Focus on sarcomas.

  title={Focus on sarcomas.},
  author={Crystal L. Mackall and Paul S. Meltzer and Lee J. Helman},
  journal={Cancer cell},
  volume={2 3},

Molecular pathology of sarcomas.

This review points out the clinical projection of sarcomagenesis elucidation and knowledge of diverse types of molecular alterations in sarcomas, as well as the identification of reliable molecular markers and possible therapeutic targets.

Molecular cytogenetic studies of soft tissue sarcoma : With focus on prognosis and acquired events

The results suggest that the clinical outcome of MFH is associated with the genetic profiles of the primary tumors, and ezrin immunoreactivity could be valuable as an additional prognostic marker for this tumor type.

Gene expression profiling of human sarcomas: insights into sarcoma biology.

An online, publicly available, searchable database housing the data from the gene expression profiles of these tumors is created, allowing the user to interactively explore this data set in depth.

The Challenges of Detecting Circulating Tumor Cells in Sarcoma

The present review provides a short overview of the most recent literature on CTCs in sarcoma to demonstrate their clinical significance as predictive and/or prognostic biomarkers, and to utilize C TCs as a tool for investigating the metastatic process in Sarcoma and to identify novel therapeutic targets.

The Biology of Ewing sarcoma.

Soft Tissue Sarcoma Cancer Stem Cells: An Overview

The published evidence for CSCs in each of the most common STSs is reviewed, then a focus is focused on the methods used to study C SCs, the developmental signaling pathways usurped byCSCs, and the epigenetic alterations critical for C SC identity that may be useful for further study of STS biology.

MicroRNAs in the Tumor Biology of Soft Tissue Sarcomas

It is shown that microRNAs can discriminate diverse liposarcoma subtype, lipomas and normal fat and fine-tune the expression of HIF3α in hypoxic tumor cells, and it is demonstrated that hypoxia inducible micro RNAs, miR-210 andMiR-485-5p, fine-Tune theexpression of Hif3 α in hyp toxic tumor cells.

Sarcoma spreads primarily through the vascular system: are there biomarkers associated with vascular spread?

The chemokine signaling demonstrated to be deeply implicated in sarcoma development as well as to have a significant role in development of metastatic disease, especially in directing tumor cells towards the preferential sites of metastases in Sarcoma, lung and bone.

Adenovirus-mediated p53 gene therapy in pediatric soft-tissue sarcoma cell lines: sensitization to cisplatin and doxorubicin

The results indicate that restoration of wild-type p53 function in pediatric sarcoma cells could provide a basis for novel approaches to treatment of this disease.

A molecular map of mesenchymal tumors

The utility of gene expression profiles and machine learning for a complex clinical problem is demonstrated, and putative origins for certain mesenchymal tumors are identified.



Chromosomal translocations and sarcomas

Basic scientific findings are reviewed that elucidate the aberrant functions of SYT-SSX in chromatin remodeling and of EWS-FLI1 in transcription and mRNA splicing that will help identify new therapeutic targets.

Gastrointestinal stromal tumors with KIT mutations exhibit a remarkably homogeneous gene expression profile.

A remarkably distinct and uniform expression profile for all of the GISTs suggests that the molecular pathogenesis of a GIST results from expansion of a clone that has acquired an activating mutation in KIT without the extreme genetic instability found in the common epithelial cancers.

Gastrointestinal stromal tumor workshop.

Early clinical results in GIST are so encouraging that oncologists may soon be wrestling with the opportunity of referring every patient with malignant GIST into clinical trials with STI-571.

Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms.

Germ line p53 mutations have been detected in all five LFS families analyzed and can now be examined in additional families with LFS, and in other cancer patients and families with clinical features that might be attributed to the mutation.

KIT activation is a ubiquitous feature of gastrointestinal stromal tumors.

It is suggested that activated KIT might represent a universal therapeutic target in GISTs, and mutations in all KIT domains were associated with high-level KIT activation/phosphorylation, and KITactivation was also demonstrated in the four Gists that lacked detectable KIT genomic and cDNA mutations.

Clinical management of gastrointestinal stromal tumors: before and after STI-571.

STI-571 is a small molecule that selectively inhibits the enzymatic activity of the ABL, platelet-derived growth factor receptor, and KIT tyrosine kinases and the BCR-ABL fusion protein and is a landmark development in cancer therapy.

Rhabdomyosarcoma in children: epidemiologic study and identification of a familial cancer syndrome.

While suggesting the role of inheritance, the familial patterns seen with rhabdomyosarcoma may result from an interaction of genetic and environmental (?viral) fadors.

Familial gastrointestinal stromal tumours with germline mutation of the KIT gene

nature genetics volume 19 august 1998 323 Gastrointestinal stromal tumour (GIST) is the most common mesenchymal tumour of the human gastrointestinal tract. Most GISTs are solitary, and

Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors.

Sequencing of c-kit complementary DNA from five GISTs revealed mutations in the region between the transmembrane and tyrosine kinase domains, suggesting that the mutations contribute to tumor development.