Resection of tumors in the caudate lobe (a deep, hard-to-reach part of the liver) is recognized as one of the most technically challenging procedures in hepatic surgery

due to its unique anatomical position and complex vascular relationships.

 

Researchers at Boston University Chobanian & Avedisian School of Medicine now show that it is possible to remove the caudate lobe safely using a surgical robot, even in an older patient, and still remove the cancer completely. The clinical case they describe in the journal Annals of Surgical Oncology, combines two “guidance” tools (1) a hanging/traction technique using the Arantius ligament and (2) Indocyanine green (ICG) “negative staining” to clearly mark the caudate lobe boundaries and guide a margin-focused cancer operation in a very difficult area.

Researchers have discovered a previously unknown signalling cascade that determines how powerful our innate immune system responds to virus infections. This discovery has broad implications for inflammatory diseases, cancer, and neurodegeneration / publication in ’Nature Cell Biology‘

Highlight：
Preclinical studies have shown that methionine restriction (MR) reduces cancer cell proliferation via different mechanisms. 
MR lowers sulfur-containing metabolite levels, reduces oxidative stress, and enhances the immune response.
Clinical trials suggest that MR, when combined with conventional treatments, may sensitize tumors to chemo/ radiotherapy.
MR disrupts methionine-dependent pathways, thereby reducing cancer cell survival.
The therapeutic potential of MR lies in its ability to synergize with other therapies, enhancing overall antitumor efficacy.

New findings show how inherited and acquired genetic mutations cause breast cancer resistance to CDK4/6 inhibitors.

Genetically altered astrocytes that express chimeric antigen receptors offer a promising immunotherapy system capable of clearing accumulations of amyloid-β in the brains of mice – a hallmark pathological feature of Alzheimer’s disease, according to a new study. Alzheimer’s disease (AD), the leading cause of dementia in aging populations worldwide, is marked by a distinctive pathological cascade: amyloid-β (Aβ) plaques accumulate in the brain, triggering harmful changes in tau proteins, which may ultimately drive widespread neurodegeneration. Although the amyloid cascade hypothesis remains debated, recently approved anti-Aβ antibody therapies have shown moderate success in slowing AD progression. However, these treatments require large doses and are associated with potentially fatal side effects. To address these shortcomings, researchers are exploring the use of engineered chimeric antigen receptors (CARs) that could program brain cells to recognize and clear Aβ with far more efficiency and precision. Although CAR immunotherapies have been transformative in cancer treatment and shown promise in early in vitro laboratory studies, significant hurdles remain towards their use in treating AD, including safe delivery of CAR cells to the brain. As a result, their effectiveness in mitigating AD in vivo has yet to be demonstrated. Here, Yun Chen and colleagues explored whether engineered CAR-expressing astrocytes – CAR-As – could be leveraged to overcome these challenges. According to Chen et al., these modified astrocytes enhanced Aβ clearance in laboratory experiments and, when delivered noninvasively into the brains of mice, substantially reduced Aβ buildup in living animals. Moreover, the authors found that a single early treatment in a mouse model of AD prevented the development of Aβ pathology. The findings establish a proof-of-concept that CAR-A designs may offer a powerful and potentially durable strategy for clearing Aβ accumulation and mitigating disease progression in AD. “The study of Chen et al. helps establish a foundation for increasingly innovative CAR strategies in AD,” write Jake Boles and David Gate in a related Perspective. “As CAR technologies mature and the ability to selectively neutralize toxic proteins improves, these approaches hold substantial promise for AD and other neurodegenerative disorders.”