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Category: biotech/medical – Page 363

Signaling pathways in the regulation of cancer stem cells and associated targeted therapy

The concept of stem cells dates back to the 18th century when scientists tried to elucidate how lower organisms developed tissues and organs. 1 These stem cells produce daughter cells that later undergo different biological processes, either continuous self‐renewal division, or differentiation into specialized cells with a limited lifespan. Normal tissue stem cells provide a life‐long source of cells for self‐renewal of tissues, which leads us to speculate that whether stem cells are capable of deriving a malignant cell population, and this lies the foundation of cancer stem cells (CSCs) theory. CSCs are defined as a subpopulation of malignant tumor cells with selective capacities for tumor initiation, self‐renewal, metastasis, and unlimited growth into bulks. 2

Despite decades of research on cancer treatment, it has been proved extremely challenging to achieve complete remission (CR) in cancer patients. Tumor relapse may be explained by the fact that antitumor therapeutics mainly target proliferative cancer cells but remain ineffective in quiescent CSCs. The role of CSC in tumor initiation was first identified in acute myeloid leukemia (AML). Since its isolation from a number of solid tumors and hematological malignancies, the CSC is believed to form the clonogenic core of these tumors. 3 Growing evidence now suggests that CSCs are responsible for multiple progressive tumor phenotypes, including recurrence, metastasis, and treatment failure. 4, 5 The intrinsic treatment resistance of tumors has partially attributed to the presence of the CSC subpopulation, 6, 7 and may also be induced by extrinsic factors, such as treatments and environments. 8, 9

Major signaling pathways are involved in the maintenance of stem cell properties and survival of CSCs, such as the Notch, Wnt, and Hedgehog (HH) pathways. 10 There is also intricate interplay network between these signal cascades and other oncogenic pathways. 11, 12, 13 Thus, targeting pathway molecules that regulate CSCs provides a new option for the treatment of therapy‐resistant or ‐refractory tumors. This review aims to provide an overview of the regulating networks and their immune interactions involved in CSC development. We also summarized the update on the development of CSC‐directed therapeutics, with a special focus on those with application approval or under clinical evaluation.

A Reflection on Movement Disorders Fellowship Training in Deep Brain Stimulation: Past and Future

A Reflection on Movement Disorders —Fellowship Training in Deep Brain Stimulation: Past and Future.

Deep brain stimulation (DBS) has been an integral part of movement disorders care for decades. However, differences exist in techniques for surgical implantation of DBS and clinician experience with DBS systems, including use of new software, programming approaches, and postsurgical management of patients. DBS technologies have been rapidly advancing, and indications for DBS are increasing, including for psychiatric symptoms and epilepsy. The heterogeneity in the scope and utility of DBS is perhaps mirrored in education and training, despite efforts to develop competency measures for trainees. These advancements in DBS and the varying opportunities offered at each fellowship contribute to challenges for program directors to establish and implement consistent expectations. Similar challenges have been observed in other fields using neuromodulation.

Scientists reverse muscle aging in mice and discover a surprising catch

A UCLA study in mice reveals that aging muscle stem cells accumulate a protein that slows repair but boosts survival. This protein, NDRG1, acts like a brake, preventing cells from activating quickly after injury. When researchers blocked it in older mice, muscle healing sped up dramatically — but stem cells became less resilient over time. The work suggests aging may reflect a survival trade-off rather than straightforward decline.

‘Off the shelf’ immunotherapy could get a lift from gene-edited natural killer cells

Since scientists first discovered that human immune cells could be modified to become cancer-fighting agents, they’ve been trying to engineer a cell that’s effective against solid tumors, which account for the vast majority of cancer cases. In a key advance in meeting this “holy grail challenge” in the field of cancer cell therapy, a team of Yale scientists led by geneticist Sidi Chen has revealed how immune cells can be “boosted” to target and eradicate solid tumors.

The field of cell therapy began to revolutionize cancer treatment several decades ago, when researchers pioneered the use of therapeutic cells. In this process, immune cells are removed from a patient, modified so that they can better fight cancer, and then reintroduced into the patient’s body.

Two major streams of this therapy exist: CAR-NK cell therapy, which uses a patient’s natural killer (NK) cells, and CAR-T cell therapy, which uses a patient’s T cells. In both cases, scientists genetically modify the cells to express Chimeric Antigen Receptor (CAR), a synthetic receptor that helps immune cells recognize proteins on cancer cells.