NRG2 (Neuregulin 2)

Afatinib-resistant cell line (HCC827AR) was established by continuously exposing HCC827 cells to afatinib (4 µM) for 6 months...This study unravels the intricate role of NDRG1 in modulating NRG2 via HECW1. The results not only illuminate Mag's promising potential as an adjunctive therapy to surmount EGFR TKI resistance, but also underscore the significant therapeutic potential of targeting the NDRG1-NRG2-HECW1 pathway as a novel strategy to reverse EGFR TKI resistance in NSCLC.

The obstruction-induced biliary proliferation is EGFR-mediated, suggesting context-specific and receptor-specific EGF signaling network contribution to EHBD regeneration after injury.

Together, our analysis maps potential nociceptive signaling pathways of different MM microenvironment cell types. These pathways extend from upstream regulatory kinases to transcription factors to secreted ligands, which can potentially stimulate sensory neuron receptors in the bone.

BIRC5 served as independent risk factors for prostate cancer prognosis, and enhanced BIRC5 expression promoted cells viability, migration, and invasion, but the autophagy activator rapamycin could counteract the effects of the BIRC5 gene...BIRC5 and NRG2 genes participate in the progression of prostate cancer by regulating autophagy. BIRC5 and NRG2 have the potential to serve as valuable biomarkers for the prognosis of prostate cancer.

Our findings highlight UBP1's pivotal role in BC progression through multiple mechanisms, including EMT induction, stemness maintenance, and macrophage polarization via activation of the NRG2/Akt axis. Moreover, higher UBP1 expression correlates with lower overall and recurrence-free survival, underscoring its potential as a prognostic marker and therapeutic target for aggressive BC.

This randomized phase III trial aimed to determine whether treatment with cisplatin and volume-directed radiation followed by carboplatin and paclitaxel for four cycles (chemoradiotherapy [C-RT]) increased recurrence-free survival (RFS) and overall survival (OS) when compared with carboplatin and paclitaxel for six cycles (chemotherapy [CT]) in locally advanced endometrial cancer (UC). None of the factors analyzed predicted OS benefit from C-RT. Although C-RT reduced the rate of local recurrence compared with CT, it did not increase OS or RFS in stage III/IVA UC.

Therefore, the development of HER3-targeted drugs possessing safety, tolerability, and sensitivity is crucial for clinical cancer treatment. This review summarizes the progress of the mechanism of HER3 in drug resistance, the HER3-targeted therapies that are conducted in preclinical and clinical trials, and some emerging molecules that could be used as future designed drugs for HER3, aiming to provide insights for future research and development of anticancer drugs targeting HER3.

The autophagy marker, LC3-II and epithelial-mesenchymal transition (EMT) marker, vimentin were increased, while P62 and E-cadherin were decreased in response to NRG2 depletion. The findings of the present study demonstrated that NRG2 acts as a tumor suppressor factor that contributes to the immune escape and anti-tumor immunity inhibition by regulating the pathological process of autophagy and EMT, suggesting that NRG2 could be used as a prognostic biomarker and clinical target for BRCA therapy.

Common treatment approaches involve pan-ERBB inhibitors, small molecule inhibitors targeting ERBB2 or ERBB3, and monoclonal antibodies. Given the current landscape of NRG1 and NRG2 in solid tumors, a consensus among diagnostic and treatment experts is proposed, and clinical trials hold promise for benefiting more patients with NRG1 and NRG2 gene fusion solid tumors.

We started from a marginal zone lymphoma cell line, Karpas-1718, kept under prolonged exposure to the PI3Kδ inhibitor idelalisib until acquisition of resistance, or with no drug...Combination with the ERBB inhibitor lapatinib was beneficial in resistant cells and in other lymphoma models already expressing the identified resistance factors...Resistance factors were also shown to be expressed in clinical specimens. In conclusion, we showed that the overexpression of ERBB4 and its ligands represents a novel mechanism of resistance for lymphoma cells to bypass the antitumor activity of BTK and PI3K inhibitors and that targeted pharmacologic interventions can restore sensitivity to the small molecules.

Fusion proteins known to be oncogenic drivers, including those of CD74, are typically detected and targeted after standard chemotherapeutic plans fail and the disease relapses. The analysis reported herein provides insights into the early intervention of CD74 fusions and highlights the need for improved routine assessment methods so that targeted therapies can be applied while they are most effective.