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Simple Summary: Theranostic robot-assisted radical prostatectomy (T-RARP) means adopting RARP as an integration of diagnosis and therapy, and this concept has rarely been discussed. Before the advancement of imaging technologies, the diagnosis of prostate cancer (PCa) needed to rely on systematic biopsies, which had certain limitation of sensitivity and specificity. In our previous reports, even with preoperative benign biopsies, there were still large portions of incidental PCa in specimens of simple prostatectomies. We first introduced the feasibility of T-RARP in 2016 in patients with clinically highly suspected prostate cancer. In 2020, we developed a nomogram to identify the potential groups. With the advantages of imaging technologies, potential groups can be more easily identified, and the concept of T-RARP can be more widely adopted. However, no studies have discussed the benefits of T-RARP in these patients. Herein, we conducted this cohort study to explore the benefits of T-RARP for such patients and topics of T-RARP that are unclear and need to be unveiled in future studies. Objective: This study aimed to explore the benefits of theranostic robot-assisted radical prostatectomy (T-RARP) for clinically highly suspicious prostate cancer (PCa) without proven biopsies. Material and Methods: Between February 2016 and December 2020, we included men with clinically highly suspicious PCa in this study. They were assessed to have possible localized PCa without any initial treatments, and were categorized into previous benign biopsies or without biopsies. Furthermore, another group of malignant biopsies with RARP in the same time frame was adopted as the control group. The endpoints were to compare the oncological outcome and functional outcome between malignant biopsies with RARP and T-RARP. p < 0.05 was considered to be significant. Results: We included 164 men with proven malignant biopsies treated with RARP as the control group. For T-RARP, we included 192 men. Among them, 129 were preoperatively benign biopsies, and 63 had no biopsies before T-RARP. Approximately 75% of men in the T-RARP group had malignant pathology in their final reports, and the other 25% had benign pathology. T-RARP provides several oncological advantages, such as a higher initial pathological T stage, lower Gleason grade, and lower odds of positive surgical margins. However, the biochemical recurrence rates were not significantly decreased. From our cohort, T-RARP (odds ratio with 95% confidence interval; erectile recovery: 3.19 (1.84–5.52), p < 0.001; continence recovery: 2.25 (1.46–3.48), p < 0.001) could result in better recovery of functional outcomes than malignant biopsies with RARP. Conclusions: For clinically highly suspicious PCa, T-RARP was able to detect around 75% of PCa cases and preserved their functional outcomes maximally. However, in 25% of men with benign pathology, approximately 6% would have incontinence and 10% would have erectile impairment. This part should be sufficiently informed of the potential groups considering T-RARP. [ABSTRACT FROM AUTHOR]

Simple Summary: Patients with pancreatic cancer and other advanced cancers suffer from progressive weight loss that reduces treatment response and quality of life and increases treatment toxicity and mortality. Effective interventions to prevent such weight loss, known as cachexia, require molecular markers to diagnose, stage, and monitor cachexia. No such markers are currently validated or in clinical use. This study used a discovery platform to measure changes in plasma proteins in patients with pancreatic cancer compared with normal controls. We found proteins specific to pancreatic cancer and cancer stage, as well as proteins that correlate with cachexia. These include some previously known proteins along with novel ones and implicates both well-known and new molecular mechanisms. Thus, this study provides novel insights into the molecular processes underpinning cancer and cachexia and affords a basis for future validation studies in larger numbers of patients with pancreatic cancer and cachexia. Patients with pancreatic ductal adenocarcinoma (PDAC) suffer debilitating and deadly weight loss, known as cachexia. Development of therapies requires biomarkers to diagnose, and monitor cachexia; however, no such markers are in use. Via Somascan, we measured ~1300 plasma proteins in 30 patients with PDAC vs. 11 controls. We found 60 proteins specific to local PDAC, 46 to metastatic, and 67 to presence of >5% cancer weight loss (FC ≥ |1.5|, p ≤ 0.05). Six were common for cancer stage (Up: GDF15, TIMP1, IL1RL1; Down: CCL22, APP, CLEC1B). Four were common for local/cachexia (C1R, PRKCG, ELANE, SOST: all oppositely regulated) and four for metastatic/cachexia (SERPINA6, PDGFRA, PRSS2, PRSS1: all consistently changed), suggesting that stage and cachexia status might be molecularly separable. We found 71 proteins that correlated with cachexia severity via weight loss grade, weight loss, skeletal muscle index and radiodensity (r ≥ |0.50|, p ≤ 0.05), including some known cachexia mediators/markers (LEP, MSTN, ALB) as well as novel proteins (e.g., LYVE1, C7, F2). Pathway, correlation, and upstream regulator analyses identified known (e.g., IL6, proteosome, mitochondrial dysfunction) and novel (e.g., Wnt signaling, NK cells) mechanisms. Overall, this study affords a basis for validation and provides insights into the processes underpinning cancer cachexia. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the efficacy and treatment rationale of Hürthle cell carcinoma (HCC) following a patient with progressive and metastatic HCC. HCC was recently shown to harbor a distinct genetic make-up and the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kiase (PI3K)/AKT signaling pathways are potential targets for anti-cancer agents in the management of recurrent HCC. The presence or absence of gene variants can give a rationale for targeted therapies that could be made available in the context of drug repurposing trials. Methods: Treatment included everolimus, sorafenib, nintedanib, lenvatinib, and panitumumab. Whole genome sequencing (WGS) of metastatic tumor material obtained before administration of the last drug, was performed. We subsequently evaluated the rationale and efficacy of panitumumab in thyroid cancer and control cell lines after epidermal growth factor (EGF) stimulation and treatment with panitumumab using immunofluorescent Western blot analysis. EGF receptor (EGFR) quantification was performed using flow cytometry. Results: WGS revealed a near-homozygous genome (NHG) and a somatic homozygous TSC1 variant, that was absent in the primary tumor. In the absence of RAS variants, panitumumab showed no real-life efficacy. This might be explained by high constitutive AKT signaling in the two thyroid cancer cell lines with NHG, with panitumumab only being a potent inhibitor of pEGFR in all cancer cell lines tested. Conclusions: In progressive HCC, several treatment options outside or inside clinical trials are available. WGS of metastatic tumors might direct the timing of therapy. Unlike other cancers, the absence of RAS variants seems to provide insufficient justification of single-agent panitumumab administration in HCC cases harboring a near-homozygous genome. [ABSTRACT FROM AUTHOR]