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PubMed1987

[Possibilities of early diagnosis of intracranial meningioma based on clinical symptoms].

In a retrospective study, 56 patients with intracranial meningiomas were investigated. The diagnosis was verified by computer tomography with subsequent selective cerebral angiography in all cases. At the time of admission, 62.5% of the patients had functional losses affecting the cranial nerves, 44% functional losses involving the long nerve tracts and 23.2% had cerebellar symptoms. Nonspecific clinical symptoms found comprised headaches in 61% of the patients; these were already present almost three and a half years before the final diagnosis. There was a marked organic psychological disorder in 50% of the patients which had already been present retrospectively for an average of 10 months. Cerebral convulsive attacks were present in 27% of the patients with partial convulsions (mainly of the "temporal lobe type") which had already been present for an average of 40 months before diagnosis; in the general tonic-clonic convulsions, the diagnosis was already made an average of six weeks after the first attack. These data show that nonspecific symptoms such as headaches, organic psychological disorders and cerebral convulsions may be early indicators for the presence of an intracranial space occupation and should be investigated further without delay.

Adult↗

PubMed2005

Accurate prediction of HIV-1 drug response from the reverse transcriptase and protease amino acid sequences using sparse models created by convex optimization.

MOTIVATION: Genotype-phenotype modeling problems are often overcomplete, or ill-posed, since the number of potential predictors-genes, proteins, mutations and their interactions-is large relative to the number of measured outcomes. Such datasets can still be used to train sparse parameter models that generalize accurately, by exerting a principle similar to Occam's Razor: When many possible theories can explain the observations, the most simple is most likely to be correct. We apply this philosophy to modeling the drug response of Type-1 Human Immunodeficiency Virus (HIV-1). Owing to the decreasing expense of genetic sequencing relative to in vitro phenotype testing, a statistical model that reliably predicts viral drug response from genetic data is an important tool in the selection of antiretroviral therapy (ART). The optimization techniques described will have application to many genotype-phenotype modeling problems for the purpose of enhancing clinical decisions. RESULTS: We describe two regression techniques for predicting viral phenotype in response to ART from genetic sequence data. Both techniques employ convex optimization for the continuous subset selection of a sparse set of model parameters. The first technique, the least absolute shrinkage and selection operator, uses the l(1) norm loss function to create a sparse linear model; the second, the support vector machine with radial basis kernel functions, uses the epsilon-insensitive loss function to create a sparse non-linear model. The techniques are applied to predict the response of the HIV-1 virus to 10 reverse transcriptase inhibitor and 7 protease inhibitor drugs. The genetic data are derived from the HIV coding sequences for the reverse transcriptase and protease enzymes. When tested by cross-validation with actual laboratory measurements, these models predict drug response phenotype more accurately than models previously discussed in the literature, and other canonical techniques described here. Key features of the methods that enable this performance are the tendency to generate simple models where many of the parameters are zero, and the convexity of the cost function, which assures that we can find model parameters to globally minimize the cost function for a particular training dataset. AVAILABILITY: Results, tables and figures are available at ftp://ftp.genesecurity.net. SUPPLEMENTARY INFORMATION: An Appendix to accompany this article is available at Bioinformatics online.

Amino Acid Sequence↗

PubMed2003

p53 loss of function enhances genomic instability and accelerates clonal evolution of murine myeloid progenitors expressing the p(210)BCR-ABL tyrosine kinase.

BACKGROUND AND OBJECTIVES: The p210 bcr-abl fusion protein has a key role in the pathogenesis of chronic myeloid leukemia (CML). However, its influence on disease progression to blast crisis is marginal and mostly due to its effect of impairing the genomic stability of clonal myeloid progenitors through pathways still largely unknown. DESIGN AND METHODS: To elucidate the role of p53 in CML progression we generated, from the 32D murine myeloid cell line, several clones co-expressing the E6 product gene of human papilloma virus (HPV) 16, which abrogates p53 function, and a temperature-sensitive bcr-abl construct encoding a fully active p210 protein only at the permissive temperature of 33 degrees C. RESULTS: Co-expression of the two proteins resulted in a significant enlargement of the G(2)/M phase of cell cycle and in the appearance of a poly-aneuploid cell population. Furthermore, with continuous in vitro passages the p210 tyrosine kinase became dispensable for growth. Increased levels of cyclin B(1) and enhanced activity of its associated cyclin-dependent kinase (cdc2) became apparent during the clonal evolution of p210 bcr-abl-transduced 32D cell clones lacking p53. INTERPRETATION AND CONCLUSIONS: The acceleration of clonal evolution of p210 bcr-abl-transduced 32D myeloid progenitors associated with p53 functional abrogation is consistent with oncosuppressor loss having a key role in CML progression. This would allow emergence of additional genomic aberrations which would lead to the fully transformed phenotype of blast crisis. Deregulated activity of the cyclin B1-cdc2 complex may be involved in the loss of temporal co-ordination of mitotic events and further free the barrier to genomic instability of CML clonal myeloid progenitors lacking p53.

Aneuploidy↗

PubMed1999

Conceptual issues in scoring radiographic progression in rheumatoid arthritis.

Radiographic scoring systems for rheumatoid arthritis (RA) should be based on current understanding of disease pathology. Evidence suggests that there may be at least two intraarticular pathologies that may result in change in different radiographic features. There is therefore a strong argument for devising a radiographic score based on the observation of features rather than broad categorizations of the total radiographic change. Features may subsequently be amalgamated in relation to other criteria such as sensitivity, specificity, and responsiveness to change, and may be related to subsequent developments in understanding the biology of RA. A second challenge is in elucidating the relationship between radiographic change and the longterm consequences of RA for the patient. Current practice is predicated on the assumption that in the longterm radiographic change correlates well with functional loss and possibly noninflammatory, endstage joint pain. Although hand and feet radiographs broadly represent destructive change in all joints, in cross sectional studies they correlate only moderately with late stage functional loss. The issue may be resolved by longterm observational studies of radiographic change and functional loss. It is recommended that specific radiographic features relevant to joint pathophysiology be used to create a radiographic damage index for comparison with current scoring systems and that longterm observational studies specifically address the relationship between radiographic joint damage and functional outcome.

Animals↗

PubMed2003

Reduced folate carrier gene silencing in multiple antifolate-resistant tumor cell lines is due to a simultaneous loss of function of multiple transcription factors but not promoter methylation.

The human reduced folate carrier (hRFC) is the major uptake route for antifolates used in cancer chemotherapy. Here we explored the molecular basis for the decrease or loss of hRFC gene expression in seventeen tumor cell lines with resistance to multiple antifolates due to impaired antifolate transport. We studied the role of various cis-acting elements including CRE/AP-1-like element and GC-box in hRFC promoters A and B, respectively, as well as AP-2, Mzf-1 and E-box that are contained within or near four tandemly repeated sequences upstream of promoter A. Decreased or abolished binding either to [32P]GC-box, Mzf-1, AP-1, E-box, or CRE oligonucleotides was detected in approximately 50-80% of antifolate-resistant cell lines. Strikingly, approximately 80% of the cell lines displayed a simultaneously decreased binding to three or more of these hRFC promoter elements, whereas normal AP-2 binding was retained. The possible contribution of promoter methylation to hRFC gene silencing was also explored. None of the antifolate-resistant cell lines, except for MDA-MB-231 cells, showed hRFC promoter methylation; consistently, MDA-MB-231 was the only cell line that retained binding to all six cis-acting elements. Western blot analysis demonstrated decreased expression of transcriptional activators (pCREB-1, pATF-1, USF-1, c-Fos, c-Jun, Sp1, and Sp3) and/or increased expression of repressors (short Sp3 isoforms), whereas normal AP2alpha levels were retained. Transient expression of the relevant transcription factors restored, at least partially, both promoter binding and hRFC gene expression. This is the first report that transcriptional silencing of the hRFC gene in multiple tumor cell lines with resistance to various novel antifolates is a result of a simultaneous loss of function of multiple transcription factors but not promoter methylation.

Amino Acid Substitution↗

PubMed2025

The curious case of a heterozygous loss-of-function PSEN1 variant associated with early-onset Alzheimer's disease.

BACKGROUND: Over 300 mutations in PSEN1 have been identified as causes of early-onset Alzheimer's disease (EOAD). While these include missense mutations and a few insertions, deletions, or duplications, none result in open reading frame shifts, and all alter γ-secretase function to increase the long/short Aβ ratio. METHODS: We identified a novel heterozygous PSEN1 nonsense variant, c.325A > T, in a patient and his father, both presenting with EOAD, resulting in the substitution of lysine 109 with a premature stop codon at position (p.K109*). This produces a truncated 109 amino acid (aa) N-terminal PSEN1 fragment. Functional characterization was performed using overexpression models and a heterozygous mouse model (Psen1K109*/+). RESULTS: In overexpression models, downstream ATGs serve as alternative starting codons, generating a > 37 kDa and a > 27 kDa PSEN1 C-terminal fragment (PSEN1-CTFA and PSEN1-CTFB, respectively) that retain the two catalytic aspartates of γ-secretase. Heterozygous Psen1K109*/+ mice exhibited subtle phenotypic defects, including reduced Pen2 expression and mild APP-CTF accumulation. Notably, aged mice demonstrated significantly increased Psen2 protein expression, potentially contributing to an elevated Aβ42/Aβ38 ratio. CONCLUSIONS: These findings indicate that PSEN1 c.325A > T (p.K109*) is not a complete loss-of-function mutation. However, to what extent and by what mechanism it contributes to EOAD pathogenesis remains unclear. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s44477-025-00004-x.

Alzheimer’s disease↗

PubMed2004

Loss-of-function analysis of EphA receptors in retinotectal mapping.

EphA tyrosine kinases are thought to act as topographically specific receptors in the well-characterized projection map from the retina to the tectum. Here, we describe a loss-of-function analysis of EphA receptors in retinotectal mapping. Expressing patches of a cytoplasmically truncated EphA3 receptor in chick retina caused temporal axons to have reduced responsiveness to posterior tectal repellent activity in vitro and to shift more posteriorly within the map in vivo. A gene disruption of mouse EphA5, replacing the intracellular domain with beta-galactosidase, reduced in vitro responsiveness of temporal axons to posterior target membranes. It also caused map abnormalities in vivo, with temporal axons shifted posteriorly and nasal axons anteriorly, but with the entire target still filled by retinal axons. The anterior shift of nasal axons was not accompanied by increased responsiveness to tectal repellent activity, in contrast to the comparable anterior shift in ephrin-A knock-outs, helping to resolve a previous ambiguity in interpreting the ephrin gene knock-outs. The results show the functional requirement for endogenous EphA receptors in retinotectal mapping, show that the receptor intracellular domain is required for a forward signaling response to topographic cues, and provide new evidence for a role of axon competition in topographic mapping.

Animals↗

PubMed2002

Adipose tissue gene expression in patients with a loss of function mutation in the leptin receptor.

BACKGROUND: In order to maintain body weight regulation, leptin directly or indirectly signals nutritional changes to key organs, but little is known about its target genes in human adipose tissue. Leptin receptor loss of function is a unique way to explore the role of leptin in the regulation of adipose tissue. OBJECTIVE: We studied the consequences of the absence of leptin signaling on adipocyte gene expression in two girls with a mutation in the leptin receptor. The expression levels of the ob gene and adipocyte transcription factors (SREBP1c, C/EPBalpha, beta, PPARgamma1, gamma2) were quantified by RT-PCR in subcutaneous adipose tissue of these patients and of 10 morbidly obese women. RESULTS: Ob mRNA levels in subjects lacking the leptin receptor were not overexpressed but were in the range that could be expected from their BMI (58 and 26 amol/ micro g total mRNA, range in obese women: 26-69). Expression of the five transcription factors was also in the same range in the affected patients and in morbidly obese women (7.7 and 6.8 amol/ micro g total mRNA, range: 2.2-9.4 for SREBP1c, 159 and 51 range: 51-406 for C/EPBalpha, 6.1 and 3.3 range: 2.4-24.8 for C/EPBbeta, 16.7 and 27.4 range: 9.4-29.7 for PPARgamma1 and 1.7 and 5.4 amol/ micro g total mRNA range: 1.7-8.8 for PPARgamma2). Significant correlation was found between the mRNA levels of leptin and PPARgamma2 and leptin and C/EBPalpha whereas no correlation was observed between leptin and SREBP1c, PPARgamma1, or C/EBPbeta mRNA levels. CONCLUSION: In patients lacking leptin signaling, the fact that ob gene expression is adequately adapted to their body fat mass argues against a direct negative feedback loop in the regulation of leptin expression in humans. The normal expression of several transcription factors, known to be dependent of the nutritional status, suggests that leptin is not a major contributor of their in vivo transcriptional regulation in human adipose tissue.

Adipocytes↗

PubMed2004

Robustifying AdaBoost by adding the naive error rate.

AdaBoost can be derived by sequential minimization of the exponential loss function. It implements the learning process by exponentially reweighting examples according to classification results. However, weights are often too sharply tuned, so that AdaBoost suffers from the nonrobustness and overlearning. Wepropose a new boosting method that is a slight modification of AdaBoost. The loss function is defined by a mixture of the exponential loss and naive error loss functions. As a result, the proposed method incorporates the effect of forgetfulness into AdaBoost. The statistical significance of our method is discussed, and simulations are presented for confirmation.

Algorithms↗

PubMed2024

Upregulation versus loss of function of NTRK2 in 44 affected individuals leads to 2 distinct neurodevelopmental disorders.

PURPOSE: Heterozygous pathogenic variants in NTRK2 (HGNC: 8032) have been associated with global developmental delay. However, only scattered cases have been described in small or general studies. The aim of our work was to consolidate our understanding of NTRK2-related disorders and to delineate the clinical presentation. METHODS: We reported an extended cohort of 44 affected individuals, of whom 19 are from the literature and 25 were previously unreported. RESULTS: Our analysis led to splitting the cohort into 2 entities. CONCLUSION: One group had variants in the cholesterol-binding motif of the transmembrane domain, with most of these being the recurrent variant c.1301A>G p.(Tyr434Cys). These variants probably lead to upregulation of tropomyosin receptor kinase B activity and to a severe phenotype of developmental delay/intellectual disability, muscular hypotonia, therapy-refractory epilepsy, visual impairment and blindness, and feeding difficulties. The second group had truncating variants or variants that presumably disturb the 3D structure of the protein leading to loss of function. These individuals had a remarkably milder phenotype of developmental delay, obesity, and hyperphagia.

Humans↗

PubMed1999

Loss of function mutations of the human melanocortin 1 receptor are common and are associated with red hair.

The melanocortin 1 receptor is a G-protein-coupled receptor that acts as a control point for control of the eumelanin/phaeomelanin ratio in mouse hair. MC1 receptor loss of function mutations lead to an increase in the ratio of phaeomelanin/eumelanin in many mammals resulting in yellow or red coat colours. We have previously shown that several common point mutations in the human MC1 receptor are overrepresented in North European redheads and in individuals with pale skin. In order to determine the functional significance of these changes we have carried out transfection and binding studies. Expression of the Val60Leu, Arg142His, Arg151Cys, Arg160Trp, and Asp294His receptors in COS 1 cells revealed that these receptors were unable to stimulate cAMP production as strongly as the wild type receptor in response to alpha-melanocyte-stimulating hormone stimulation. None of the mutant receptors displayed complete loss of alphaMSH binding, with only the Arg142His and Asp294His displaying a slight reduction in binding affinity.

Amino Acid Sequence↗

PubMed1995

Introduction of a loss-of-function point mutation from the SH3 region of the Caenorhabditis elegans sem-5 gene activates the transforming ability of c-abl in vivo and abolishes binding of proline-rich ligands in vitro.

We have introduced two loss-of-function point mutations from highly conserved regions of the src homology 3 (SH3) domains of the Caenorhabditis elegans sem-5 gene into the SH3 domain of the murine type IV c-abl tyrosine kinase proto-oncogene. One of the mutations, P131L, activated abl to transform fibroblasts while the other, G128R, did not. When combined with independent activating mutations in the c-abl kinase domain or NH2-terminus, the G128R mutation blocked transformation by the double mutant, suggesting that the G128R mutant was unable to transform cells for trivial reasons. The c-Abl G128R mutant, like wild type c-Abl protein, was localized to the nucleus and actin cytoskeleton and had normal tyrosine kinase activity in vitro, while the transforming c-Abl P131L protein was localized exclusively to the cytoplasm and exhibited decreased in vitro kinase activity. By real-time biospecific interaction analysis, the wild type Abl SH3 domain bound to two proteins containing proline-rich motifs with dissociation constants of 0.2 and 17 microM; the G128R mutant bound with 50-fold lower affinity, and no binding was detected by the P131L mutant. Both mutations completely abolished binding of the Abl SH3 domain to proline-rich target proteins in a filter-binding assay. These results suggest that the transforming activity of Abl is regulated in vivo by an inhibitor protein which associates with the SH3 domain via a proline-rich sequence.

3T3 Cells↗

PubMed2001

The arginine-552-cysteine (R1315C) mutation within the A1 loop of von Willebrand factor induces an abnormal folding with a loss of function resulting in type 2A-like phenotype of von Willebrand disease: study of 10 patients and mutated recombinant von Willebrand factor.

The study identified 10 patients from 6 families with prolonged bleeding time, decreased von Willebrand factor (vWF) ristocetin cofactor activity (RCoF) to vWF:Ag (antigen) ratio, and reduced ristocetin-induced platelet agglutination as well as ristocetin- or botrocetin-induced binding of plasma vWF to platelet glycoprotein Ib (GpIb). In addition, all patients showed a decrease of intermediate-molecular-weight (intermediate-MW) and high-molecular-weight (HMW) multimers of vWF. In the heterozygous state, a cysteine-to-threonine (C --> T) transversion was detected at nucleotide 4193 of the VWF gene of all patients and lead to the arginine (R)522C substitution in the A1 loop of vWF mature subunit (R1315C in the preprovWF). By in vitro mutagenesis of full-length complementary DNA (cDNA) of vWF and transient expression in COS-7 cells, the mutated C552 recombinant vWF (C552rvWF) was found to exhibit decreased expression, abnormal folding, and lack of intermediate-MW and HMW multimers. In addition, direct binding of botrocetin to C552rvWF, as well as ristocetin- and botrocetin-induced binding of C552rvWF to GpIb, was markedly decreased. Although being localized in an area of the A1 loop of vWF where most of the type 2B mutations that induce a gain-of-function have been identified, the R552C mutation induces a 2A-like phenotype with a decrease of intermediate-MW and HMW multimers as well as a loss-of-function of vWF in the presence of either ristocetin or botrocetin. (Blood. 2001;97:952-959)

Adult↗

PubMed2005

Loss of function of def selectively up-regulates Delta113p53 expression to arrest expansion growth of digestive organs in zebrafish.

Transcription factor p53 forms a network with associated factors to regulate the cell cycle and apoptosis in response to environmental stresses. However, there is currently no direct genetic evidence to show if or how the p53 pathway functions during organogenesis. Here we present evidence to show that the zebrafish def (digestive-organ expansion factor) gene encodes a novel pan-endoderm-specific factor. A loss-of-function mutation in def confers hypoplastic digestive organs and selectively up-regulates the expression of Delta113p53, counterpart to a newly identified isoform of p53 produced by an alternative internal promoter in intron 4 of the p53 gene in human. The increased Delta113p53 expression is limited to within the mutant digestive organs, and this increase selectively induces the expression of p53-responsive genes to trigger the arrest of the cell cycle but not apoptosis, resulting in compromised organ growth in the mutant. Our data demonstrate that, while induction of expression of p53 and/or its isoforms is crucial to suppress abnormal cell growth, Delta113p53 is tightly regulated by an organ/tissue-specific factor Def, especially during organogenesis, to prevent adverse inhibition of organ/tissue growth.

Animals↗

PubMed2005

Loss-of-function of Nkx3.1 promotes increased oxidative damage in prostate carcinogenesis.

Despite the significance of oxidative damage for carcinogenesis, the molecular mechanisms that lead to increased susceptibility of tissues to oxidative stress are not well-understood. We now report a link between loss of protection against oxidative damage and loss-of-function of Nkx3.1, a homeobox gene that is known to be required for prostatic epithelial differentiation and suppression of prostate cancer. Using gene expression profiling, we find that Nkx3.1 mutant mice display deregulated expression of several antioxidant and prooxidant enzymes, including glutathione peroxidase 2 and 3 (GPx2 and GPx3), peroxiredoxin 6 (Prdx6), and sulfyhydryl oxidase Q6 (Qscn6). Moreover, the formation of prostatic intraepithelial neoplasia in these mutant mice is associated with increased oxidative damage of DNA, as evident by increased levels of 8-hydroxy-2'-deoxyguanosine. We further show that progression to prostate adenocarcinoma, as occurs in compound mutant mice lacking Nkx3.1 as well as the Pten tumor suppressor, is correlated with a further deregulation of antioxidants, including superoxide dismutase enzymes, and more profound accumulations of oxidative damage to DNA and protein, the latter manifested by increased levels of 4-hydroxynonenal. We propose that the essential role of Nkx3.1 in maintaining the terminally differentiated state of the prostate epithelium provides protection against oxidative damage and, thereby, suppression of prostate cancer. Thus, our findings provide a molecular link between a gene whose inactivation is known to be involved in prostate carcinogenesis, namely Nkx3.1, and oxidative damage of the prostatic epithelium.

Animals↗

PubMed1996

CAG-repeat expansion in androgen receptor in Kennedy's disease is not a loss of function mutation.

Expansion of CAG trinucleotide repeats in androgen receptor gene is present in patients with a rare X-linked inherited form of motor neuron disorder termed Kennedy's disease or spinal and bulbar muscular atrophy (SBMA). This is a late onset progressive disease often associated with mild signs of androgen insensitivity. Defects in androgen receptor (AR) action have been linked to the expansion of the CAG trinucleotide repeats and postulated to be the cause of the disease. We have identified a trinucleotide repeat of 45 in the N-terminus of the AR in two brothers with SBMA and several members in their family (range in the general population is 11-35). Treatment of the patients with androgens failed to improve their clinical symptoms and provided no hint of an anomalous function of the AR. Consistently, functional analysis of the mutant receptor showed hormone binding, transactivation and transrepression potentials identical to that of the wild-type receptor. These results together argue against SBMA being a loss of function mutation of the AR.

Androgens↗

PubMed2026

RETRACTION: Loss-of-Function CARS1 Variants in a Patient With Microcephaly, Developmental Delay, and a Brittle Hair Phenotype.

C. Del Greco, M. E. Kuo, D. E. C. Smith, M. I. Mendes, G. S. Salamons, M. Nemcovic, R. Kodrikova, S. Sestak, M. Stancheva, and A. Antonellis, "Loss-of-Function CARS1 Variants in a Patient With Microcephaly, Developmental Delay, and a Brittle Hair Phenotype," Molecular Genetics & Genomic Medicine 13, no. 2 (2025): e70078, https://doi.org/10.1002/mgg3.70078. The above article, published online on 18 February 2025 in Wiley Online Library (https://onlinelibrary.wiley.com/), has been retracted by agreement between the authors; the journal Editor-in-Chief, Paraminder Dhillon; and Wiley Periodicals, LLC. The retraction has been agreed upon due to the lack of appropriate authorization for the publication of the CARS1 variants related to the specific patient described in this clinical report. In addition, written consent for publication was not obtained from the child's legal guardian.

Journal Article↗

PubMed1996

Peritonitis, functional catheter loss and the sitting of the Dacron cuff in chronic peritoneal dialysis catheters in children.

Functional peritoneal dialysis catheter loss due to persistent or recurrent peritonitis is a common clinical problem in paediatric patients. To examine the effect of positioning of the cuff on infection and loss rate we compared catheters where the cuff was buried in the rectus sheath (deep cuffs) with those where the cuff was sutured to the external oblique muscle, just below the subcutaneous fascia (superficial cuffs). Of 62 catheters inserted into 35 patients (median age 7.76 yrs, range 0-17 yrs) 28 were lost through peritonitis of which 19 (68%) were due to Staph. aureus infection, usually associated with exit site colonisation or infection. 12 out of 20 catheters with superficial cuffs were lost through infection compared with 16 out of 42 with deep cuffs (relative risk reduction 37%, p = ns). Controlling for patient age and infecting organism made no difference to this statistic. 15 out of 21 catheters inserted into patients < 2yrs of age were lost through peritonitis compared to 13 out of 41 catheters inserted into patients over 2 yrs of age (p = 0.037). We conclude that although siting of the Dacron cuff in the rectus sheath is somewhat protective against penetrating infection this is still a major problem in the infant and young child where alternative strategies for the prevention of Staph. aureus infection need to be sought.

Adolescent↗