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Category: biotech/medical – Page 7

Engineered nanoparticles could deliver better targeted cancer treatment to lymph nodes

Scientists at McGill University and the Rosalind and Morris Goodman Cancer Institute have developed a new way to deliver cancer immunotherapy that caused fewer side effects compared to standard treatment in a preclinical study. The work is published in the journal Proceedings of the National Academy of Sciences.

The experimental approach is designed to treat cancer that has spread to the lymph nodes, a difficult-to-treat stage of the disease. Today, most immunotherapies are delivered by intravenous (IV) infusion and circulate throughout the body. This can trigger immune responses in healthy tissues, leading to serious side effects.

“Some immunotherapies cause such severe side effects that clinicians are forced to lower the dose, making treatment less effective,” said senior author Guojun Chen, Assistant Professor in McGill’s Department of Biomedical Engineering and member of the Goodman Cancer Institute. “Our approach could allow for higher, more effective doses while limiting toxicity, which is a major goal in cancer treatment.”

Nanotubes unlock new wavelengths for smarter sensing

Sensors made of carbon nanotubes that can measure infrared and terahertz radiation are being tested for uses ranging from detecting damaged cables after earthquakes, to collecting health data via ultrathin wearable devices, and assisting with pharmaceutical quality control, say researchers in Japan.

“Accurately visualizing the internal structures of organisms and objects is integral to our daily lives, from medical imaging to security scanning in airports,” and terahertz sensors built from carbon nanotubes are uniquely suited to this purpose, says Yukio Kawano is a professor of engineering at Chuo University in Tokyo, and project leader at the Kanagawa Institute of Industrial Science and Technology (KISTEC) in Japan.

Compared with many sensor technologies that can only detect one part of the electromagnetic spectrum, Kawano’s team is working to create sensors that can detect terahertz and a broader range of radiation, and use them to produce high-resolution images.

Tailored COX-2 Inhibition for Precision Adjuvant Therapy of Localized Metastatic Colon Cancer

💬 Editorial: Precision adjuvant therapy for stage III ColonCancer may be enhanced through molecular profiling for ctDNA status and PIK3CA mutation, informing use of celecoxib or aspirin alongside standard treatment.

CALGB/SWOG 80,702 Alliance was a placebo-controlled randomized clinical trial (RCT) of daily celecoxib (400 mg/d vs placebo) as an adjuvant therapy to fluorouracil, leucovorin, and oxaliplatin (FOLFOX) toward improving disease-free survival (DFS) of minimal residual localized (stage III) metastatic colon cancer.1 The rationale for the trial was a preponderance of evidence from RCTs and observational studies showing that selective cyclooxygenase 2 (COX-2 or prostaglandin-endoperoxide synthase 2 [PTGS2]) inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs) such as celecoxib and rofecoxib, reduce the incidence of premalignant colorectal polyps and colorectal cancer (CRC). Although the primary trial results did not show daily celecoxib to be statistically significantly associated with improvement in DFS or overall survival (OS),1 the results raised the possibility that yet-to-be-determined subgroups may experience a significant benefit. Indeed, Nowak et al2 reported in 2024 that a significant protective effect was observed among patients with tumors harboring mutations to exons 9 or 20 of the PIK3CA gene within the subset of the Alliance trial population with available whole-exome tumor sequencing data.

The possibility for molecular selection for NSAID adjuvant therapy of CRC, specifically on the basis of PIK3CA mutation was first raised in a prospective observational study by Liao and colleagues3 in 2012 for aspirin—a less selective COX-2 inhibitor. This finding for aspirin was later corroborated with post hoc observational follow-up of the VICTOR RCT of daily rofecoxib (20 mg vs placebo),4 which, like the Alliance trial, did not demonstrate a significant protective benefit for rofecoxib among unselected patients.5 Most recently, 2 RCTs of daily low-dose aspirin, ALASSCA6 and SAKK41/13,7 showed that aspirin, among patients enrolled using molecular selection for tumor PIK3CA mutation, led to a similar survival benefit of approximately 50% compared to placebo.

Frontiers: Psoriasis is a complex, chronic relapsing and inflammatory skin disorder with a prevalence of approximately 2% in the general population worldwide

Psoriasis can be triggered by infections, physical injury and certain drugs. The most common type of psoriasis is psoriasis vulgaris, which primarily features dry, well-demarcated, raised red lesions with adherent silvery scales on the skin and joints. Over the past few decades, scientific research has helped us reveal that innate and adaptive immune cells contribute to the chronic inflammatory pathological process of psoriasis. In particular, dysfunctional helper T cells (Th1, Th17, Th22, and Treg cells) are indispensable factors in psoriasis development. When stimulated by certain triggers, antigen-presenting cells (APCs) can release pro-inflammatory factors (IL-23, IFN-α and IL-12), which further activate naive T cells and polarize them into distinct helper T cell subsets that produce numerous cytokines, such as TNF, IFN-γ, IL-17 and IL-22, which act on keratinocytes to amplify psoriatic inflammation. In this review, we describe the function of helper T cells in psoriasis and summarize currently targeted anti-psoriatic therapies.

Psoriasis is a complex, chronic relapsing and inflammatory skin disorder with an overall prevalence of 2% in the general population worldwide (1). The most common type of psoriasis is psoriasis vulgaris, which primarily manifests as dry, well-demarcated, raised red lesions with adherent silvery scales on the skin and joints and accounts for nearly 90% of all psoriasis cases. Psoriasis is also associated with multiple comorbidities, such as arthritis, obesity, diabetes mellitus, depression, hypertension, cardiovascular disease, and reduced quality of life (2).

Although the exact mechanism that triggers psoriasis remains unclear, it is currently accepted that psoriasis is induced or exacerbated by either nonspecific triggers, such as infections [such as Streptococcus ], physical injury [such as scratching and tattoos ], drugs [such as β blockers, lithium and antimalarials (5, 6)] or some specific autoantigens [such as cathelicidin LL-37, melanocytic ADAMTSL5, lipid antigen PLA2G4D and keratin 17 ]. Pathologically, psoriasis is characterized by epidermal acanthosis (thickening of the viable layers), hyperkeratosis (thickened cornified layer), and parakeratosis (cell nuclei present in the cornified layer).

Intraductal Papillary Mucinous Neoplasm and Pancreatic… : Official journal of the American College of Gastroenterology

Intraductal papillary mucinous neoplasm and pancreatic cancer: opportunity knocks twice hamada, et al.

📕 doi.org/10.14309/ajg.

L, the wide variation in cancer risk necessitates prolonged surveillance for most patients. There is an unmet need to optimize surveillance strategies for patients with IPMNs to address the rising global mortality associated with pancreatic cancer and to balance early cancer detection against healthcare resource allocation. While published guidelines outline common risk factors of carcinoma derived from IPMN, the resource-intensive nature of surveillance underscores the need for more granular management strategies—a need not yet reflected in current recommendations. Moreover, it is important to appreciate that patients with IPMNs also face an elevated risk of developing pancreatic carcinoma arising concomitantly with IPMN. This type of carcinoma presents unique challenges for surveillance but also offers novel opportunities for the timely identification of incident pancreatic cancer.

Engineered CAR-NK cells appear more ‘attack-ready’

Researchers at the Ribeirao Preto Blood Center and the Center for Cell-Based Therapy (CTC) conducted a study using the NK-92 cell line to test new models of chimeric antigen receptors (CARs) with specific costimulatory domains, such as 2B4 and DAP12. The tests showed that these components helped make the cells “ready to attack,” thereby increasing their ability to destroy tumors. The results were published in the journal Frontiers in Immunology.

The CTC is one of the Research, Innovation, and Dissemination Centers (RIDCs) supported by FAPESP. It is based at the Ribeirao Preto Blood Center and is linked to the general and teaching hospital (“Hospital das Clínicas”) of the Ribeirao Preto Medical School of the University of São Paulo (FMRP-USP).

CAR-based cell therapies are revolutionizing cancer treatment, especially for hematological tumors. However, although it is already known which components work best in CAR-T cells, many questions remain about which intracellular signals make CAR-NK cells more effective.

What Growing Up On Mars Would Do to the Human Body

An enjoyable article exploring the science of reproduction in space. I appreciate the genuine curiosity and hopeful outlook here!

The annual SXSW conference in Austin, Texas, can be a bit overwhelming. What started as a fairly modest four-day music festival in 1987, drawing some 700 attendees, has become a ten-day extravaganza of panel presentations featuring celebrities and business leaders, film screenings, technology showcases, and—yes—music. These days hundreds of thousands of people converge on downtown Austin for “South By,” as it’s called by those in the know. When I was a graduate student at the University of Texas in the early 2000s, I always avoided the festival and its inevitable crowds, which was relatively easy to do since it tended to be held the same week as the university’s Spring Break.

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But when I received an invitation in 2023 to attend a SXSW panel presentation with the title “Sex in Space: Sex and Reproduction Beyond Earth,” I knew I had to go. After all, any plans to create a permanent settlement on Mars or elsewhere in space wouldn’t last long if we can’t have kids there.

Astrocytes enable amygdala neural representations supporting memory

A thorough study exploring how astrocytes affect fear conditioning and fear extinction in the basolateral amygdala of mice. Subpopulations of astrocytes were found to interact with neurons in such a way as to help encode representations of fear. [ https://www.nature.com/articles/s41586-025-10068-0](https://www.nature.com/articles/s41586-025-10068-0)

Gq G-protein-coupled receptor (GPCR) signalling increases astrocyte Ca2+ activity through IP3-mediated release of intracellular Ca2+ stores42,43 and hM3Dq actuation causes a Ca2+ surge preceded by prolonged quiescence, possibly due to intracellular Ca2+ depletion24,44,45. Replicating these effects in the BLA, we expressed hM3Dq in BLA astrocytes and used in vivo cyto-GCaMP6f photometry and observed that clozapine–N-oxide (CNO) injection markedly increased Ca2+ activity within around 10 min but, thereafter, decreased and remained low for at least 2 h (Fig. 2c and Extended Data Figs. 6a–e and 8e, f). A lower hM3Dq virus concentration or lower CNO dose had modest or negligible effects on Ca2+ activity and behaviour (Extended Data Fig. 6h–p). On the basis of these data, we posited that BLA astrocyte Ca2+ dynamics would be constrained by hM3Dq actuation at timepoints relevant to behavioural testing. Consistent with this supposition, hM3Dq-actuation essentially abolished Ca2+ responses to a potent stimulus (footshock) given 30 min after CNO injection (Extended Data Fig. 6f, g).

We leveraged these effects of hM3Dq actuation to test how constraining astrocyte Ca2+ dynamics affected memory acquisition, retrieval, consolidation and extinction by injecting separate groups of animals with 3 mg per kg CNO either before or immediately after F-Con, or before fear retrieval/extinction training. We found that CNO given before extinction training reduced CS-related freezing during E-Ext—consistent with impaired memory retrieval—in hM3Dq-expressing mice compared with viral controls (Fig. 2d, e). In vivo fibre photometry confirmed that this behavioural effect was accompanied by loss of CS-related astrocyte Ca2+ responses (Fig. 2f and Extended Data Fig. 7a–c). In contrast to these memory-retrieval-impairing effects, CNO had no behavioural effect when injected before or after F-Con26,27 and did not alter uncued freezing, shock-induced flinching or various measures of anxiety-like behaviour (Extended Data Fig. 7d–i). Behavioural effects were also absent when CNO was injected in mice not expressing hM3Dq or when vehicle was injected in hM3Dq-expressing animals, excluding potential non-specific CNO and hM3Dq-virus effects, respectively (Extended Data Fig. 7j–n).

We next compared these effects with those of another DREADD, hM4Di, that produces effects on cortical, striatal and (as we show here; Fig. 2g–i) BLA astrocyte Ca2+ activity that mirror those of hM3Dq, that is, increase Ca2+ transients24,46,47. Accordingly, we found that hM4Di actuation produced effects on memory retrieval that were opposite to hM3Dq: pre-Ext CNO injection produced increases in CS-related freezing and astrocyte Ca2+ responses during E-Ext in hM4Di-expressing mice compared with viral controls (Fig. 2j–l and Extended Data Fig. 8a–f). Pre-Ext hM4Di actuation also increased freezing during (CNO-free) E-Ret, indicative of a deficit in extinction memory formation, and attenuated CS-related Ca2+ activity during this test stage. This latter effect is notable given that hM3Dq actuation produced a similar extinction deficit and blunted the CS-related Ca2+ response on E-Ret (Fig. 2e and Extended Data Fig. 7b), despite the two manipulations having opposite effects on fear retrieval and neither affecting extinction memory when CNO was given before E-Ret (Extended Data Fig. 8g, h). This convergence of extinction-impairing effects suggests that extinction is sensitive to perturbations—whether increases or decreases—in astrocyte Ca2+ activity and, by extension, implies an important role for BLA astrocytes in the plastic adaptations underlying extinction memory formation.

Phagocyte NADPH Oxidase NOX2-Derived Reactive Oxygen Species in Antimicrobial Defense: Mechanisms, Regulation, and Therapeutic Potential—A Narrative Review

ROS derived from NADPH oxidase, particularly NOX2, are central to antimicrobial defense, coupling direct pathogen killing with redox signaling that shapes inflammation. This narrative review integrates recent advances on NOX2 structure, assembly, and spatiotemporal control in phagocytes, and outlines how ROS interact with NF-κB, MAPK, and Nrf2 networks to coordinate microbicidal activity and immune modulation. We summarize evidence that both ROS deficiency, as in chronic granulomatous disease, and uncontrolled excess, as in sepsis and severe COVID-19, drive clinically significant pathology, emphasizing the need for precise redox balance.

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