Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Large neurofibroma of trunk.

ABSTRACT:

Unlabelled

Neurofibroma is a benign tumor of cutaneous nerves. These are benign tumors which may have a varied presentations ranging from a cosmetic problem to a spinal tumor which may lead to neural complications. We here by present a case where the patient has become an appendage of the tumor and its the mass of the tumor that has handicapped the patient.

Electronic supplementary material

The online version of this article (doi:10.1007/s12262-010-0129-x) contains supplementary material, which is available to authorized users.

SUBMITTER: Agarwal A

PROVIDER: S-EPMC3087064 | biostudies-literature | 2011 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Large neurofibroma of trunk.

Agarwal Akhilesh A Agarwal Anshu A Sil B D BD Choudhury Chandan R CR Bhattacharya Saptarshi S

The Indian journal of surgery 20110201 3

<h4>Unlabelled</h4>Neurofibroma is a benign tumor of cutaneous nerves. These are benign tumors which may have a varied presentations ranging from a cosmetic problem to a spinal tumor which may lead to neural complications. We here by present a case where the patient has become an appendage of the tumor and its the mass of the tumor that has handicapped the patient.<h4>Electronic supplementary material</h4>The online version of this article (doi:10.1007/s12262-010-0129-x) contains supplementary m ...[more]

PMID: 22654333

Similar Datasets

Neurofibroma

Project description:Neurofibroma

| PRJNA484782 | ENA

A large vegetation on a xenopericardial roll elephant trunk graft.

Project description: Not available

| S-EPMC8300915 | biostudies-literature

Neurofibroma

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-03-03 | GSE118186 | GEO

<i>Cdkn2a</i> Loss in a Model of Neurofibroma Demonstrates Stepwise Tumor Progression to Atypical Neurofibroma and MPNST.

Project description:Plexiform neurofibromas are benign nerve sheath Schwann cell tumors characterized by biallelic mutations in the neurofibromatosis type 1 (NF1) tumor suppressor gene. Atypical neurofibromas show additional frequent loss of CDKN2A/Ink4a/Arf and may be precursor lesions of aggressive malignant peripheral nerve sheath tumors (MPNST). Here we combined loss of Nf1 in developing Schwann cells with global Ink4a/Arf loss and identified paraspinal plexiform neurofibromas and atypical neurofibromas. Upon transplantation, atypical neurofibromas generated genetically engineered mice (GEM)-PNST similar to human MPNST, and tumors showed reduced p16INK4a protein and reduced senescence markers, confirming susceptibility to transformation. Superficial GEM-PNST contained regions of nerve-associated plexiform neurofibromas or atypical neurofibromas and grew rapidly on transplantation. Transcriptome analyses showed similarities to corresponding human tumors. Thus, we recapitulated nerve tumor progression in NF1 and provided preclinical platforms for testing therapies at each tumor grade. These results support a tumor progression model in which loss of NF1 in Schwann cells drives plexiform neurofibromas formation, additional loss of Ink4a/Arf contributes to atypical neurofibromas formation, and further changes underlie transformation to MPNST. SIGNIFICANCE: New mouse models recapitulate the stepwise progression of NF1 tumors and will be useful to define effective treatments that halt tumor growth and tumor progression in NF1.

| S-EPMC7968129 | biostudies-literature

BCRP expression in schwannoma, plexiform neurofibroma and MPNST.

Project description:peripheral nerve sheath tumors comprise a broad spectrum of neoplasms. Vestibular schwannomas and plexiform neurofibromas are symptomatic albeit benign, but a subset of the latter pre-malignant lesions will transform to malignant peripheral nerve sheath tumors (MPNST). Surgery and radiotherapy are the primary strategies to treat these tumors. Intrinsic resistance to drug therapy characterizes all three tumor subtypes. The breast cancer resistance protein BCRP is a transmembrane efflux transporter considered to play a key role in various biological barriers such as the blood brain barrier. At the same time it is associated with drug resistance in various tumors. Its potential role in drug resistant tumors of the peripheral nervous system is largely unknown.to assess if BCRP is expressed in vestibular schwannomas, plexiform neurofibromas and MPNST.immunohistochemical staining for BCRP was performed on a tissue microarray composed out of 22 vestibular schwannomas, 10 plexiform neurofibromas and 18 MPNSTs.sixteen out of twenty-two vestibular schwannomas (73%), nine out of ten plexiform neurofibromas (90%) and six out of eighteen MPNST (33%) expressed BCRP in the vasculature. Tumor cells were negative.BCRP is present in the vasculature of vestibular schwannomas, plexiform neurofibromas and MPSNT. Therefore, it may reduce the drug exposure of underlying tumor tissues and potentially cause failure of drug therapy.

| S-EPMC5687642 | biostudies-literature

Runx1 contributes to neurofibromatosis type 1 neurofibroma formation.

Project description:Neurofibromatosis type 1 (NF1) patients are predisposed to neurofibromas but the driver(s) that contribute to neurofibroma formation are not fully understood. By cross comparison of microarray gene lists on human neurofibroma-initiating cells and developed neurofibroma Schwann cells (SCs) we identified RUNX1 overexpression in human neurofibroma initiation cells, suggesting RUNX1 might relate to neurofibroma formation. Immunostaining confirmed RUNX1 protein overexpression in human plexiform neurofibromas. Runx1 overexpression was confirmed in mouse Schwann cell progenitors (SCPs) and mouse neurofibromas at the messenger RNA and protein levels. Genetic inhibition of Runx1 expression by small hairpin RNA or pharmacological inhibition of Runx1 function by a Runx1/Cbfβ interaction inhibitor, Ro5-3335, decreased mouse neurofibroma sphere number in vitro. Targeted genetic deletion of Runx1 in SCs and SCPs delayed mouse neurofibroma formation in vivo. Mechanistically, loss of Nf1 increased embryonic day 12.5 Runx1(+)/Blbp(+) progenitors that enable tumor formation. These results suggest that Runx1 has an important role in Nf1 neurofibroma initiation, and inhibition of RUNX1 function might provide a novel potential therapeutic treatment strategy for neurofibroma patients.

| S-EPMC4679719 | biostudies-literature

Trunk Stability, Trunk Strength and Sport Performance Level in Judo.

Project description:Although trunk muscle function has been suggested to be a determinant of judo performance, its contribution to high-level performance in this sport has been poorly studied. Therefore, several tests were used to assess the differences in trunk muscle function between 11 international and 14 national level judo practitioners (judokas). Trunk strength and endurance were assessed using isokinetic tests and core stability was assessed using two protocols: 1) sudden loading, to assess trunk responses to unexpected external perturbations; 2) stable and unstable sitting, to assess the participants' ability to control trunk balance. No differences between groups were found for trunk flexor isokinetic strength, trunk responses against lateral and posterior loading and trunk control while sitting. However, international level judokas showed significantly higher trunk extensor isokinetic strength (p <0.05) and lower trunk angular displacement after anterior trunk loading (p <0.05) than national level judokas. Few and low (r < 0.512) significant correlations were found between strength, endurance and stability parameters, which suggests that trunk strength and endurance are not limiting factors for trunk stability in competitive judokas. These results support the importance of trunk extensor strength and trunk stability against forward perturbations in elite judo performance.

| S-EPMC4883759 | biostudies-literature

Management of cutaneous neurofibroma: current therapy and future directions.

Project description:Neurofibromatosis type 1 (NF1) is a life-long neurocutaneous disorder characterized by a predisposition to tumor development, including cutaneous neurofibroma (cNF), the hallmark of the disease. cNF is a histologically benign, multicellular tumor formed in virtually most individuals with NF1. It is considered the most burdensome feature of the disorder due to their physical discomfort, cosmetically disfiguring appearance, and psychosocial burden. Management of cNF remains a challenge in the medical field. Effective medicinal treatment for cNF does not exist at this time. Trials aimed at targeting individual components of the neoplasm such as mast cells with Ketotifen have not shown much success. Physical removal or destruction has been the mainstay of therapy. Surgical removal gives excellent cosmetic results, but risk in general anesthesia may require trained specialists. Destructive laser such as CO2 laser is effective in treating hundreds of tumors at one time but has high risk of scarring hypopigmentation or hyperpigmentation that alter cosmetic outcomes. A robust, low-risk surgical technique has been developed, which may be performed in clinic using traditional biopsy tools that may be more accessible to NF1 patients worldwide than contemporary techniques including Er:YAG or Nd:YAG laser. In this review, specific recommendations for management of cNFs are made based on symptoms, clinical expertise, and available resources. Additionally, antiproliferative agents aimed at stimulating cellular quiescence are explored.

| S-EPMC7317049 | biostudies-literature

Contributions of inflammation and tumor microenvironment to neurofibroma tumorigenesis.

Project description:Neurofibromatosis type 1 associates with multiple neoplasms, and the Schwann cell tumor neurofibroma is the most prevalent. A hallmark feature of neurofibroma is mast cell infiltration, which is recruited by chemoattractant stem cell factor (SCF) and has been suggested to sustain neurofibroma tumorigenesis. In the present study, we use new, genetically engineered Scf mice to decipher the contributions of tumor-derived SCF and mast cells to neurofibroma development. We demonstrate that mast cell infiltration is dependent on SCF from tumor Schwann cells. However, removal of mast cells by depleting the main SCF source only slightly affects neurofibroma progression. Other inflammation signatures show that all neurofibromas are associated with high levels of macrophages regardless of Scf status. These findings suggest an active inflammation in neurofibromas and partly explain why mast cell removal alone is not sufficient to relieve tumor burden in this experimental neurofibroma model. Furthermore, we show that plexiform neurofibromas are highly associated with injury-prone spinal nerves that are close to flexible vertebras. In summary, our study details the role of inflammation in neurofibromagenesis. Our data indicate that prevention of inflammation and possibly also nerve injury at the observed tumor locations are therapeutic approaches for neurofibroma prophylaxis and that such treatment should be explored.

| S-EPMC6025974 | biostudies-literature

A rare cause of cervical swelling: Solitary plexiform neurofibroma.

Project description:IntroductionPlexiform cervical neurofibromas are benign neoplasm, extremely rare, difficult to diagnose and to manage. Only some cases have been reported in the literature.Case presentationWe report the case of a 60-year-old man admitted for a lateral neck mass, for which the surgical indication was the increase in volume of this mass, as well as the aesthetical impairment, the surgical exploration found the tumor attached to the cervical plexus. The excision of the mass was performed without damaging nerve. The pathological study was in favor of a plexiform neurofibroma.DiscussionEven though Plexiform cervical neurofibroma are extremely rare, and their diagnosis are not often primary evoked in front of any growing mass of this region, the surgeon must keep in mind the existence of these neoplasms as a differential diagnosis of a neck tumor.ConclusionSurgery remains the gold standard in the treatment of these locally invasive tumors. It is essential that the surgeon keep in mind the possibility of these tumors as a differential diagnosis of a neck tumor.

| S-EPMC7988485 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data