CellLoom

Recent research is introducing a new way to approach cancer immunotherapy — by reprogramming immune cells directly inside the tumor.

Scientists have developed a nanoparticle-based therapy that delivers mRNA into tumor-associated macrophages, one of the most abundant immune cells within the tumor microenvironment. These macrophages are normally suppressed by the tumor and lose their ability to attack cancer cells.

Using lipid nanoparticles, the therapy induces these macrophages to express CAR (chimeric antigen receptor) proteins in vivo, effectively turning them into CAR-macrophages without removing them from the patient’s body.

Once reprogrammed, these immune cells regain their anti-tumor activity, directly attacking cancer cells and stimulating broader immune responses within the tumor environment.

In preclinical models, this strategy significantly slowed tumor growth and activated systemic anti-cancer immunity.

The key implication is conceptual as much as technical: instead of engineering immune cells outside the body and reinfusing them, it may be possible to reprogram immune function in place, inside the tumor itself.

This approach could simplify immunotherapy workflows and open new directions for targeting the tumor microenvironment.

If this topic aligns with your interests in cancer biology or immunotherapy, feel free to share it with others engaged in science-driven research and discussion.

For many years, cancer research has focused on the genetic and molecular changes that occur inside tumour cells themselves. But cancer does not develop in isolation. Tumours grow within complex biological environments, shaped by constant interaction with surrounding cells.

Among these surrounding cells are neurons.

Until recently, neurons were thought to influence cancer mainly through signaling molecules and nerve growth factors. Their role was considered indirect. That assumption is now being challenged.

New evidence discussed in Nature suggests that neurons can transfer mitochondria directly into neighbouring tumour cells. Mitochondria are not just sources of energy. They regulate metabolism, stress responses, and cell survival. When tumour cells acquire additional mitochondria, their ability to endure hostile conditions and continue growing may be fundamentally altered.
This finding reframes how scientists think about tumour–nerve interactions.

Rather than acting only as messengers, neurons may provide metabolic support that actively fuels cancer progression. In this context, the nervous system becomes a structural component of the tumour ecosystem, capable of shaping how aggressively a cancer behaves.

The implications extend beyond basic biology.

If tumour cells rely on mitochondrial input from neurons, then interrupting this transfer could represent a new therapeutic strategy.

Targeting cancer may require not only attacking malignant cells, but also disrupting the supportive networks that sustain them.

For the first time, the influence of nerves on cancer is no longer limited to signaling pathways. It includes the direct transfer of cellular power.

If you find this research relevant, consider sharing it with others interested in how biology and disease are studied. Thoughtful discussion and informed sharing help scientific knowledge reach beyond the laboratory.

📌 Source: comments

For more than two decades, the scientific community has recognized that the three-dimensional organization of the human genome plays a critical role in how genetic information is accessed and utilized within living cells. However, comprehensive integration of structural data with functional insights remained a significant challenge—until now.

In a major advance by the 4D Nucleome Project, researchers have assembled an integrated and high-resolution view of the human 4D nucleome by combining diverse genomic datasets from two widely studied human cell types: embryonic stem cells (H1) and immortalized fibroblasts (HFFc6). This effort has allowed the generation of detailed structural annotations of chromosome folding, nuclear positioning, and looping interactions, enabling quantitative connections between genome architecture and core biological processes such as transcription and DNA replication.

The integrated dataset includes extensive catalogues of more than 140,000 looping interactions per cell type, mapped alongside classifications of chromosomal domains and their subnuclear locations. These loop structures bring distant regulatory elements into physical proximity with target genes, shaping the regulatory landscape of the genome and influencing gene activity in a cell-type-dependent manner.

A key feature of this work is the development and benchmarking of complementary genomic assays that contribute unique perspectives on genome folding, as well as computational models that can predict aspects of 3D structure directly from DNA sequence. This integrated approach offers a framework for interpreting how genetic variants, including those linked to disease, may perturb genome organization and function.

Beyond producing comprehensive structural models, the study provides a practical user guide for future 4D nucleome research, outlining the strengths of different experimental methods and offering strategies for their application. By uniting structural and functional genomics, the work deepens our understanding of the relationship between physical genome architecture and biological function.

This integrated view of the human genome’s four-dimensional structure represents a significant milestone in genomics—one that moves the field closer to deciphering how chromosome folding dynamics contribute to health, development, and disease.









#علم

🧬 Intercellular Mitochondrial Transfer: Rethinking Cellular Communication

Mitochondria have long been recognized as the primary organelles responsible for cellular energy production. However, growing evidence over the past decade suggests that their role extends far beyond ATP generation, encompassing metabolic regulation, immune signaling, and cellular stress responses. Recent studies indicate that mitochondria are not always confined within individual cells, but can be transferred between neighboring cells under specific physiological and pathological conditions.

Experimental observations have revealed multiple mechanisms through which mitochondrial transfer can occur, including tunneling nanotubes, extracellular vesicles, and direct cell-to-cell contact. These processes have been documented in diverse biological contexts, such as tissue repair, immune modulation, and tumor microenvironments, suggesting that mitochondrial exchange may represent a conserved form of intercellular communication.

Functionally, transferred mitochondria can influence the metabolic state of recipient cells. In some cases, the acquisition of healthy mitochondria restores oxidative phosphorylation and improves cellular survival following injury. In other contexts, mitochondrial transfer alters redox balance, reactive oxygen species production, and gene expression patterns, effectively reprogramming cellular behavior.

The role of mitochondrial transfer in disease remains complex and context-dependent. While some studies suggest that mitochondrial donation from healthy cells may support tissue regeneration, others indicate that cancer cells can exploit this process to enhance metabolic flexibility, resist stress, and survive therapeutic interventions. This duality highlights the need for a deeper mechanistic understanding of when mitochondrial transfer is beneficial versus pathological.

Despite increasing recognition of this phenomenon, key questions remain unresolved, including how mitochondrial transfer is regulated, what signals initiate or inhibit it, and whether the process can be selectively targeted for therapeutic benefit. Addressing these questions may open new avenues in regenerative medicine, cancer therapy, and the treatment of metabolic and inflammatory disorders.

🔗 Source: comments

دراسة جديدة من معهد ماساتشوستس التكنولوجي (MIT) بتفسر ليه الأكل عالي الدهون ممكن يخلي الكبد أكثر عرضة للإصابة بالسرطان. وجدت الدراسة إن التعرض الطويل لنظام غذائي غني بالدهون بيخلي خلايا الكبد المتطورة ترجع لحالة أشبه بالخلايا الجذعية — وضع يساعدها على النجاة من الإجهاد لكن كمان يرفع من احتمال تحولها لخلايا سرطانية بمرور الوقت.

الدراسة اتعملت على فئران، وبيّن الباحثين إن تغيّر الجينات ده بيحصل تدريجيًا مع تراكم الدهون في الكبد، وبيشبه نفس التغييرات اللي بتظهر في بيانات مرضى الكبد عند البشر.

الدهون مش بس بتتراكم في الكبد، لكن بتغيّر سلوك خلاياه بشكل يخلي السرطان أسهل في الظهور مع الوقت.

📍 اقرأ التفاصيل الكاملة هنا:
https://scitechdaily.com/mit-reveals-how-high-fat-diets-quietly-prime-the-liver-for-cancer/

#صحة #الكبد #تغذية #علم #أبحاث

علماء من مشروع 4D Nucleome قدروا يرسموا خريطة ثلاثية الأبعاد لأكثر من 140,000 حلقة DNA داخل نواة الخلية البشرية، موضحين كيف يتشكل الكروموسوم في الفضاء الخلوي وكيف تتفاعل أجزاء الحمض النووي مع بعضها. الاكتشاف ده بيساعدنا نفهم إزاي الجينات بتتعامل وتتفاعل ـ وبيفتح باب لفهم أفضل للوراثة والأمراض الجينيّة.

📌 الفريق استخدم نماذج حاسوبية متقدمة تقدر تتنبأ بتكوين الجينوم من تسلسل الـDNA نفسه، ده ممكن يساعد في فهم تأثير التغيرات الوراثية المرتبطة بالأمراض.

🔗 اللينك :
https://phys.org/news/2025-12-scientists-dna-loops-human-chromosomes.html