The purpose was to compare and comment on use of the SF-36 and MOS-HIV instruments in studies of persons with HIV disease. Three medical information databases were searched to identify examples of HIV studies that included the MOS-HIV or SF-36. Thirty-nine and 14 published articles were identified for illustration in comparing the use of the MOS-HIV and SF-36 in HIV disease, respectively. Support for the reliability and construct validity of the MOS-HIV and SF-36 was found. Ceiling and floor effects were reported for both the MOS-HIV and SF-36; however, ceiling effects were more common for the MOS-HIV, in part due to fewer items in the physical, social, and role functioning domains. The MOS-HIV measures three domains hypothesized to be associated with the health deterioration of HIV disease not measured by the SF-36; however, these domains may not assess aspects of HIV disease that typify the majority of the persons with HIV disease today. National norms for the U.S. adult population (and other nations) are available for the SF-36. In addition, the SF-36 has been used in a wide variety of patient populations, enabling comparisons of HIV-infected persons with persons with other health conditions. No national norms for the MOS-HIV are available. We conclude that there is currently insufficient evidence in the literature to recommend the use of the MOS-HIV over the SF-36 in HIV-infected persons. Although the SF-36 is not targeted at HIV, it may be preferable to use the SF-36 over the MOS-HIV due to fewer ceiling effects, availability of national norms, and the vast amount of data for other populations in the U.S. and around the world. Head-to-head comparisons demonstrating the unique value of the MOS-HIV over the SF-36 are clearly needed. More importantly, additional work needs to be directed at comparing the MOS-HIV and other putatively HIV-targeted instruments to one another to help demarcate aspects of HRQOL that are truly generic versus specific to HIV disease. Using both a generic and targeted HRQOL measure is a good general strategy, but this has not been a typical practice in studies of HIV because the MOS-HIV is so similar in content to the SF-36.

Introduction

Contrast-enhanced MRI (CE-MRI) represents the current mainstay for monitoring treatment response in glioblastoma multiforme (GBM), based on the premise that enlarging lesions reflect increasing tumor burden, treatment failure, and poor prognosis. Unfortunately, irradiating such tumors can induce changes in CE-MRI that mimic tumor recurrence, so called post treatment radiation effect (PTRE), and in fact, both PTRE and tumor re-growth can occur together. Because PTRE represents treatment success, the relative histologic fraction of tumor growth versus PTRE affects survival. Studies suggest that Perfusion MRI (pMRI)-based measures of relative cerebral blood volume (rCBV) can noninvasively estimate histologic tumor fraction to predict clinical outcome. There are several proposed pMRI-based analytic methods, although none have been correlated with overall survival (OS). This study compares how well histologic tumor fraction and OS correlate with several pMRI-based metrics.

Methods

We recruited previously treated patients with GBM undergoing surgical re-resection for suspected tumor recurrence and calculated preoperative pMRI-based metrics within CE-MRI enhancing lesions: rCBV mean, mode, maximum, width, and a new thresholding metric called pMRI-fractional tumor burden (pMRI-FTB). We correlated all pMRI-based metrics with histologic tumor fraction and OS.

Results

Among 25 recurrent patients with GBM, histologic tumor fraction correlated most strongly with pMRI-FTB (r = 0.82; P < .0001), which was the only imaging metric that correlated with OS (P<.02).

Conclusion

The pMRI-FTB metric reliably estimates histologic tumor fraction (i.e., tumor burden) and correlates with OS in the context of recurrent GBM. This technique may offer a promising biomarker of tumor progression and clinical outcome for future clinical trials.

We describe the landscape of genomic alterations in cutaneous melanomas through DNA, RNA, and protein-based analysis of 333 primary and/or metastatic melanomas from 331 patients. We establish a framework for genomic classification into one of four subtypes based on the pattern of the most prevalent significantly mutated genes: mutant BRAF, mutant RAS, mutant NF1, and Triple-WT (wild-type). Integrative analysis reveals enrichment of KIT mutations and focal amplifications and complex structural rearrangements as a feature of the Triple-WT subtype. We found no significant outcome correlation with genomic classification, but samples assigned a transcriptomic subclass enriched for immune gene expression associated with lymphocyte infiltrate on pathology review and high LCK protein expression, a T cell marker, were associated with improved patient survival. This clinicopathological and multi-dimensional analysis suggests that the prognosis of melanoma patients with regional metastases is influenced by tumor stroma immunobiology, offering insights to further personalize therapeutic decision-making.