Cells are constantly exposed to agents that can damage our DNA. These can be from internal sources, such as products of metabolism and errors in DNA duplication, or from external sources, such as carcinogens and UV light (Jackson and Bartek, 2009). DNA damage left unresolved or inaccurately repaired results in genome instability, leading to mutations, chromosome breakages and translocations, events that can promote tumorigenesis (Khanna and Jackson, 2001). To counteract this constitutive DNA damage, cells have intricate mechanisms in place for surveillance and repair of DNA damage. DNA double-strand breaks (DSBs) are the most deleterious type of DNA damage and two main mechanisms exist to repair this type of lesion: non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ is an homology- independent method of repair which relies on KU, DNA-PK and LIG IV to carry out minimal processing and ligation of broken DNA ends (Chiruvella et al., 2013). Such processes very often introduce ...
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Background: PARP inhibition is a promising therapeutic strategy for the treatment of men with metastatic castration-resistant prostate cancer whose tumors harbor homologous recombination DNA repair gene alterations. However, questions remain for many practicing clinicians about which patients are ideally suited for PARP inhibitor treatment. This report details our institutional experience using PARP inhibitor therapy in patients whose tumors harbored specific DNA repair gene alterations. Patients and Methods: We performed a retrospective chart review to identify patients at Oregon Health & Science University who were treated with PARP inhibition. We identified 8 patients and determined the impact of the specific DNA repair gene alterations on tumor response and time on treatment with PARP inhibition. Results: A number of DNA repair gene alterations were identified. Three patients had pathogenic BRCA2 mutations and one had a BRCA2 mutation of uncertain significance. Conversely, the 4 other ...
BACKGROUND: ATR is a critical regulator of the homologous recombination DNA repair pathway and the cellular response to replication stress. Inhibition of ATR is predicted to selectively enhance the sensitivity of tumor cells, in which DNA repair is often compromised, to standard of care DNA damaging agents, while relatively sparing non-tumor cells which have DNA repair mechanisms to compensate for the loss of ATR. VX-970 is a potent and selective inhibitor of ATR with a Ki | 0.2 nM and intracellular IC50 of 19 nM. RESULTS: VX-970 substantially increases the cytotoxic activity of multiple DNA damaging agents in a broad panel of tumor cell lines, with minimal increase in non-tumor cell cytotoxicity. VX-970 markedly synergizes with cytotoxic agents in mouse xenograft models of several tumor types. At concentrations of VX-970 which inhibit tumor growth, phosphorylation of the downstream biomarker, Chk1, is observed, as is up-modulation of markers of unrepaired double strand DNA breaks, including gamma-H2AX.
Purpose: We aimed to identify DNA methylation biomarkers of progression-free survival (PFS) to platinum-based chemotherapy in high-grade serous ovarian cancer (HGSOC) within biologically relevant ovarian cancer-associated pathways.. Experimental Design: Association with PFS of CpG island (CGI) promoter DNA methylation at genes in the pathways Akt/mTOR, p53, redox, and homologous recombination DNA repair was sought with PFS as the primary objective in a prospectively collected ovarian cancer cohort (n = 150). Significant loci were validated for associations between PFS, methylation, and gene expression in an independent The Cancer Genome Atlas (TCGA) data set of HGSOC (n = 311).. Results: DNA methylation at 29 CGI loci linked to 28 genes was significantly associated with PFS, independent from conventional clinical prognostic factors (adjusted P , 0.05). Of 17 out of the 28 genes represented in the TCGA data set, methylation of VEGFB, VEGFA, HDAC11, FANCA, E2F1, GPX4, PRDX2, RAD54L, and RECQL4 was ...
The BRCT domains of the BRCA1 and BARD1 tumor suppressors differentially regulate homology-directed repair and stalled fork protection. Billing et al.
Homology-directed repair of a defective glabrous gene in Arabidopsis with Cas9-based gene targeting [Florian Hahn, Marion Eisenhut, Otho Mantegazza, Andreas P.M. Weber, January 5, 2018, BioRxiv] [https://doi.org/10.1101/243675]Overview and take-home
Allyson Ocean, MD, a medical oncologist and attending physician in gastrointestinal oncology at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, commented on the Know Your Tumor study. This study by Pishvaian et al highlights the importance of genomics in guiding treatment decisions in patients with advanced pancreatic cancer, she said.. Based on a large study of 822 patients from the Know Your Tumor program, the investigators showed that treatment with a platinum agent was associated with a significant survival benefit in patients with advanced disease who have homologous recombination DNA damage response mutations. In 2018, the National Comprehensive Cancer Network® (NCCN®) updated the Clinical Practice Guidelines in Oncology to state that all individuals with a diagnosis of pancreatic cancer meet criteria for hereditary cancer testing, including but not necessarily limited to testing of the BRCA1 and BRCA2 genes, said Dr. Ocean. With the hopeful increase in genomic ...
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The transcriptome is extensively and dynamically regulated by a network of RNA modifying IPI-493 factors. by RNA interference. In addition tRNA base modifications processing and regulated cleavage have been shown to alter global patterns of mRNA translation in response to cellular stress pathways. Recent studies some of which were discussed at this workshop have rekindled interest in the emerging roles of RNA modifications in health and disease. On September 10th 2014 the Division of Cancer Biology NCI sponsored a workshop to explore the role of epitranscriptomic RNA modifications and tRNA processing in cancer progression. The workshop attendees spanned a scientific range including chemists virologists and RNA and cancer biologists. The goal of the workshop was to explore the interrelationships between RNA editing epitranscriptomics and RNA processing and the enzymatic pathways that regulate these activities in cancer initiation and progression. At the conclusion of the workshop a general ...
Background Retinal ganglion cell (RGC) differentiation in vivo is definitely a highly stereotyped process, most likely resulting from the interaction of cell type-specific transcription factors and tissue-derived signaling factors. In addition, we knocked-down and and and translational initiation: and mRNA: [28] was capable to generate a well-known but fairly fragile ciliary phenotype at low dosages (3?ng/embryo) in the genetic history of our seafood lines. At somewhat higher dosages (4?ng/embryo), however, it all caused generalized embryo fatality and severe problems that were not reverted by g53 MO co-injection (Fig.?7a). Another translation-blocking MO, in this full case against [27], was not really capable to generate a proclaimed ciliary phenotype, actually at incredibly high dosages, such as 20?ng/embryo (Fig.?7b). Therefore, we determined to style two splice-blocking MOs aimed against these two genetics (and knock-down. a-c Exterior phenotype of 48 hpf embryos shot with different ...
Tumor cure with conventional fractionated radiotherapy is 65%, dependent on tumor cell-autonomous gradual buildup of DNA double-strand break (DSB) misrepair. Here we report that single-dose radiotherapy (SDRT), a disruptive technique that ablates more than 90% of human cancers, operates a distinct dual-target mechanism, linking acid sphingomyelinase-mediated (ASMase-mediated) microvascular perfusion defects to DNA unrepair in tumor cells to confer tumor cell lethality. ASMase-mediated microcirculatory vasoconstriction after SDRT conferred an ischemic stress response within parenchymal tumor cells, with ROS triggering the evolutionarily conserved SUMO stress response, specifically depleting chromatin-associated free SUMO3. Whereas SUMO3, but not SUMO2, was indispensable for homology-directed repair (HDR) of DSBs, HDR loss of function after SDRT yielded DSB unrepair, chromosomal aberrations, and tumor clonogen demise. Vasoconstriction blockade with the endothelin-1 inhibitor BQ-123, or ROS ...
Tumor cure with conventional fractionated radiotherapy is 65%, dependent on tumor cell-autonomous gradual buildup of DNA double-strand break (DSB) misrepair. Here we report that single-dose radiotherapy (SDRT), a disruptive technique that ablates more than 90% of human cancers, operates a distinct dual-target mechanism, linking acid sphingomyelinase-mediated (ASMase-mediated) microvascular perfusion defects to DNA unrepair in tumor cells to confer tumor cell lethality. ASMase-mediated microcirculatory vasoconstriction after SDRT conferred an ischemic stress response within parenchymal tumor cells, with ROS triggering the evolutionarily conserved SUMO stress response, specifically depleting chromatin-associated free SUMO3. Whereas SUMO3, but not SUMO2, was indispensable for homology-directed repair (HDR) of DSBs, HDR loss of function after SDRT yielded DSB unrepair, chromosomal aberrations, and tumor clonogen demise. Vasoconstriction blockade with the endothelin-1 inhibitor BQ-123, or ROS ...
Tumor cure with conventional fractionated radiotherapy is 65%, dependent on tumor cell-autonomous gradual buildup of DNA double-strand break (DSB) misrepair. Here we report that single-dose radiotherapy (SDRT), a disruptive technique that ablates more than 90% of human cancers, operates a distinct dual-target mechanism, linking acid sphingomyelinase-mediated (ASMase-mediated) microvascular perfusion defects to DNA unrepair in tumor cells to confer tumor cell lethality. ASMase-mediated microcirculatory vasoconstriction after SDRT conferred an ischemic stress response within parenchymal tumor cells, with ROS triggering the evolutionarily conserved SUMO stress response, specifically depleting chromatin-associated free SUMO3. Whereas SUMO3, but not SUMO2, was indispensable for homology-directed repair (HDR) of DSBs, HDR loss of function after SDRT yielded DSB unrepair, chromosomal aberrations, and tumor clonogen demise. Vasoconstriction blockade with the endothelin-1 inhibitor BQ-123, or ROS ...
Tumor cure with conventional fractionated radiotherapy is 65%, dependent on tumor cell-autonomous gradual buildup of DNA double-strand break (DSB) misrepair. Here we report that single-dose radiotherapy (SDRT), a disruptive technique that ablates more than 90% of human cancers, operates a distinct dual-target mechanism, linking acid sphingomyelinase-mediated (ASMase-mediated) microvascular perfusion defects to DNA unrepair in tumor cells to confer tumor cell lethality. ASMase-mediated microcirculatory vasoconstriction after SDRT conferred an ischemic stress response within parenchymal tumor cells, with ROS triggering the evolutionarily conserved SUMO stress response, specifically depleting chromatin-associated free SUMO3. Whereas SUMO3, but not SUMO2, was indispensable for homology-directed repair (HDR) of DSBs, HDR loss of function after SDRT yielded DSB unrepair, chromosomal aberrations, and tumor clonogen demise. Vasoconstriction blockade with the endothelin-1 inhibitor BQ-123, or ROS ...
Alt-R HDR Design Tool & Templates are a complete solution for achieving higher homology-directed repair (HDR) rates. See the quality of our designs and oligos.
Complete information for SWI5 gene (Protein Coding), SWI5 Homologous Recombination Repair Protein, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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Participant has recurrent or refractory osteosarcoma, neuroblastoma, adrenocortical carcinoma, Ewing sarcoma, rhabdomyosarcoma, or any other solid tumor (excluding tumors of the central nervous system [CNS]) previously documented to have breast cancer susceptibility gene (BRCAness) mutational signature (mutational signature 3) on deoxyribonucleic acid (DNA) sequencing of tumor obtained in the relapsed/recurrent disease setting, within 6 (preferably 3) months prior to enrolment. For participants with documented BRCAness mutational signature: Existing information on molecular profiling of the participants tumor tissue must be through a molecular profiling platform such as Individualized Therapy for Relapsed Malignancies in Childhood (INFORM). Molecular profile information must contain information from whole exome sequencing or whole genome sequencing, including the mutation status of BRCA1/2 and other homologous recombination DNA repair (HRR) pathway genes, mutational signatures including ...
Studies in the model eukaryote Saccharomyces cerevisiae have revealed that homologous recombination (HR) is an important tool for the repair of chromosomes inju...
The HRD score appears capable of detecting homologous recombination defects regardless of aetiology or mechanism. This score could facilitate the use of PARP inhibitors and platinum in breast, ovarian, and other cancers.
Considerations for design of an optimal ssDNA donor for CRISPR-Cas9-mediated precise gene editing. Insertion of an epitope tag, mutation or other genomic modification can be readily accomplished by using CRISPR-Cas9 to cause a double-strand break (DSB) followed by homology-directed repair (HDR) using a repair template (donor oligo or donor plasmid). Knock-in of shorter sequences such as a single nucleotide (nt) change, or insertion of exogenous DNA up to ~100 nts can be performed with a single-stranded, synthetic DNA oligo (Figure 1). The design of a single-stranded donor template plays a big role in your knock-in efficiency; important parameters include homology arm length, homology arm symmetry and chemical modifications. Our top recommendations for each of these, thanks to our great R&D team, are provided here to help you obtain the best results possible for your experiment.. ...
L-755,507 is characterized as a potent and selective β3 adrenergic receptor partial agonist with EC50 of 0.43 nM. It is also recently identified to enhance CRISPR-mediated homology-directed repair (HDR) efficiency in human induced pluripotent stem cells (iPSCs) and other cell types. ...
Chk1 and Chk2 are differentially involved in homologous recombination repair and cell cycle arrest in response to DNA double-strand breaks induced by camptothecins ...
Your story must start with Today, and end with FML. TXT language is forbidden and spelling mistakes hurt peoples eyeballs, so the use of either would result in the direct dismissal of your FML. Dont use this space for discussions, advertising or spam, or for posting anything which isnt an FML. Furthermore, its not possible to obtain badges by posting keywords, so stop believing things youve read on message boards. Dont try reposting old FMLs, were not that daft ...
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Toxoplasma gondii is an apicomplexan parasite of medical and veterinary importance which causes toxoplasmosis in humans. Great effort is currently being devoted toward the identification of novel drugs capable of targeting such illness. In this context, we believe that the thorough understanding of the life cycle of this model parasite will facilitate the identification of new druggable targets in T. gondii. It is important to exploit the available knowledge of pathways which could modulate the sensitivity of the parasite to DNA damaging agents. The homologous recombination repair (HRR) pathway may be of particular interest in this regard as its inactivation sensitizes other cellular models such as human cancer to targeted therapy. Herein we discuss the information available on T. gondiis HRR pathway from the perspective of its conservation with respect to yeast and humans. Special attention was devoted to BRCT domain-containing and end-resection associated proteins in T. gondii as in other ...
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Eukaryotic cells deploy overlapping repair pathways to resolve DNA damage. Advancements in genome editing take advantage of these pathways to produce permanent genetic changes. Despite recent improvements, genome editing can produce diverse outcomes that can introduce risks in clinical applications. Although homology-directed repair is attractive for its ability to encode precise edits, it is particularly difficult in human cells. Here we discuss the DNA repair pathways that underlie genome editing and strategies to favour various outcomes. Harnessing DNA repair pathways in genome editing In this Review, Yeh, Richardson and Corn discuss the DNA repair pathways that underlie genome editing and recent improvements and strategies to yield desired genomic alterations in cells and organisms.
The CRISPR-Cas9 system is an RNA-guided genome-editing tool that provides researchers a simple, easy, and quick way to modify the genomes of various organisms. Using this system, Cas9 is gudied to a target sequence where it cleaves the DNA to form a double-stranded DNA break (DSB). Cells repair the break through one of two approaches, non-homologous end joining (NHEJ) or by homology-directed repair (HDR). Most commonly, cells will utilize NHEJ, which has been shown to have high efficiencies in Cas9-mediated genome modification. However, NHEJ is notably imprecise, typically resutling in insertions or deletions (INDELS) that result in unpredictable outcomes. Many investigators desire precision targeting to modify exact DNA sequences (including SNPs, knock-ins, conditional knock-outs, etc) in a controlled setting. In these cases HDR from a provided DNA template is the preferred mechanism of repair; however, this pathway is utilized by the cell less frequently than NHEJ. A number of studies have ...
Sodium, Homologous Recombination, Recombination, Butyrate, Cell Cycle, DNA, DNA Damage, Histone, Histone Deacetylase, Histone Deacetylase Inhibitor, Homologous Recombination Repair, Recombination Repair, Cell, Cells, Hela Cells, Treatment, Oxygen, Chromatin, Communication, Phosphorylation
Cell culture and transfection. All cell lines used in this study were cultured for 2 passages to expand the cell population and frozen for future use. The CHO AA8, UV41, UV5, UV135, EM9, UV20, and HCC1806 cells were obtained from the American Type Culture Collection and the SUM149 cells from Asterand Bioscience. CHO irs1SF and hamster V79 and irs1 cells were provided by L.H. Thompson (Lawrence Livermore National Laboratory, Livermore, California, USA), human U2OS-DR-GFP cells by M. Jasin (Memorial Sloan Kettering Cancer Center, New York, New York, USA), PW human B lymphoma cells by S.J. Knox (Stanford University, Palo Alto, California, USA), MDA-MB-231-BR3 cells by J.E. Price (M.D. Anderson Cancer Center, Houston, Texas, USA), the BRCA1-deficient HCC1937 cell line and its derivatives bearing an empty pcDNA3.1 or a plasmid with BRCA1 cDNA (62, 63) by S.N. Powell (Memorial Sloan Kettering Cancer Center), and the human 293/1040 and HT1080 cells with an inducible knockdown of RAD51 by A. Aroumougame ...
LOC100420930 (SWI5 recombination repair homolog (yeast) pseudogene), Authors: Dessen P. Published in: Atlas Genet Cytogenet Oncol Haematol.
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Abstract: Poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitors have shown clinical activity in epithelial ovarian cancer, leading both the US Food and Drug Administration (FDA) and the European Medicines Agency to approve olaparib for tumors characterized by BRCA1 and BRCA2 mutations. However, it is becoming increasingly evident that tumors that share molecular features with BRCA-mutant tumors-a concept known as BRCAness-also may exhibit defective homologous recombination DNA repair, and therefore will respond to PARP inhibition. A number of strategies have been proposed to identify BRCAness, including identifying defects in other genes that modulate homologous recombination and characterizing the mutational and transcriptional signatures of BRCAness. In addition to olaparib, a number of other PARP inhibitors are in clinical development. This article reviews the development of PARP inhibitors other than olaparib, and discusses the evidence for PARP inhibitors beyond BRCA1/2-mutant ...
DNA repair is essential to maintain genome integrity, and genes with roles in DNA repair are frequently mutated in a variety of human diseases. Repair via homologous recombination typically restores the original DNA sequence without introducing mutations, and a number of genes that are required for homologous recombination DNA double-strand break repair (HR-DSBR) have been identified. However, a systematic analysis of this important DNA repair pathway in mammalian cells has not been reported. Here, we describe a genome-scale endoribonuclease-prepared short interfering RNA (esiRNA) screen for genes involved in DNA double strand break repair. We report 61 genes that influenced the frequency of HR-DSBR and characterize in detail one of the genes that decreased the frequency of HR-DSBR. We show that the gene KIAA0415 encodes a putative helicase that interacts with SPG11 and SPG15, two proteins mutated in hereditary spastic paraplegia (HSP). We identify mutations in HSP patients, discovering KIAA0415/SPG48
The presentation reviews the modus operandi of the dose modifying drug Pentoxifylline and the dose enhancement factors which can be achieved in different cell types. Preclinical and clinical data show that Pentoxifylline improves the oxygenation of hypoxic tumours and enhances tumour control by irradiation. In vitro experiments demonstrate that Pentoxifylline also operates when oxygen is not limiting and produces dose modifying factors in the region of 1.2 - 2.0. This oxygen independent effect is poorly understood. In p53 mutant cells irradiation induces a G2 block which is abrogated by Pentoxifylline. The enhancement of cell kill observed when Pentoxifylline and irradiation are given together could arise from rapid entry of damaged tumour cells into mitosis and propagation of DNA lesions as the result of curtailment of repair time. Recovery ratios and repair experiments using CFGE after high dose irradiation demonstrate that Pentoxifylline inhibits repair directly and that curtailment of repair ...
To change the message: RNA editing for neurodegenerative disorders. RNA has long been sought as a therapeutic target to provide transient amelioration of disease status without making permeant changes to the genetic markup. The recently reported RNA Editing for Programmable A-to-I Replacement (REPAIR) system is an ingenious combination of gRNA-mediated RNA-binding capability of a kinase domain-dead Cas13b and an adenosine deaminase to achieve single-base-pair RNA editing (a term coined way back at 1986). Such a system offers a highly efficient RNA editing tool to repair single-nucleotide mutations, so the bad message can be changed and lost in translation.. REPAIR is especially advantageous for studying pathogenesis and the development of gene therapy for neurodegenerative disorders. First, because the REPAIR system does not need to involve the endogenous DNA damage repair mechanisms, such as non-homologous end-joining or homology-directed repair, it provides more efficient editing in ...
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OmniSeq INSIGHTSM is a comprehensive genomic and immune profiling test that is clinically and analytically validated for all solid tumors. OmniSeq INSIGHTSM interrogates the full exonic coding region of 523 genes by next generation sequencing for mutations, select copy number alterations, and fusions/splice variants including genes associated with homologous recombination repair deficiency (HRR/HRD), microsatellite instability (MSI) and tumor mutational burden (TMB), expression of 64 immune genes, and PD-L1 by immunohistochemistry (IHC). The test informs treatment decisions, including targeted and immunotherapy options to which the patient may be more likely to respond, clinical trials, and mechanisms of decreased response and resistance to therapies based on the individual genomic and immune profile for each patients tumor. ...
The mutational signature AC3, which has been associated with defects in homologous recombination repair (HRR), was detected in both sporadic meningioma and Mrad, but widely distributed across the genome in sporadic cases and enriched near genomic breakpoints in Mrad. Compared to the other MCs, the number of
Your story must start with Today, and end with FML. TXT language is forbidden and spelling mistakes hurt peoples eyeballs, so the use of either would result in the direct dismissal of your FML. Dont use this space for discussions, advertising or spam, or for posting anything which isnt an FML. Furthermore, its not possible to obtain badges by posting keywords, so stop believing things youve read on message boards. Dont try reposting old FMLs, were not that daft ...
Your story must start with Today, and end with FML. TXT language is forbidden and spelling mistakes hurt peoples eyeballs, so the use of either would result in the direct dismissal of your FML. Dont use this space for discussions, advertising or spam, or for posting anything which isnt an FML. Furthermore, its not possible to obtain badges by posting keywords, so stop believing things youve read on message boards. Dont try reposting old FMLs, were not that daft ...
Your story must start with Today, and end with FML. TXT language is forbidden and spelling mistakes hurt peoples eyeballs, so the use of either would result in the direct dismissal of your FML. Dont use this space for discussions, advertising or spam, or for posting anything which isnt an FML. Furthermore, its not possible to obtain badges by posting keywords, so stop believing things youve read on message boards. Dont try reposting old FMLs, were not that daft ...
Your story must start with Today, and end with FML. TXT language is forbidden and spelling mistakes hurt peoples eyeballs, so the use of either would result in the direct dismissal of your FML. Dont use this space for discussions, advertising or spam, or for posting anything which isnt an FML. Furthermore, its not possible to obtain badges by posting keywords, so stop believing things youve read on message boards. Dont try reposting old FMLs, were not that daft ...
Your story must start with Today, and end with FML. TXT language is forbidden and spelling mistakes hurt peoples eyeballs, so the use of either would result in the direct dismissal of your FML. Dont use this space for discussions, advertising or spam, or for posting anything which isnt an FML. Furthermore, its not possible to obtain badges by posting keywords, so stop believing things youve read on message boards. Dont try reposting old FMLs, were not that daft ...
Your story must start with Today, and end with FML. TXT language is forbidden and spelling mistakes hurt peoples eyeballs, so the use of either would result in the direct dismissal of your FML. Dont use this space for discussions, advertising or spam, or for posting anything which isnt an FML. Furthermore, its not possible to obtain badges by posting keywords, so stop believing things youve read on message boards. Dont try reposting old FMLs, were not that daft ...
Your story must start with Today, and end with FML. TXT language is forbidden and spelling mistakes hurt peoples eyeballs, so the use of either would result in the direct dismissal of your FML. Dont use this space for discussions, advertising or spam, or for posting anything which isnt an FML. Furthermore, its not possible to obtain badges by posting keywords, so stop believing things youve read on message boards. Dont try reposting old FMLs, were not that daft ...
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