Malignant high-grade histological transformation of inflammatory myofibroblastic tumour associated with amplification of<i>TPM3-ALK</i>: Figure 1

Zhang, Hongying; Erickson-Johnson, Michele R.; Wang, Xiaoke; Bahrami, Armita; Medeiros, Fabíola; Lonzo, Melissa L.; Oliveira, André M.

doi:10.1136/jcp.2010.080705

Cited by 6 publications

(6 citation statements)

References 5 publications

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“…The most commonly reported TPM3 breakpoints in both ALK and NTRK1 fusion transcripts involve intron 7, resulting in incorporation of sequences N‐terminal to exon 8 which include the dimerization domain, as seen in our cases. An increased metastatic potential has been suggested in cell lines harboring TPM3‐ALK compared with other ALK fusion transcripts (Armstrong et al, ), and isolated case reports have suggested a more aggressive clinical behavior in ALCL and IMT harboring TPM3‐ALK fusion transcripts (Zhang et al, ; Shin et al, ; Hoshino et al, ). Although five out of six patients presented here showed advanced local stage with extra‐renal extension and/or lymph node metastases, no firm conclusions about clinical behavior can be drawn at this time due to the short follow up time and limited clinical information.…”

Section: Discussionmentioning

confidence: 99%

ALK‐rearranged renal cell carcinomas in children

Cajaíba

Jennings

Rohan

et al. 2016

Genes Chromosomes & Cancer

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Knowledge of the clinicopathological and molecular spectrum of pediatric renal cell carcinomas (RCC) remains limited, and approximately 16%-24% of these neoplasms cannot be classified into specific subtypes. In this review of 168 pediatric RCC prospectively registered on Children's Oncology Group AREN03B2 protocol, six RCC (3.5%) that demonstrated a unique epithelioid morphology and a peculiar immunophenotypic profile that includes expression of ALK, TFE3, and retention of INI1 was identified. Further investigation revealed ALK rearrangements in all cases, manifested molecularly by fusion transcripts of either VCL-ALK (3 patients all with sickle cell trait which had been previously reported) or TPM3-ALK (3 patients, none with sickle cell trait). Based on the shared unique morphologic, immunophenotypic, and genetic features, it was proposed that these neoplasms belonged to a distinct subgroup of RCC frequently occurring in pediatric patients, which they have termed as ALK-rearranged RCC. Importantly, additional therapeutic options may be available for these patients.

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Section: Discussionmentioning

confidence: 99%

ALK‐rearranged renal cell carcinomas in children

Cajaíba

Jennings

Rohan

et al. 2016

Genes Chromosomes & Cancer

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“…99 Furthermore, chromosomal translocation of the tpm3 gene to other DNA regions has also been reported to lead to carcinogenesis. Thus examples of the fusion of the tpm3 gene to the anaplastic lymphoma kinase ALK gene, resulting in the chimera TPM3-ALK has been linked to inflammatory myofibroblastic tumors 100 and anaplastic large cell lymphoma, 101 whereas fusion of the tpm3 gene to the TRK kinase gene leads to human thyroid papillary carcinoma. 102 In all these cases, a direct role for tpm3 as an oncogene has always been in question since it could potentially act indirectly by promoting dimerization/multimerization which would be sufficient to lead to activation of the associated kinase protein.…”

Section: Regulation Of Specific Actin Binding Proteins In Cancer Progmentioning

confidence: 99%

Actin binding proteins

Gross

2013

Cell Adhesion & Migration

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In order to metastasize away from the primary tumor site and migrate into adjacent tissues, cancer cells will stimulate cellular motility through the regulation of their cytoskeletal structures. Through the coordinated polymerization of actin filaments, these cells will control the geometry of distinct structures, namely lamella, lamellipodia and filopodia, as well as the more recently characterized invadopodia. Because actin binding proteins play fundamental functions in regulating the dynamics of actin polymerization, they have been at the forefront of cancer research. This review focuses on a subset of actin binding proteins involved in the regulation of these cellular structures and protrusions, and presents some general principles summarizing how these proteins may remodel the structure of actin. The main body of this review aims to provide new insights into how the expression of these actin binding proteins is regulated during carcinogenesis and highlights new mechanisms that may be initiated by the metastatic cells to induce aberrant expression of such proteins.

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“…These lesions show similar pathological characteristics, but differ biologically. IMT, a distinctive neoplasm with a few reactive inflammatory cells that occurs primarily in viscera and soft tissues, predominantly affects children and young adults (9). As IMT of the neck is a rare disease, to the best of our knowledge, the present study is the first case report of the lesion.…”

Section: Discussionmentioning

confidence: 72%

A case report of an inflammatory myofibroblastic tumor of the neck: A focus on the computed tomography and magnetic resonance imaging findings

2015

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Abstract. Inflammatory myofibroblastic tumors (IMTs) of the neck are rare, with only a few patients reported in the literature. The present study discusses the clinical manifestations, radiographic characteristics and management of these tumors, with a focus on imaging modalities. A case of IMT of the neck is presented and the associated literature is reviewed. In total, seven patients in seven English-language studies, including the present case, and one patient in one Chinese-language study were found. On CT scans, all tumors appeared as soft-tissue densities. Upon magnetic resonance imaging (MRI), all tumors displayed a heterogeneous hypointense-isointense signal on T1-weighted sequences and an isointense-hyperintense signal on T2-weighted sequences. All tumors showed enhancement on enhanced CT and MR images. The imaging features of the neck IMTs can be summarized as follows: i) When enhanced, the tumor displays enhancement on CT and MR images; ii) MRI is superior to CT scans in the differential diagnosis of this disease; iii) in general, the lesion displays a hypointense-isointense signal on T1-weighted sequences and an isointense-hyperintense signal on T2-weighted sequences; iv) due to the fibrous tissue in the tumor, delayed enhancement may be observed on gadolinium-enhanced MR images; and v) due to its benign or intermediate features, the tumor is usually a well-defined mass.

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Malignant high-grade histological transformation of inflammatory myofibroblastic tumour associated with amplification ofTPM3-ALK: Figure 1

Cited by 6 publications

References 5 publications

ALK‐rearranged renal cell carcinomas in children

ALK‐rearranged renal cell carcinomas in children

Actin binding proteins

A case report of an inflammatory myofibroblastic tumor of the neck: A focus on the computed tomography and magnetic resonance imaging findings

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