ERBB3 positive

Of 52 patients (55.8% female; mean age 64.5 years), 59.6% received chemotherapy and 40.4% received an EGFR TKI as first-line treatment; erlotinib constituted 71.2% of targeted therapies. These results suggest that HER3 expression may warrant further investigation as a candidate biomarker for treatment sequencing decisions and as a potential therapeutic target in EGFR-mutant NSCLC. Prospective studies evaluating chemotherapy-TKI sequencing and HER3-directed agents such as patritumab deruxtecan (HER3-DXd) in HER3-positive patients are needed to confirm these preliminary observations.

HER3 positivity was observed in 3/5 of the intermediate MutL cases and HER2 positivity in only one. MMR deficiency and potential MSI-H status were identified to be relevant prognostic biomarkers for pancreatic cancer patients, with MSI-H patients displaying a younger age and distinct tumor features.

HER2 and HER3 overexpression often coexisted with pathological features, such as perineural invasion, in cases of combined HER2 and HER3 positivity. These findings support the involvement of the ErbB receptor family in pancreatic carcinogenesis and suggest their potential as targets for future (neo)adjuvant therapeutic strategies.

The increase in HER3 expression induced by osimertinib treatment was associated with increased payload release in PC-9 cells. Our results indicate that HER3 dynamics, as well as baseline HER3 expression, modulate payload release from HER3-DXd and support combination strategies to potentiate the antitumor activity of HER3-DXd.

In an orthotopic metastatic TNBC model, systemic treatment with HPK2.0 corrole assemblies achieved 67 to 83% tumor regression, near-complete suppression of spontaneous lung metastasis, and a ~2 fold improvement in survival relative to mock treatment, with minimal off-target toxicity. By integrating tumor specificity with therapeutic potency, this next-generation protein corrole platform establishes a clinically scalable strategy for treating metastatic HER3 positive TNBC.

P1, N=42, Not yet recruiting, Actinium Pharmaceuticals Australia Pty Limited

TK-hu A3 emerged as the lead candidate, showing specific HER3 targeting, strong pathway inhibition, and antitumor efficacy in vivo. Beyond standalone use, it could support novel strategies such as T-cell engagers, ADCs, CAR-T, and bispecific antibodies. These findings highlight TK-hu A3 as a promising therapy for HER3-positive, treatment-resistant cancers, meriting further development.

HER3 expression may serve as a critical biomarker for guiding therapeutic strategies in HER2-positive breast cancer patients. The combinatorial effect of HER3 overexpression and PIK3CA mutations may exacerbate therapeutic resistance, while dual-targeted strategies against the HER3/PI3K pathway could potentially improve clinical outcomes in treatment-resistant populations.

Our findings also suggest that evaluating the response of SBAs to anti-HER3 therapies should be considered in future clinical trials. Additionally, evidence of spatial heterogeneity in biomarker expression emphasizes the importance of assessing biomarkers in metastatic tissue to identify actionable alterations that may not be present in the primary tumor.

It was found that the new affiprobe allowed the detection of HER3 expressing cells with a detection limit of 14578 cells per 200 μl assay volume and a working range of 14000 to 50000 cells. The new affiprobe can be used for detecting, studying and monitoring the HER3-expressing cells using a luminometer in fast and inexpensive assays.

Claudin 18.2, nectin-4, and HER3 are potential therapeutic targets in SBA, and nectin-4 positivity is independently associated with an unfavorable prognosis. These proteins may represent new therapeutic targets for SBA.

This multifaceted approach could ultimately lead to more personalized treatment options for patients with HER3-positive breast cancers, thereby improving overall patient management and outcomes in this challenging disease landscape. This study presents recombinant affibodies tailored to bind to HER3 for cancer cell identification, along with novel methods for producing a range of affibody molecules.