Pigmented villonodular synovitis (PVNS) is a benign proliferative disorder of the synovium that usually involves joints, tendon sheaths, and bursae. It presents rarely, however, in the temporomandibular joints (TMJs). This paper reports a 59-year-old female patient with PVNS of the TMJ and its clinico-pathologic features are discussed. The patient was treated with surgery and postoperative radiotherapy (PORT). Follow-up was conducted, and there were no recurrences, metastases, skin changes or joint stiffness noted. The main treatment of PVNS is surgical resection. However, postoperative radiotherapy is important for local control of extensive tumors or positive margins. We conducted a literature review for postoperative radiotherapy case reports related to PVNS of the TMJ.
Cancer is becoming the largest threat to human health. Apart from classical anti-cancer therapies such as surgery, chemotherapies, and radiotherapy, many new therapies are being developed or translated into clinical use. These therapies include various neoadjuvant chemotherapies, minimally invasive treatments, and molecular-targeted therapies. However, none of these methods benefit all patients because treatment should be personalized according to the response of each patient. A futile therapy makes a patient miss the optimum time for treatment and increases the medical burden to the society. Thus, a great challenge is encountered in monitoring such therapies. Classical methods based on anatomical changes such as computed tomography (CT) and magnetic resonance imaging (MRI) have well-known limitations in early response evaluation. Positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) as tracer is a promising method especially when integrated with CT or MRI in one system. This article reviews the current status of monitoring anti-cancer therapies, including the evolution of evaluation criteria from the World Health Organization to the Response Evaluation Criteria in Solid Tumor and the PET Response Criteria in Solid Tumor. The advantages of 18F-FDG PET/CT for response evaluation are analyzed in various malignant tumors, and the pertinent weaknesses are discussed. Finally, several future directions in monitoring anti-cancer therapies are prospected. Keywords: Anatomical imaging, EORTC, 18F-fluorodeoxyglucose, Molecular imaging, PERCIST, PET/CT, RECIST, Response evaluation.
Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi), have gained approval for treating patients with castration-resistant prostate cancer (CRPC). Maternally expressed gene 3 (MEG3), a long non-coding RNA (lncRNA), plays a role in inhibiting tumorigenesis through regulating DNA repair genes. This study aimed to investigate the association between the anti-prostate cancer (PCa) effect of niraparib, a representative PARPi, and MEG3 expression, as well as explore the downstream pathway involved.The levels of MEG3, miR-181-5p, GATA binding protein 6 (GATA6) in clinical samples from PCa patients were accessed by RT-qPCR. PC3 cells were treated with niraparib, and the expression of MEG3, miR-181-5p, GATA6 expression was tested. PC3 cell proliferation, migration, and invasion were tested by CCK-8, wound healing, and Transwell assays, respectively. The bindings between miR-181-5p and MEG3/GATA6 were determined by dual-luciferase reporter gene assay. Furthermore, rescue experiments were conducted to investigate the underlying mechanism of MEG3/miR-181-5p/GATA6 axis in PCa progression. Additionally, mice were injected with PC3 cells transfected with sh-MEG3 and treated with niraparib, and the xenograft tumor growth was observed.MEG3 and GATA6 were upregulated and miR-181-5p was downregulated in PCa patients. Niraparib treatment substantially upregulated MEG3 and GATA6, and downregulated miR-181-5p expression in PCa cells. Niraparib effectively restrained PC3 cell proliferation, migration, and invasion. MiR-181-5p targeted to MEG3, and the inhibitory effects of MEG3 overexpression on PC3 cell proliferation and metastasis were abrogated by miR-181-5p overexpression. Moreover, GATA6 was identified as a target of miR-181-5p, and GATA6 silencing abolished the inhibitory effects of miR-181-5p inhibition on PC3 cell proliferation and metastasis. Besides, MEG3 silencing could abrogate niraparib-mediated tumor growth inhibition in mice.Niraparib restrains prostate cancer cell proliferation and metastasis and tumor growth in mice by regulating the lncRNA MEG3/miR-181-5p/GATA6 pathway.
Large maxillofacial venous malformation (VM) lesions can affect the craniofacial skeleton, causing occlusal and craniofacial deformity. Few studies have discussed the management of these skeletal disorders. It is unclear whether orthodontic treatment and orthognathic surgery are necessary after such a VM lesion has been significantly reduced.A 13-year-old boy with a large, extensive maxillofacial VM lesion, severe facial asymmetry, macroglossia, and lower lip hypertrophy visited our department in 2010. He received more than 100 sclerotherapy treatments and 20 laser treatments in the past 8 years.The patient's cosmetic disfigurement greatly improved, and the VM lesion diminished by more than 80%. Changes in the bite and craniofacial skeleton progressed from "normal" to "open bite with skeletal deformity" and finally to "spontaneously close to normal".During the progression of VM, removal of pathogenic factors can inhibit the aggravation of open bite deformity and promote the spontaneous improvement, thereby circumventing the need for complicated osteotomy, orthodontic intervention and/or orthognathic surgery.
Purpose: Extracranial Arteriovenous Malformations(AVMs) were primarily caused by somatic mutations in KRAS and MAP2K1 genes. Targeted chemotherapies are emerging but require molecular diagnosis. Since the AVMs were high flow and high pressure. It is hard to acquire the AVM lesion tissue where the mutant variants were only detected in. Few were detected in Cell-free DNA(CfDNA). Since absolute ethanol embolism is one of the effective methods for treating AVM. We hypothesized that CfDNA of post-embolism could provide the genotype of patients with AVMs. Methods: Peripheral Blood, lesion tissue specimens under the guidance of digital subtraction angiography(DSA), CfDNAs isolated from plasma of 40 patients underwent interventional embolism(before and after as T1(1h, setting first injecting ethanol moment as T0 )). 4 patients ‘s CfDNAs were collaborated in 8h(T8), 16h(T16), 24h(T24), 48h(T48), and 72h(T72) after T0. All the specimen were sequenced by a targeted NGS panel of vascular anomalies Results: Variants were detected in tissue and CfDNA but none in peripheral blood. The prevalence for tissue, CfDNA of pre-embolism and post-embolism(1h) were 73%(27/37), 27.5%(11/40), and 90%(36/40), respectively. KRAS(p.Gln61, p.Gly12) and MAP2K1(p.Gln56, p.Lys57) were the mutant hot spots. Novel mutations in BRAF, RASA1, KRAS, and MAP2K1 were also detected in tissue and cfDNA. As for specificity, area under the ROC curve were 0.8125(P<0.0001), 0.6375(P=0.0343), and 0.9500(P<0.0001). For the variants allele frequency(VAF) of CfDNA, the VAF reached a surge at T1, then a second surge at T24. Conclusion: AVMs were caused by mutations in RAS/MAPK pathway where cfDNA of post-embolism(T1) of absolute ethanol interventional therapy could provide the accurate genotype of the patients in sensitivity and specificity. VAF detected in T24 could provide information related to the natural metabolism such as the indications or prognosis of targeted chemotherapy. Overall, CfDNA of post-embolism provides us a new method for approaching the precise medicine of AVM.
Microsurgical anastomosis is technically difficult especially for less-experienced surgeons. Traditionally, surgeons in training could only accomplish these surgeries under intensive guiding and supervision from senior surgeons. This study presents and characterises a new method for microsurgical trainees to objectively evaluating the quality of vascular anastomosis intraoperatively.We conducted a prospective study to determine the utility of patency test of vascular anastomosis with assistance of high-speed video recording (PTHVR) to evaluate the quality of vascular anastomosis during microsurgery. To determine whether the use of PTHVR outperformed traditional supervision from senior surgeons (historical control), we compared the outcomes of microsurgeries including free flap transfer and replantation between the two groups.A total of 211 patients were enrolled, of which 98 underwent surgery under traditional supervision and 113 underwent surgery with PTHVR. Of the 211 patients, 102 underwent digit replantation (48%), 22 underwent limb replantation (10%), and 87 underwent free flap transfer (42%). There was no statistical difference between the two groups in age, gender, BMI, pre-existing comorbidities, smoking status, alcohol consumption, and duration of surgery. Use of PTHVR as an intraoperative guide significantly decreased the rate of re-exploration surgeries (PTHVR, 8.0% [9/113]; control, 23.5% [23/98]; P = 0.002) and replantation/free flap failures (PTHVR, 8.8% [10/113]; control, 19.4% [19/98]; P = 0.029) compared with historical control under traditional supervision.PTHVR is a useful tool for improving the success rate of microsurgery for less-experienced surgeons when compared with traditional supervision mode.
Abstract Congenital melanocytic nevus (CMN) represent a benign proliferative skin disease in the epidermis and dermis. CMN are historically known to be associated with activating NRAS or BRAF mutations. Melanoma frequently harbors the BRAF p.Val600Glu mutation, which is also commonly found in benign nevi. A recent study reported mutation of MAP2K1, a downstream effector of the RAS-RAF-MEK pathway, in melanoma with an overall frequency of 8%. Later, in 2019, Jansen P detected one activating MAP2K1 mutation in acral nevi. However, it is unknown whether MAP2K1 mutations are common in CMN, and how MAP2K1 contributes to the pathogenesis of CMN remains to be determined. In this study, we report one patient clinically and histologically diagnosed with CMN, with the MAP2K1 germline mutation and a BRAF p.Val600Glu somatic hit in the lesion. To the best of our knowledge, this is the first report of the coexistence of mutated BRAF and MAP2K1 in CMN, which may suggest that MAP2K1 mutations contribute to the occurrence and development of nevus expanding our knowledge of the genetics of CMN.
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