Participants completed the IPSS and the LUTS Tool. Prevalence rates of symptoms captured by the LUTS Tool were compared using IPSS summary scores: 0, 1-7, 8-19, and >= 20. LUTS Tool subscale scores were calculated.
Pearson correlations between the LUTS Tool symptoms and subscales and IPSS symptoms were performed. Logistic regressions evaluated the associations of IPSS scores and LUTS Tool subscales with treatment seeking for LUTS. Results: The IPSS did not assess some symptoms (i. e., incontinence) for which there was a high prevalence among participants. Correlations between the 7 symptoms assessed by the IPSS and LUTS Tool were moderate to high ranging between 0.37 (nocturia women) and GPCR Compound Library order 0.77 (weak stream men), indicating concordance. While the LUTS Tool subscales and the total IPSS score were all significantly associated with treatment seeking, the LUTS Tool OAB subscale in men and Voiding subscale in women most strongly predicted treatment seeking. Conclusion: LUTS that are excluded from the IPSS, most notably incontinence, were prevalent even among mildly symptomatic participants. Since storage symptoms appear to drive treatment seeking, identifying, and treating these symptoms is essential when caring for patients with LUTS. Neurourol. Urodynam. 31: 448-454,
I-BET151 nmr 2012. (C) 2012 Wiley Periodicals, Inc.”
“Background: Pancreatic cancer is one of the most lethal and molecularly diverse malignancies. Repurposing of therapeutics that target specific molecular mechanisms in different disease types offers potential for rapid improvements in
outcome. Although Ricolinostat HER2 amplification occurs in pancreatic cancer, it is inadequately characterized to exploit the potential of anti-HER2 therapies.
Methods: HER2 amplification was detected and further analyzed using multiple genomic sequencing approaches. Standardized reference laboratory assays defined HER2 amplification in a large cohort of patients (n = 469) with pancreatic ductal adenocarcinoma (PDAC).
Results: An amplified inversion event (1 MB) was identified at the HER2 locus in a patient with PDAC. Using standardized laboratory assays, we established diagnostic criteria for HER2 amplification in PDAC, and observed a prevalence of 2%. Clinically, HER2-amplified PDAC was characterized by a lack of liver metastases, and a preponderance of lung and brain metastases. Excluding breast and gastric cancer, the incidence of HER2-amplified cancers in the USA is >22,000 per annum.
Conclusions: HER2 amplification occurs in 2% of PDAC, and has distinct features with implications for clinical practice. The molecular heterogeneity of PDAC implies that even an incidence of 2% represents an attractive target for anti-HER2 therapies, as options for PDAC are limited. Recruiting patients based on HER2 amplification, rather than organ of origin, could make trials of anti-HER2 therapies feasible in less common cancer types.