Evaluation of alternative prognostic thresholds for SP142 and 22C3 immunohistochemical PD-L1 expression in triple-negative breast cancer: results from a population-based cohort.

Background: Immune checkpoint inhibitors are now a part of the treatment arsenal for triple-negative breast cancer (TNBC) but refinement of PD-L1 as a prognostic and predictive biomarker is a clinical priority. We aimed to evaluate the relevance of novel PD-L1 immunohistochemical (IHC) thresholds in TNBC with regard to PD-L1 gene expression, prognostic value, tumor infiltrating lymphocytes (TILs), and TNBC molecular subtypes.

Material & Methods: PD-L1 was scored in a tissue microarray with the SP142 (immune cell (IC) score) and the 22C3 (combined positive score; CPS) IHC assays and TIL abundance evaluated in whole slides in a population-based cohort of 237 early-stage TNBC patients.

Quest for Cooper Pair Transfer in Heavy-Ion Reactions: The ^{206}Pb+^{118}Sn Case.

In this Letter we report on effects of nucleon-nucleon correlations probed in nucleon transfer reactions with heavy ions. We measured with high efficiency and resolution a complete set of observables for neutron transfer channels in the ^{206}Pb+^{118}Sn system employing a large solid angle magnetic spectrometer, which allowed us to study a wide range of internuclear distances via a detailed excitation function. The coupled channel theory, based on an independent particle transfer mechanism, follows the experimental transfer probabilities for one- and two-neutron pick-up and stripping channels.

Proteomic profiling reveals that ESR1 mutations enhance cyclin-dependent kinase signaling.

Three quarters of all breast cancers express the estrogen receptor (ER, ESR1 gene), which promotes tumor growth and constitutes a direct target for endocrine therapies. ESR1 mutations have been implicated in therapy resistance in metastatic breast cancer, in particular to aromatase inhibitors. ESR1 mutations promote constitutive ER activity and affect other signaling pathways, allowing cancer cells to proliferate by employing mechanisms within and without direct regulation by the ER.