUCH COMPOSITIONS; CONDITION RESPONSIVE CONTROL IN MICROBIOLOGICAL OR ENZYMOLOGICAL PROCESSES
- C12Q2600/00—Oligonucleotides characterized by their use
- C12Q2600/158—Expression markers
Similar Documents
Publication | Publication Date | Title |
---|---|---|
Lee et al. | Synthetic lethal and convergent biological effects of cancer-associated spliceosomal gene mutations | |
Samarasinghe et al. | Targeted degradation of transcription factors by TRAFTACs: transcription factor targeting chimeras | |
Dingler et al. | Two aldehyde clearance systems are essential to prevent lethal formaldehyde accumulation in mice and humans | |
Wang et al. | Targeting an RNA-binding protein network in acute myeloid leukemia | |
Volk et al. | A CHAF1B-dependent molecular switch in hematopoiesis and leukemia pathogenesis | |
Kim et al. | SRSF2 mutations contribute to myelodysplasia by mutant-specific effects on exon recognition | |
Brunetti et al. | Mutant NPM1 maintains the leukemic state through HOX expression | |
Xiao et al. | B-cell-specific diversion of glucose carbon utilization reveals a unique vulnerability in B cell malignancies | |
Cimmino et al. | Restoration of TET2 function blocks aberrant self-renewal and leukemia progression | |
Ma et al. | APOL1 renal-risk variants induce mitochondrial dysfunction | |
Qi et al. | HDAC8 inhibition specifically targets Inv (16) acute myeloid leukemic stem cells by restoring p53 acetylation | |
Colla et al. | Telomere dysfunction drives aberrant hematopoietic differentiation and myelodysplastic syndrome | |
Li et al. | Tumor suppression in the absence of p53-mediated cell-cycle arrest, apoptosis, and senescence | |
Nagamachi et al. | Haploinsufficiency of SAMD9L, an endosome fusion facilitator, causes myeloid malignancies in mice mimicking human diseases with monosomy 7 | |
Biddle et al. | Phenotypic plasticity determines cancer stem cell therapeutic resistance in oral squamous cell carcinoma | |
Abdel-Wahab et al. | ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression | |
Pignatti et al. | Beta-catenin causes adrenal hyperplasia by blocking zonal transdifferentiation | |
Cole et al. | Histone H2B monoubiquitination: roles to play in human malignancy | |
Rathinam et al. | Myeloid leukemia development in c-Cbl RING finger mutant mice is dependent on FLT3 signaling | |
Gu et al. | Discovery of dual inhibitors of MDM2 and XIAP for cancer treatment | |
Wakabayashi et al. | Impaired KLHL3-mediated ubiquitination of WNK4 causes human hypertension | |
Sanz et al. | Cell-type-specific isolation of ribosome-associated mRNA from complex tissues | |
Vasileiou et al. | Chromatin-remodeling-factor ARID1B represses Wnt/β-catenin signaling | |
Tollini et al. | Regulation of p53 by Mdm2 E3 ligase function is dispensable in embryogenesis and development, but essential in response to DNA damage | |
Sondalle et al. | Fanconi anemia protein FANCI functions in ribosome biogenesis |