• 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2020-03
  • 2020-07
  • 2020-08
  • 2021-03
  • As has been reported in other malignancies


    As has been reported in other malignancies, we found that the appearance of the radiographic characteristics of LC on post-surgical follow-up CT was associated with a statistically worse OS and PFS compared to patients that did not develop radiographic evidence of LC on CT. In our cohort of 44 patients status post EPD, the median overall survival in those that developed LC was 21 months compared to 51 months in patients that did not develop LC. Kadota et al. [3] reported an OS of 11 months for patients with lymphatic invasion compared to 21 months for patients that did not develop invasion in their Cytochalasin D of patients with MPM. Other studies have demonstrated a prognostic significance for the development of LC. For example, a reported 2–4% 2-year survival in breast cancer [21] and mean survival of 13 months in lung cancer in patients that developed LC [22]. Harold et al reported a 3-month survival for patients with cancer that developed LC [23]. Our study has several limitations to be considered. As this data was not collected prospectively, clinical variables that may influence the manifestation of LC on imaging cannot be controlled for including surgical and PDT factors. Our results may not be generalizable to patients that do not undergo EPD with intraoperative PDT. In addition, due to the retrospective nature of this study, surgical pathology was not collected prospectively for direct review. As a result, while none of the clinical surgical pathology reports described the presence of LC in resected specimens, the presence of LC in resected specimens at surgery can not be assessed for specifically, though felt to be unlikely. Finally, the diagnosis of LC was made based on radiographic changes on computed tomography (CT) rather than histologic confirmation since none of the patients who developed LC had available biopsy or autopsy data. However, while LC is a histologic diagnosis, it manifests with a characteristic radiographic pattern on CT [24] that has a reported diagnostic accuracy of 85% [25]. Since CT is the primary imaging modality used for therapeutic surveillance in MPM, it remains important to understand the prognostic implications of this radiographic pattern on CT imaging, even in the absence of histological correlation. In conclusion, for the first time, we report LC as a common pattern of failure in MPM patients who have undergone EPD and that the manifestation of LC portends a poor prognosis. Awareness of the implications of this radiographic pattern on CT is useful for therapy surveillance and prognostication in this patient population. It would also be interesting to explore FDG-PET/CT as a modality for characterization of LC in the patients with MPM following EPD since this modality has shown value in detection of LC [26]. Further studies are warranted to determine if any evidence of preoperative LC should be an absolute contraindication to EPD and may warrant alternative consideration of either EPP or non-surgical management.
    Conflict of interest statement
    Introduction MicroRNAs (miRNAs) are small noncoding RNAs of approximately 22nts in length. They suppress target genes via binding to the 3′-untranslated region (UTR) [1,2]. miRNAs regulate cellular functions including metabolism, development, senescence, proliferation, and apoptosis [3]. These miRNAs regulate networks of specific target genes that are involved in specific biological processes. For example, miR-23a/b regulates glutamine metabolism by suppression of c-Myc [4], miR-124 directly inhibits the SCP1 expression that blockades the REST/SCP1 network during embryonic CNS development [5], and the miR-29 and -30 family represses B-mybshown to induce cellular senescence [6]. Additionally the overexpression of let-7a repressed cell proliferation by significantly targeting the RAS gene and by playing a tumor suppressor role in human lung cancer [7]. miR-34 induces apoptosis and prevents tumorigenesis by targeting Bcl-2 CCND1 or c-Myc [8].