Cell cycle and apoptosis regulatory proteins, proliferative markers, cell signaling molecules, CD209, and decorin immunoreactivity in low-grade myxofibrosarcoma and myxoma

Cates, Justin M.; Memoli, Vincent A.; González, Raúl

doi:10.1007/s00428-015-1778-8

Cited by 12 publications

(10 citation statements)

References 24 publications

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“…In a recent study, on the other hand, Cates et al [28] saw no difference in decorin immunoreactivity between myxoma and myxofibrosarcoma. In fact, none of the 19 potential diagnostic markers tested distinguished myxoma from myxofibrosarcoma [28]. The authors concluded that the distinction between these tumors must still be made based on morphologic criteria.…”

Section: Discussionmentioning

confidence: 90%

“…Both decorin immunoreactivity and mRNA expression of DCN (the gene coding for decorin) were positive in the former but not in the latter [27]. In a recent study, on the other hand, Cates et al [28] saw no difference in decorin immunoreactivity between myxoma and myxofibrosarcoma. In fact, none of the 19 potential diagnostic markers tested distinguished myxoma from myxofibrosarcoma [28].…”

Section: Discussionmentioning

confidence: 99%

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Karyotyping and analysis of GNAS locus in intramuscular myxomas

et al. 2017

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Intramuscular myxoma is a benign soft tissue tumor about which very limited genetic information exists. We studied 68 intramuscular myxomas by means of chromosome banding analysis finding abnormal karyotypes in 21 of them. The most clearly nonrandom involvement was of chromosome 8 which was found gained in seven tumors (+8 was the sole change in five myxomas) and structurally rearranged in another two. Since mutation of the gene GNAS (20q13) has been implicated in the pathogenesis of both solitary and hereditary multiple myxomas, we assessed the transcription and mutation status of this gene in five tumors from which we had suitable RNA. All five intramuscular myxomas expressed biallelic transcripts. The mutated GNAS allele found in one tumor was also biallelically transcribed. In none of the five myxomas were maternally expressed transcripts detected. Collectively, the data suggest that intramuscular myxomas have acquired genetic abnormalities that often include chromosome 8 changes but may also involve alterations of GNAS. To what extent these aberrations are pathogenetically important, remains uncertain.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Karyotyping and analysis of GNAS locus in intramuscular myxomas

et al. 2017

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“…It has been reported that GMNN is associated with different diseases including cancer. GMNN have been found to associate with regulation of apoptosis, regulatory proteins of cell cycle, cell proliferation markers, signaling molecules and extracellular matrix moieties [3]. Proliferation and labeling index are the two parameters that are used to measure dividing cells in particular tumor and mitotic activity of a cell population respectively.…”

Section: Editorialmentioning

confidence: 99%

Geminin as an Emerging Anticancer Drug Target

Kumar¹

2016

JOJCS

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EditorialFor normal cell division, one time replication origin firing is mandatory. The mutual interaction and levels of Cdt1 and geminin (GMNN) proteins are known to be involved in this regulatory mechanism. Imbalance between these protein levels may cause defects in replication of DNA leading to genome instability. This might cause cancer. In different stem cells, such as leukemic and hematopoietic stem cells, significant levels of GMNN have been recorded. It has been observed that siRNA mediated GMNN suppression can arrest cancer cell proliferation without affecting the normal cells. Two molecules of GMNN and one molecule of Cdt1 form a heterotrimer, and two heterotrimer combines and form heterohexamer which inhibits the DNA licensing process. Any moiety that is able to inhibit the formation of GMNN-Cdt1 heterohexamer might act as regulatory source and could be utilized as a DNA replication inhibitor in cancer cells (Figure 1).

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“…Benign myxoid tumors include myxomas and angiomyxomas; and malignant myxoid tumors include fibromyxoid sarcomas, extraskeletal myxoid chondrosarcomas, ossifying fibromyxoid tumors, myxoid liposarcomas, myxoinflammatory fibroblastic tumors and myxofibrosarcomas [1]. Each myxoid neoplasms has key chromosomal translocations or immunohistochemical markers that are pathognomic for its diagnosis except for myxomas and myxofibrosarcomas [1–8]. Myxofibrosarcomas and myxomas are not associated with any particular translocation or gene expression product, and their diagnoses are based on their histological appearances [1, 8–10].…”

Section: Introductionmentioning

confidence: 99%

“…Each myxoid neoplasms has key chromosomal translocations or immunohistochemical markers that are pathognomic for its diagnosis except for myxomas and myxofibrosarcomas [1–8]. Myxofibrosarcomas and myxomas are not associated with any particular translocation or gene expression product, and their diagnoses are based on their histological appearances [1, 8–10]. Therefore, one of the greatest diagnostic dilemmas for a pathologist lies in differentiating a myxoma from a myxofibrosarcoma, and particularly differentiating a cellular myxoma from some low-grade myxofibrosarcomas [1, 8–10].…”

Section: Introductionmentioning

confidence: 99%

Radiomic features from MRI distinguish myxomas from myxofibrosarcomas

Martin-Carreras

Cooper

et al. 2019

BMC Med Imaging

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Background Myxoid tumors pose diagnostic challenges for radiologists and pathologists. All myxoid tumors can be differentiated from each other using fluorescent in-situ hybridization (FISH) or immunohistochemical markers, except for myxomas and myxofibrosarcomas. Myxomas and myxofibrosarcomas are rare tumors. Myxomas are benign and histologically bland, whereas myxofibrosarcomas are malignant and histologically heterogenous. Because of the histological heterogeneity, low grade myxofibrosarcomas may be mistaken for myxomas on core needle biopsies. We evaluated the performance of T1-weighted signal intensity (T1SI), tumor volume, and radiomic features extracted from magnetic resonance imaging (MRI) to differentiate myxomas from myxofibrosarcomas. Methods The MRIs of 56 patients (29 with myxomas, 27 with myxofibrosarcomas) were analyzed. We extracted 89 radiomic features. Random forests based classifiers using the T1SI, volume features, and radiomic features were used to differentiate myxomas from myxofibrosarcomas. The classifiers were validated using a leave-one-out cross-validation. The performances of the classifiers were then compared. Results Myxomas had lower normalized T1SI than myxofibrosaromas ( p = 0.006) and the AUC using the T1SI was 0.713. However, the classification model using radiomic features had an AUC of 0.885 (accuracy = 0.839, sensitivity = 0.852, specificity = 0.828), and outperformed the classification models using T1SI (AUC = 0.713) and tumor volume (AUC = 0.838). The classification model using radiomic features was significantly better than the classifier using T1SI values ( p = 0.039). Conclusions Myxofibrosarcomas are on average higher in T1-weighted signal intensity than myxomas. Myxofibrosarcomas are larger and have shape differences compared to myxomas. Radiomic features performed best for differentiating myxomas from myxofibrosarcomas compared to T1-weighted signal intensity and tumor volume features. Electronic supplementary material The online version of this article (10.1186/s12880-019-0366-9) contains supplementary material, which is available to authorized users.

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Cell cycle and apoptosis regulatory proteins, proliferative markers, cell signaling molecules, CD209, and decorin immunoreactivity in low-grade myxofibrosarcoma and myxoma

Cited by 12 publications

References 24 publications

Karyotyping and analysis of GNAS locus in intramuscular myxomas

Karyotyping and analysis of GNAS locus in intramuscular myxomas

Geminin as an Emerging Anticancer Drug Target

Radiomic features from MRI distinguish myxomas from myxofibrosarcomas

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