Internal medicine Oncology

Physician-scientists at Kanazawa University have demonstrated, for the first time worldwide, the clinical efficacy of chemoimmunotherapy in patients with ultra-rare urachal cancer. Furthermore, their reverse translational research elucidated the mechanism by which the addition of immunotherapy enhances the efficacy of chemotherapy.

Researchers studied 23 cases of oral cancer with a burrowing growth pattern and found that rare carcinoma cuniculatum has a unique genetic fingerprint. The research found genetic alterations in FAT1, NOTCH1, PIK3CA, and CASP8, suggesting a potential explanation for its slow growth and favorable prognosis. These findings suggest that genetic testing could improve diagnosis and inform treatment decisions in oral cancer.

Researchers from The University of Osaka found that only a small subset of tumor-killing T cells undergoes extensive expansion during immunotherapy for multiple myeloma. By tracking individual cells, the team showed that the T-cell clones that later became dominant had already begun expanding shortly after the treatment started. The findings also suggest that highly proliferative immune cells show lower levels of exhaustion-related markers, offering new insights into why some patients respond better to immunotherapy.

Hiroshima University researchers have developed a practical framework to identify candidate pathogenic variants hidden among the large number of variants of uncertain significance (VUS) detected in comprehensive genomic profiling (CGP) of cancers. This framework could improve the accuracy of precision oncology by more reliable prioritization of VUS.

Researchers from The University of Osaka found that leukemia caused by NUTM1 rearrangements is distinguished from other forms of B-cell acute lymphoblastic leukemia (B-ALL) by a unique pattern of gene activity and gene regulation. Unlike the common form of B-ALL caused by KMT2A rearrangement, which is resistant to treatment, leukemic cells with NUTM1 rearrangements are highly sensitivity to chemotherapy.

Through protein binding, molecular heavy drugs are effectively transported to cancerous tissues

Researchers at the Cancer Research Institute and the Nano Life Science Institute (WPI-NanoLSI), Kanazawa University, have uncovered a critical mechanism that enables gastric cancer to spread to distant organs. Their study shows that cancer cells stimulate Wnt signaling in surrounding stromal fibroblasts to produce hyaluronan, creating a supportive microenvironment that promotes metastasis. These findings provide new insight into how metastatic tumors establish themselves and suggest promising strategies to prevent gastric cancer progression.

A research team at The University of Osaka revealed that the loss of heterochromatin can cause a chain reaction leading to genetic changes and the subsequent development of diseases including cancer. Using fission yeast, the study specifically found that loss of Clr4, which encodes a methyltransferase, can induce an increase in R-loop levels at pericentromeric repeats, and the later conversion of R-loops into ADR-loops can prompt gross chromosomal rearrangements.

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Researchers at The University of Osaka developed the Balloon-Assisted Bronchoscope Delivery (BDBD) technique and in a first-in-human clinical trial, the team successfully demonstrated that this technique is both safe and effective, enabling access to lesions smaller than 20 mm. By using a small balloon to gently widen airways, it allows endoscopes to reach deep, peripheral lung tumors, promising more accurate cancer diagnosis and new minimally invasive treatment options.

Researchers have developed an eco-friendly method to create gold nanoparticles (AuNPs) using microalgae. This "green synthesis" avoids harsh chemicals, resulting in nanoparticles that are more stable than conventional ones. When activated by a laser, these AuNPs effectively destroy cancer cells while showing lower toxicity to healthy cells. This breakthrough promises a more sustainable and safer approach to photothermal cancer therapy and other applications in nanomedicine.

UOsaka and MIT scientists revealed that the motor proteins KIF18A and CENP-E work together to align chromosomes during mitosis. Cancer cells with reduced CENP-E levels are especially sensitive to KIF18A inhibition, and dual inhibition of both proteins leads to efficient cell death. The discovery offers new insights into chromosome mechanics and a potential strategy for targeted cancer therapy.

A joint team has uncovered how soft, deformable particles, like cells, behave in microfluidic channels. Using precisely fabricated hydrogel particles and simulations on the supercomputer "Fugaku," they demonstrated that particle softness dramatically alters their focusing patterns, deviating significantly from rigid particle behavior. These findings reveal distinct "phase transitions" in focusing, shifting from mid-edge to eight-point, diagonal-edge, and finally center focusing as deformability increases. This breakthrough, explained by a new theoretical model incorporating inertia and deformability, offers crucial insights for designing next-generation microfluidic devices for highly efficient cell sorting and other biomedical applications like early cancer detection. The ability to control particle focusing based on deformability opens exciting possibilities for advanced particle manipulation and separation technologies.

Researchers at The University of Osaka and Kanazawa University have developed a novel method for analyzing cancer metabolism, revealing new insights into cancer's inefficient energy process. This breakthrough, published in Metabolic Engineering, combines biological experiments with advanced information science techniques to uncover the role of cancer-specific inefficient metabolism.

Researchers at the Nano Life Science Institute (WPI-NanoLSI), Kanazawa University observe and model how the enzyme ADAR1 interacts with double-stranded RNA, which may be useful for future cancer treatment strategies.

A surgeon can excise breast cancer from the body, but even the most skilled scalpel may not be able to remove every cell — especially when the cells have spread from the original disease site elsewhere in the body. This proliferation and migration of breast cancer cells involves many still unknown molecular means, but researchers at Hiroshima University have elucidated at least one mechanism, involving protein receptors that bind to one another. With the discovery, they may have also uncovered how short chains of protein building blocks could serve as a novel anticancer drug.

Researchers from The University of Osaka found that the Wnt5a protein, secreted by inflammatory fibroblasts within cancerous tumors, inhibits angiogenesis and consequently promotes hypoxia within tumors. Hypoxic conditions help sustain the inflammatory fibroblasts, which also secrete the growth factor epiregulin, thereby promoting tumor growth. This newly proposed mechanism for tumor growth offers a promising new target for cancer therapies and possibly other conditions linked to inflammation, such as inflammatory bowel disease.

Researchers discover that inflammation and aging contribute to non-viral liver cancer development. Green tea's role in reversing some of the pathway dysregulation that may contribute to the cancer development and other therapies explored.

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Researchers at Kanazawa University report in Cancer Research how Kras and p53 mutations influence the tumor suppressor and promoter functions of a TGF- ß pathway. The findings may lead to a new approach for colorectal cancer therapy.

A research team led by Osaka University developed a theranostics approach to both diagnose and treat certain pancreatic cancer cases. They radioactively labeled a monoclonal antibody targeting glypican-1, which is highly expressed in pancreatic cancer, then administered it to disease model mice. One label, 89Zr, showed high uptake in tumors, which would allow early detection of pancreatic cancer with PET scans. Another label, 211At, was used with alpha therapy to significantly slow tumor growth.

AXL and EGFR inhibitors combined hold promise in fighting certain head, neck, and lung cancers

Researchers at Kanazawa University report in Cell Reports how alterations in the nuclear pores lead to the degradation of anti-tumor proteins.

Researchers from Osaka University have revealed that the expression of a specific isoform of GREB1 Is4 is induced in malignant melanoma cells by the melanocyte-specific transcription factor, MITF. They revealed that GREB1 Is4 stimulates pyrimidine biosynthesis and promotes cancer cell proliferation. Furthermore, the anti-tumor effect of antisense nucleic acids against GREB1 showed a potential new modality for malignant melanoma.

The researchers from Osaka University showed how bone erosion caused by cholesteatoma occurs. This study showed that a subset of cells called osteoclastogenic fibroblasts expresses a protein, activin A, which causes the breakdown of the bones. Because of this discovery, novel medical treatments can be developed as first-line management for cholesteatomas.

Researchers from Osaka University have revealed the mechanism by which increased signaling through a pathway associated with a molecule called Wnt leads to the development of liver cancer. They identified a gene called GREB1 as a target of Wnt specifically in liver cancer. This gene alters the function of a protein called HNF4α, leading to the development of cancer. They also showed that treatment of mice with antisense oligonucleotides against GREB1 had significant anti-cancer effects.

Broccoli may contain advantages beyond nutrition. A molecule found in broccoli, cabbage and more digests down into DIM, a compound with brighter benefits than the name implies, such as inducing cell death in breast, prostate and colon cancer. Now, researchers are beginning to understand the mechanism underpinning this molecular behavior — information that could help elucidate future anti-cancer treatments.

We have succeeded in establishing a mouse model that develops gastric cancer closely resembling advanced human gastric cancer. Using this model, we have discovered gastric cancer stem cells, i.e. Lgr5+ gastric cancer cells, essential for the development, maintenance, and metastasis of cancer. Our study provides an experimental system that enables detailed analysis of highly malignant gastric cancer and is expected to lead to the development of a breakthrough treatment for advanced human gastric cancer.

Malfunctioning of the so-called Hippo signalling pathway within animal cells leads to irregular activity of proteins that regulate genes involved in cell proliferation. Researchers have identified a key step in the process of this aberration, opening the door to new therapeutics for cancers such as head-and-neck squamous cell carcinoma and lung adenocarcinoma.

A synthetic CDK4/6 inhibitor exerts antitumor effects by forcing RB1 tumor-suppressor into an active status, but its single administration is not sufficiently effective. We find its combinatorial administration with an IKKβ inhibitor is significantly more effective in hepatocellular carcinoma treatment. Also, blockage of the IKK-NF-κB or AKT pathway enhances its effects on RB1-intact K-Ras mutated lung and colon cancers. CDK4/6 inhibitors have potential to treat various RB1-intact cancers when combined with an appropriate kinase inhibitor.