To propose minimally invasive percutaneous techniques in the management of high output chylous ascites, a known potential complication of retroperitoneal surgery associated with significant morbidity and mortality. Management has traditionally been based on successful treatment reported in the literature. However, refractory or high-output leaks often prove difficult to treat and there is little evidence on superior management. We report percutaneous maceration and embolization for the management of high-volume abdominal chyle leak after robot-assisted laparoscopic (RAL) radical nephrectomy and lymph node dissection for renal cell carcinoma. A 68-year-old male with incidentally found renal cell carcinoma underwent RAL radical nephrectomy with paraaortic lymph node dissection. He initially improved after surgery but developed significant abdominal pain and distension approximately 7 weeks postoperative. This proved to be chyloperitoneum. Conservative management was initiated, but after continued high-output (>1 L) fluid drainage, we pursued adjunct intervention involving Interventional Radiological percutaneous procedures. This included lymphatic maceration and glue embolization of leaking lymphatics. The patient tolerated the percutaneous procedures well with significant improvement in drain output ultimately leading to complete resolution of ascites without further complication. Similar interventions have previously been reported in the literature for cases of chylothorax with success. However, there is a lack of reports on utilizing this minimally invasive procedure for chyloperitoneum after retroperitoneal urologic surgery. We report our successful experience with percutaneous lymphatic maceration and embolization for high output chylous ascites after RAL radical nephrectomy with lymphadenectomy. We believe that early initiation utilizing these percutaneous techniques can achieve timely resolution and should be considered in the management of these patients.
Objective. The study investigates the prostate-specific antigen threshold for adding targeted, software-based, magnetic resonance imaging-ultrasound fusion biopsy during a standard 12-core biopsy in biopsy-naïve patients. It secondarily explores whether the targeted biopsy is necessary in setting of abnormal digital rectal examination. Methods. 260 patients with suspected localized prostate cancer with no prior biopsy underwent prostate magnetic resonance imaging and were found to have Prostate Imaging Reporting and Data System score ≥ 3 lesion(s). All 260 patients underwent standard 12-core biopsy and targeted biopsy during the same session. Clinically significant cancer was Gleason ≥ 3 + 4. Results. Percentages of patients with prostate-specific antigen 0–1.99, 2–3.99, 4–4.99, 5–5.99, 6–9.99, and ≥ 10 were 3.0%, 4.7%, 20.8%, 16.9%, 37.7%, and 16.9%, respectively. Cumulative frequency of clinically significant prostate cancer increased with the addition of targeted biopsy compared with standard biopsy alone across all prostate-specific antigen ranges. The difference in clinically significant cancer detection between targeted plus standard biopsy compared to standard biopsy alone becomes statistically significant at prostate-specific antigen >4.3 ( p = 0.031 ). At this threshold, combination biopsy detected 20 clinically significant prostate cancers, while standard detected 14 with 88% sensitivity and 20% specificity. Excluding targeted biopsy in setting of a positive digital rectal exam would save 12.3% magnetic resonance imaging and miss 1.8% clinically significant cancers in our cohort. Conclusions. In biopsy-naïve patients, at prostate-specific antigen >4.3, there is a significant increase in clinically significant prostate cancer detection when targeted biopsy is added to standard biopsy. Obtaining standard biopsy alone in patients with abnormal digital rectal examinations would miss 1.8% clinically significant cancers in our cohort.
Cholangiocarcinoma, a primary liver cancer of the bile ducts, effects 6,000 patients yearly and incidence has been growing consistently over the past 15 years. Current therapies for cholangiocarcinoma are not curative and patient survival is less than 1 year after diagnosis. Strides toward new treatment rest on better understanding tumor biology. The expression of microRNAs in cholangiocarcinoma cells was analyzed by RNAseq after knockdown of fibroblast growth factor receptor 4 (FGFR4) to identify potential microRNAs regulated by FGFR4. Caspase activity was used to evaluate miR-10a roles in anti-apoptotic signaling. Cell scratch assays were used to test cell migration and cell counting was used to determine proliferation. Quantitative real time PCR was used to measure miR-10a levels in cholangiocarcinoma cell lines Mz-ChA-1, HUCCT-1 and KMCH after FGFR4 knockdown with siRNA. Potential target proteins of miR-10a were evaluated by western blot. Preliminary data showed dozens of microRNAs (miRs) in cholangiocarcinoma cells were modulated by FGFR4 knockdown. Treatment with siRNA to FGFR4 caused increased sensitivity to TRAIL-induced apoptosis, and also reduced miR-10a expression in Mz-ChA-1, HuCCT-1, and KMCH cell lines. Importantly, apoptosis sensitization was reversed by restoring miR-10a expression in cells. miR-10a helped regulate both cell proliferation and cell migration in cholangiocarcinoma cells. When miR-10a was increased in cholangiocarcinoma cells, migration and proliferation increased. When miR-10a was decreased these effects also decreased. Protein targets of miR-10a included the MAP Kinase-related proteins MLK-1 & TAK-1. Other protein targets such as PHLDA1 & AKTIP were also identified. Notably, microRNA binding prediction programs did not include MLK-1 as a target, though our sequence analysis shows multiple stable binding sites. MLK-1 showed the most dramatic response to miR-10a. We investigated the role miR-10a plays for cholangiocarcinoma and the mechanism through which this pathway is regulated. Data supports miR-10a as a key player in cell survival, proliferation and migration. We have identified a set of proteins that are regulated by miR-10a in cholangiocarcinoma cells. Looking forward, identification of the function of these proteins will help elucidate how miR-10a functions in cholangiocarcinoma progression. Citation Format: Matthieu Spriet, Cody Wehrkamp, Brandon Henslee, Ashley Mohr, Steve Kachman, Justin Mott. Function of microRNA-10a in cholangiocarcinoma [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 2518.
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