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AJCC eighth edition for soft tissue sarcoma of the extremities and trunk.
Cates JMM
(2018) Ann Oncol 29: 2023
MeSH Terms: Extremities, Humans, Neoplasm Staging, Sarcoma, Soft Tissue Neoplasms, United States
Added November 1, 2018
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6 MeSH Terms
Intraoperative Raman spectroscopy of soft tissue sarcomas.
Nguyen JQ, Gowani ZS, O'Connor M, Pence IJ, Nguyen TQ, Holt GE, Schwartz HS, Halpern JL, Mahadevan-Jansen A
(2016) Lasers Surg Med 48: 774-781
MeSH Terms: Adult, Algorithms, Humans, Intraoperative Care, Logistic Models, Margins of Excision, Multivariate Analysis, Sarcoma, Sensitivity and Specificity, Soft Tissue Neoplasms, Spectrum Analysis, Raman
Show Abstract · Added September 15, 2017
BACKGROUND AND OBJECTIVE - Soft tissue sarcomas (STS) are a rare and heterogeneous group of malignant tumors that are often treated through surgical resection. Current intraoperative margin assessment methods are limited and highlight the need for an improved approach with respect to time and specificity. Here we investigate the potential of near-infrared Raman spectroscopy for the intraoperative differentiation of STS from surrounding normal tissue.
MATERIALS AND METHODS - In vivo Raman measurements at 785 nm excitation were intraoperatively acquired from subjects undergoing STS resection using a probe based spectroscopy system. A multivariate classification algorithm was developed in order to automatically identify spectral features that can be used to differentiate STS from the surrounding normal muscle and fat. The classification algorithm was subsequently tested using leave-one-subject-out cross-validation.
RESULTS - With the exclusion of well-differentiated liposarcomas, the algorithm was able to classify STS from the surrounding normal muscle and fat with a sensitivity and specificity of 89.5% and 96.4%, respectively.
CONCLUSION - These results suggest that single point near-infrared Raman spectroscopy could be utilized as a rapid and non-destructive surgical guidance tool for identifying abnormal tissue margins in need of further excision. Lasers Surg. Med. 48:774-781, 2016. © 2016 Wiley Periodicals, Inc.
© 2016 Wiley Periodicals, Inc.
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11 MeSH Terms
Differential diagnostic considerations of desmoid-type fibromatosis.
Goldstein JA, Cates JM
(2015) Adv Anat Pathol 22: 260-6
MeSH Terms: Diagnosis, Differential, Fibroma, Fibromatosis, Aggressive, Fibrosarcoma, Humans, Soft Tissue Neoplasms
Show Abstract · Added February 15, 2016
Fibrous and myofibroblastic tumors of soft tissue often present the surgical pathologist with a difficult differential diagnosis because of the number of diagnostic possibilities and morphologic similarities among cytologically bland spindle-cell tumors. Prototypical in this regard is desmoid-type fibromatosis. In a review of 320 surgical specimens diagnosed as desmoid tumor, 94 (29%) were discovered to be misclassified as such. The most common lesions in this series were Gardner fibroma, scar tissue, superficial fibromatosis, nodular fasciitis, myofibroma, and collagenous fibroma. Four sarcomas were also misinterpreted as desmoid-type fibromatosis (3 low-grade fibromyxoid sarcomas and 1 unclassified spindle-cell sarcoma). We take this opportunity to compare and contrast desmoid tumor and several of the soft tissue tumors that should be considered in the differential diagnosis thereof.
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6 MeSH Terms
Expression of ROS1 predicts ROS1 gene rearrangement in inflammatory myofibroblastic tumors.
Hornick JL, Sholl LM, Dal Cin P, Childress MA, Lovly CM
(2015) Mod Pathol 28: 732-9
MeSH Terms: Adolescent, Adult, Child, Child, Preschool, Female, Gene Rearrangement, High-Throughput Nucleotide Sequencing, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Infant, Inflammation, Male, Middle Aged, Myofibroma, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Reverse Transcriptase Polymerase Chain Reaction, Soft Tissue Neoplasms, Young Adult
Show Abstract · Added September 10, 2020
Inflammatory myofibroblastic tumor is a distinctive, rarely metastasizing mesenchymal neoplasm composed of fascicles of spindle cells with a prominent inflammatory infiltrate. Roughly 50% of inflammatory myofibroblastic tumors harbor ALK receptor tyrosine kinase gene rearrangements. Such tumors are usually positive for ALK by immunohistochemistry. The molecular pathogenesis of ALK-negative inflammatory myofibroblastic tumors is largely unknown. A recent study identified rearrangements of ROS1 (another tyrosine kinase receptor) in a subset of ALK-negative inflammatory myofibroblastic tumors. Immunohistochemistry for ROS1 has been shown to correlate with ROS1 rearrangement in lung adenocarcinomas. The purpose of this study was to determine whether immunohistochemistry for ROS1 could predict ROS1 rearrangement in inflammatory myofibroblastic tumor. In total, 30 inflammatory myofibroblastic tumors were evaluated, including 21 ALK-positive tumors (10 confirmed to harbor ALK rearrangements, with TPM3, CLTC, RANPB2, and FN1 fusion partners) and 9 ALK-negative tumors (including 2 known to harbor ROS1 rearrangements). Immunohistochemistry was performed on whole tissue sections following pressure cooker antigen retrieval using a rabbit anti-ROS1 monoclonal antibody. The results were scored as 'positive' or 'negative,' and the pattern of staining was recorded. Three ALK-negative inflammatory myofibroblastic tumors (including both tumors with known ROS1 rearrangements) showed immunoreactivity for ROS1, whereas all ALK-positive inflammatory myofibroblastic tumors were negative for ROS1. One ROS1-positive inflammatory myofibroblastic tumor (with YWHAE-ROS1 fusion) showed strong, diffuse cytoplasmic and nuclear staining; one case (with TFG-ROS1 fusion) showed weak, diffuse and dot-like cytoplasmic staining; and one case (fusion partner unknown) showed moderate, diffuse and dot-like cytoplasmic staining. Expression of ROS1 correlates with ROS1 gene rearrangement in inflammatory myofibroblastic tumor. These findings suggest that immunohistochemistry for ROS1 may be useful to support the diagnosis of a subset of inflammatory myofibroblastic tumors and may select some clinically aggressive cases for targeted therapy directed against ROS1.
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MeSH Terms
MFH and high-grade undifferentiated pleomorphic sarcoma-what's in a name?
Delisca GO, Mesko NW, Alamanda VK, Archer KR, Song Y, Halpern JL, Schwartz HS, Holt GE
(2015) J Surg Oncol 111: 173-7
MeSH Terms: Aged, Cohort Studies, Female, Histiocytoma, Malignant Fibrous, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Neoplasm Metastasis, Neoplasm Recurrence, Local, Prognosis, Retrospective Studies, Sarcoma, Soft Tissue Neoplasms, Terminology as Topic
Show Abstract · Added January 20, 2015
BACKGROUND AND OBJECTIVES - In 2002, with the advent of better classification techniques, the World Health Organization declassified malignant fibrous histiocytoma (MFH) as a distinct histological entity in favor of the reclassified entity high-grade undifferentiated pleomorphic sarcoma (HGUPS). To date, no study has evaluated comparative outcomes between patients designated historically in the MFH group and those classified in the new HGUPS classification. Our goal was to determine the presence of clinical prognostic implications that have evolved with this new nomenclature.
METHODS - Sixty-eight patients were retrospectively evaluated between January 1998 and December 2007. Forty-five patients diagnosed with MFH between 1998 and 2003 were compared to 23 patients in the HGUPS group, from 2004 to 2007. Primary prognostic outcomes assessed included overall survival, metastatic-free, and local recurrence-free survival.
RESULTS - Five-year survivorship between MFH and HGUPS populations, using Kaplan-Meier or competing risk methods, did not show statistical difference for overall survival (60% vs. 74%, P=0.36), 5-year metastasis-free survival (31% vs. 26%, P=0.67), or local recurrence-free survival (13% vs. 16%, P=0.62).
CONCLUSION - Despite new classification nomenclature, there appears to be no identifiable prognostic implications for sarcomas that remain in the unclassifiable HGUPS group, as compared to the previously accepted MFH group.
© 2014 Wiley Periodicals, Inc.
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15 MeSH Terms
Syndrome-associated soft tissue tumours.
Coffin CM, Davis JL, Borinstein SC
(2014) Histopathology 64: 68-87
MeSH Terms: Humans, Soft Tissue Neoplasms, Syndrome
Show Abstract · Added March 7, 2014
Soft tissue neoplasms may be associated with a variety of genetic disorders and malformation syndromes, especially when they arise in children, adolescents and early adulthood. This review summarizes the principal histopathological types of soft tissue tumours which occur in various syndromes, with an emphasis on pathological features, genetic aspects and considerations for the diagnostic pathologist.
© 2013 John Wiley & Sons Ltd.
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3 MeSH Terms
Myxoinflammatory fibroblastic sarcoma in children and adolescents: clinicopathologic aspects of a rare neoplasm.
Weiss VL, Antonescu CR, Alaggio R, Cates JM, Gaskin D, Stefanovici C, Coffin CM
(2013) Pediatr Dev Pathol 16: 425-31
MeSH Terms: Adolescent, Biomarkers, Tumor, Child, Child, Preschool, Female, Fibrosarcoma, Humans, Immunohistochemistry, Male, Soft Tissue Neoplasms
Show Abstract · Added March 7, 2014
Myxoinflammatory fibroblastic sarcoma (MIFS), originally described as a low-grade malignant soft-tissue tumor in adults, has recently been reported in children and in non-acral sites. This report describes the clinicopathologic features of a series of 5 MIFS in children and adolescents (3 males, 2 females), ranging in age from 5 to 17 years (mean, 13 years). These tumors presented as small, superficial, slowly growing soft-tissues masses of the scalp, neck, middle finger, forearm, and thigh. Histologically, the tumors were composed of spindled and plump polygonal cells with prominent nuclear pleomorphism, nuclear pseudoinclusions; large eosinophilic nucleoli; myxoid foci intermingled with spindled foci; and an accompanying inflammatory infiltrate of lymphocytes, plasma cells, and variable neutrophils. Immunohistochemical analysis revealed variable reactivity for CD34 and smooth muscle actin in the tumor cells. Genetic analysis in 3 cases showed no rearrangements of TGFBR3 or MGEA5. Follow up in 4 cases revealed no recurrence or metastasis. These 5 cases of childhood and adolescent MIFS demonstrate an expanded age range and topographic distribution and a favorable outcome. The differential diagnosis and importance of recognizing this rare neoplasm in young patients are discussed.
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10 MeSH Terms
Cyclin-dependent kinase inhibitor 2A (p16) distinguishes well-differentiated liposarcoma from lipoma.
Gonzalez RS, McClain CM, Chamberlain BK, Coffin CM, Cates JM
(2013) Histopathology 62: 1109-11
MeSH Terms: Biomarkers, Tumor, Cyclin-Dependent Kinase Inhibitor p16, Diagnosis, Differential, Female, Humans, Lipoma, Liposarcoma, Male, Middle Aged, Soft Tissue Neoplasms
Added March 7, 2014
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10 MeSH Terms
Tumor size increase following preoperative radiation of soft tissue sarcomas does not affect prognosis.
Delisca GO, Alamanda VK, Archer KR, Song Y, Schwartz HS, Holt GE
(2013) J Surg Oncol 107: 723-7
MeSH Terms: Adult, Aged, Chemotherapy, Adjuvant, Disease-Free Survival, Female, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Neoadjuvant Therapy, Prognosis, Radiotherapy, Adjuvant, Retrospective Studies, Sarcoma, Soft Tissue Neoplasms, Treatment Outcome
Show Abstract · Added March 7, 2014
BACKGROUND AND OBJECTIVES - Administration of preoperative radiotherapy for extremity soft tissue sarcoma improves local control, while allowing for a more conservative surgical resection. During radiation treatment tumor size typically decreases or remains constant. In a subset of patients, however, a size increase in the tumor occurs. Our goal was to investigate the prognosis of patients who had a size increase of at least 20% over the course of preoperative radiotherapy versus those who did not.
METHODS - This retrospective study evaluated 70 patients treated for localized primary STS of the extremities between January 2000 and December 2008. Kaplan-Meier curves for disease-specific and metastasis-free survival were calculated for both groups.
RESULTS - Sixty-one patients had stable or decrease local tumor size following preoperative radiotherapy and nine patients had an increase of at least 20% in tumor size. There were no statistically significant differences found in disease-specific survival and metastasis-free survival (Gray's test, P = 0.93 and P = 0.68, respectively) among the two groups.
CONCLUSION - Our results indicate that a 20% increase in tumor size following preoperative radiotherapy did not result in a worse outcome for patients when compared to those who had stable or decrease local tumor size following preoperative radiotherapy.
Copyright © 2013 Wiley Periodicals, Inc.
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16 MeSH Terms
SMARCB1 protein and mRNA loss is not caused by promoter and histone hypermethylation in epithelioid sarcoma.
Papp G, Changchien YC, Péterfia B, Pecsenka L, Krausz T, Stricker TP, Khoor A, Donner L, Sápi Z
(2013) Mod Pathol 26: 393-403
MeSH Terms: Adolescent, Adult, Aged, Aged, 80 and over, Child, Chromosomal Proteins, Non-Histone, DNA Methylation, DNA Mutational Analysis, DNA-Binding Proteins, Down-Regulation, Enhancer of Zeste Homolog 2 Protein, Female, Gene Deletion, Gene Expression Regulation, Neoplastic, Genetic Predisposition to Disease, Histones, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Laser Capture Microdissection, Male, Middle Aged, Mutation, Phenotype, Poland, Polycomb Repressive Complex 2, Promoter Regions, Genetic, RNA, Messenger, Real-Time Polymerase Chain Reaction, Retrospective Studies, Reverse Transcriptase Polymerase Chain Reaction, SMARCB1 Protein, Sarcoma, Soft Tissue Neoplasms, Transcription Factors, United States, Young Adult
Show Abstract · Added March 28, 2014
About 10% of epithelioid sarcomas have biallelic mutation of the SMARCB1 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily b, member 1) gene resulting in a lack of this nuclear protein. It has been suggested that SMARCB1 may be silenced by epigenetic changes in the remaining 90% of tumors. Thus, we hypothesized that the promoter of SMARCB1 is hypermethylated. We also examined SMARCB1 mRNA level to determine if a post-translational change was possible. Thirty-six cases of epithelioid sarcomas were studied. Immunohistochemistry and mutation analysis of the SMARCB1 gene were performed to select appropriate cases. Methylation status was assessed by methylation-specific PCR. Laser capture microdissection of tumor cells followed by real-time PCR was applied to examine the expression of SMARCB1 mRNA. Of 36 epithelioid sarcomas, 31 (86%) displayed a lack of SMARCB1 nuclear protein. In all, 4 (13%) of 31 SMARCB1-negative cases harbored biallelic deletion while 9 (33%) cases showed single-allelic deletion. One (4%) frameshift deletion of exon 3 and one point mutation of exon 7 were also found. In 16 (59%) cases, both alleles were intact. Altogether, 25/31 (81%) SMARCB1-negative cases had at least one intact allele. None of these cases demonstrated promoter hypermethylation. Low levels of SMARCB1 mRNA were found in all cases with tumor tissue extracted RNA (because of the minimal normal cell contamination) but no mRNA could be detected in laser dissected cases (containing only tumor cells). Enhancer of zeste homolog 2 (EZH2) overexpression was not characteristic of epithelioid sarcoma. Thus, loss of SMARCB1 expression in epithelioid sarcoma is caused neither by DNA hypermethylation nor by post-translational modifications. Most likely it is the microRNA destruction of SMARCB1 mRNA but further investigations are needed to elucidate this issue.
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37 MeSH Terms