BRCA1 (Breast cancer 1, early onset)

P1/2, N=210, Recruiting, Shanghai SciBrunch Therapeutics Co., Ltd. | Not yet recruiting --> Recruiting

BRCA2 is the most common gene with germline variations, while CDK12 is the most frequently mutated gene in somatic HRR variants. This study suggests that HRR gene testing in patients with high-risk HSPC would help identify those with more aggressive clinical features and guide prognostication and potential targeted therapeutic strategies.

In an in vivo TNBC xenograft mouse model, combination treatment with paclitaxel and compound 12 significantly increased BRCA1 stability, reduced the final tumor weight, and decreased the number of Ki-67-positive proliferative cells. Our findings suggest that combination therapy with compound 12 can enhance BRCA1 function and improve chemotherapeutic efficacy. This study highlights CTSS inhibition as a promising therapeutic strategy for TNBC patients with wild-type BRCA1.

The use of PARP inhibitors and targeted therapies adds complexity to surgical decisions. Ongoing trials and new therapeutic strategies are expected to enhance the management and outcomes of OC.

Paeonol attenuates PH by rebalancing the BMP/TGF-β signaling through interacting with BRCC3 activation, thereby inhibiting vascular remodeling. These findings suggest that paeonol is a promising therapeutic candidate for PAH.

A few were predicted to be carcinogenic, immunotoxic, and/or cytotoxic. Overall, the clerodane-type furano-diterpenoids from T. crispa show encouraging results in in-silico studies and may be considered for further modification and lead development.

P=N/A, N=42, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027

For women electing imaging surveillance over risk-reducing surgery, our results may offer reassurance that their breast cancer-specific survival and OS are unlikely to be compromised. However, breast cancer incidence rates are significantly reduced after BRRM compared with imaging surveillance, which may be important information for women with pvBRCA1/2 considering BRRM.

Despite some significantly different clinicopathological features, there is no solid evidence to support HER2-ultralow, HER2-low and HER2-null cancers as individual TNBC clinical-molecular entities. Particularly, assigning TNBC samples to the HER2-null, -ultralow and -low categories did not bring any additional prognostic value.

Isogenic PDX models of TNBC provide a powerful platform to define molecular mechanisms of acquired carboplatin resistance and uncover actionable therapeutic strategies. Our findings reveal multiple adaptive routes to platinum resistance, including restoration of homologous recombination and activation of alternative DNA repair programs. Synergistic interactions between SG and mTOR inhibition offer a promising avenue for overcoming resistance, supporting further clinical investigation of these combinations in TNBC.

P2, N=80, Active, not recruiting, Gilead Sciences | Trial completion date: Dec 2025 --> Dec 2027

P1, N=18, Recruiting, Pamela Munster | Trial completion date: Feb 2027 --> Jan 2028 | Trial primary completion date: Jan 2026 --> Jan 2028