Abstract:IntroductionDesmoid tumor (DT) is a rare neoplasm with high local recurrence rates, composed of fibroblastic cells that are characterized by the expression of key molecules, including the intermediate filament vimentin, cyclooxygenase-2 (COX-2), and nuclear β-catenin, and lack of epithelial markers. Circulating tumor cells (CTCs) isolated from the peripheral blood of patients with sarcomas and other neoplasms can be used as early biomarkers of tumor invasion and dissemination. Moreover, CTCs can also re-coloni… Show more
“…As TGF‐β is a universal driver of fibrosis and has been implicated in the growth of DTs, 18 , 19 , 20 we next performed immunohistochemistry for p‐Smad2 and TGF‐β1 in DTs of C mice. The frequency of p‐Smad2‐positive cells in DTs on day 15 was elevated compared with normal tissues and slightly decreased on day 40.…”
Section: Resultsmentioning
confidence: 99%
“…As TGF-β is a universal driver of fibrosis and has been implicated in the growth of DTs, [18][19][20] smaller in size and mass than those in C mice (Figure 3B,C). Histological analysis showed that tumors in CS mice contained numerous cysts (Figure 3D).…”
Section: Tgf-β Signaling Promotes Dt Formation In Mouse Modelsmentioning
Desmoid tumors (DTs), also called desmoid‐type fibromatoses, are locally aggressive tumors of mesenchymal origin. In the present study, we developed a novel mouse model of DTs by inducing a local mutation in the Ctnnb1 gene, encoding β‐catenin in PDGFRA‐positive stromal cells, by subcutaneous injection of 4‐hydroxy‐tamoxifen. Tumors in this model resembled histologically clinical samples from DT patients and showed strong phosphorylation of nuclear SMAD2. Knockout of SMAD4 in the model significantly suppressed tumor growth. Proteomic analysis revealed that SMAD4 knockout reduced the level of Cysteine‐and‐Glycine‐Rich Protein 2 (CSRP2) in DTs, and treatment of DT‐derived cells with a TGF‐β receptor inhibitor reduced CSRP2 RNA levels. Knockdown of CSRP2 in DT cells significantly suppressed their proliferation. These results indicate that the TGF‐β/CSRP2 axis is a potential therapeutic target for DTs downstream of TGF‐β signaling.
“…As TGF‐β is a universal driver of fibrosis and has been implicated in the growth of DTs, 18 , 19 , 20 we next performed immunohistochemistry for p‐Smad2 and TGF‐β1 in DTs of C mice. The frequency of p‐Smad2‐positive cells in DTs on day 15 was elevated compared with normal tissues and slightly decreased on day 40.…”
Section: Resultsmentioning
confidence: 99%
“…As TGF-β is a universal driver of fibrosis and has been implicated in the growth of DTs, [18][19][20] smaller in size and mass than those in C mice (Figure 3B,C). Histological analysis showed that tumors in CS mice contained numerous cysts (Figure 3D).…”
Section: Tgf-β Signaling Promotes Dt Formation In Mouse Modelsmentioning
Desmoid tumors (DTs), also called desmoid‐type fibromatoses, are locally aggressive tumors of mesenchymal origin. In the present study, we developed a novel mouse model of DTs by inducing a local mutation in the Ctnnb1 gene, encoding β‐catenin in PDGFRA‐positive stromal cells, by subcutaneous injection of 4‐hydroxy‐tamoxifen. Tumors in this model resembled histologically clinical samples from DT patients and showed strong phosphorylation of nuclear SMAD2. Knockout of SMAD4 in the model significantly suppressed tumor growth. Proteomic analysis revealed that SMAD4 knockout reduced the level of Cysteine‐and‐Glycine‐Rich Protein 2 (CSRP2) in DTs, and treatment of DT‐derived cells with a TGF‐β receptor inhibitor reduced CSRP2 RNA levels. Knockdown of CSRP2 in DT cells significantly suppressed their proliferation. These results indicate that the TGF‐β/CSRP2 axis is a potential therapeutic target for DTs downstream of TGF‐β signaling.
“…Histologically, desmoid tissue is also positive for nuclear beta-catenin, intermediate vimentin, and COX-2 and will appear as intertwining bundles of spindle cells within a collagen matrix (Fig. 2 ) [ 14 , 15 ]. Fig.…”
Background
Desmoid-type fibromatosis (DTF) is a rare benign lesion that usually arises from the abdominal wall or extremities and rarely from the mesentery or intrabdominal organs. Malignant peritoneal mesothelioma is also a rare, yet aggressive disease. To our knowledge, this is the first case report of desmoid-type fibromatosis in the setting of malignant peritoneal mesothelioma.
Case presentation
An early 30-year-old female was referred to our center for large intra-abdominal mass concerning for recurrent malignant peritoneal mesothelioma after previous cytoreductive surgery with hyperthermic intraperitoneal chemotherapy and adjuvant chemotherapy. Further investigation revealed a large mesenteric mass, which was resected en bloc with the cecum and terminal ileum. Pathologic findings confirmed a surprising diagnosis of desmoid-type fibromatosis.
Conclusions
No adjuvant therapy was offered to this patient due to negative tumor margins; however, close follow-up will be provided for recurrence of both malignant peritoneal mesothelioma and desmoid-type fibromatosis, which can be differentiated in the future via biopsy in this patient.
“…However, EMT in CTC down-regulates epithelial phenotypes, such as EpCAM, making accurate CTCs detection challenging. Other commonly used detection and isolation methods include the CellSearch system, 38 immunocytochemistry (ICC), 39 and membrane filtration methods. 40 …”
This review summarizes the application of various photothermal materials in the detection of circulating tumor cells (CTCs), and describes the significance of CTCs detection for early tumor diagnosis and tumor prognosis.
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