Notably, recent innovation in ICR-cell technology potentially provides similar performance at a lower magnetic field strength [33]. The statistical analysis of profiles generated from a clinical cohort of samples allowed the discrimination between healthy individuals and PC patients with sensitivity and specificity comparable with those reported by other authors using MALDI-TOF MS. A total of 273 serum samples was processed and mass analyzed within a time frame of 24 h and the high quality of the data both facilitated the interpretation and evaluation of the generated profiles. These ultrahigh resolution mass spectra represent selleck kinase inhibitor a “next-generation” of MS-based peptidome profiles and provide a new

tool for a more detailed description of the high-abundant proteins in clinical serum sample cohorts aiming for new diagnostic leads. “
“Breast cancer, the most frequent cancer entity among women, is nowadays recognized as a heterogeneous disease in terms of tumor morphology as well as at the molecular selleck chemical level [[1], [2] and [3]]. Treatment of breast cancer patients with similar clinicopathologic features can result in different outcomes regarding disease progression and survival. Over the last few years, gene expression profiling has provided insights into molecular mechanisms

associated with observed heterogeneous clinical outcome [4]. The seminal work of Sorlie and Perou identified intrinsic molecular subtypes, termed luminal A, luminal B, basal-like, and HER2-enriched, with unique biological Celecoxib and prognostic features [5]. The largest group of breast cancer patients suffers from luminal breast cancer with overexpression of hormone receptors as molecular hallmark. Luminal breast cancer comprises patients of the luminal A subtype with good prognosis whereas patients of the luminal B subtype are at a higher risk to suffer from recurrence [6]. Treatment of patients in these two groups is fundamentally different,

with patients at higher recurrence risk requiring chemo-endocrine treatment, whereas others do not benefit from chemotherapy. Hence, to avoid over- or under-treatment of patients with luminal breast cancer, tools allowing a clear-cut distinction of low and high risk are required. Although different approaches employing gene expression signatures or protein-based assays were introduced [[7], [8], [9], [10] and [11]], a robust assessment of the recurrence risk in luminal breast cancer has remained a challenge. To differentiate between low and high risk tumors, proliferation rate has emerged as a prominent feature, mainly supported by gene expression profiling data [4,12]. This is in line with information provided by histologic grade which is beside age, tumor size, and lymph node status a well-established independent prognostic factor, combining information on tumor proliferation and differentiation status.