HMGN1 (High Mobility Group Nucleosome Binding Domain 1)

Therapy acute myeloid leukemia (AML) is a heterogeneous malignant hematopoietic disease that arises either from an antecedent hematologic disorder, including myelodysplastic syndromes, myeloproliferative neoplasms, aplastic anemia, or as a result of exposure to genotoxic chemotherapeutic agents or radiotherapy (therapy-related AML). In this study, we describe a case of therapy AML after treatment for breast, uterine, and rectal malignancies in a patient with a special fusion gene-RUNX1::HMGN1.

The combined treatment of the anti-TNFR2 antibody and HMGN1 therapy synergistically alleviates immunosuppression by decreasing tumor-infiltrating regulatory T cells (Treg cells). This decrease in Treg cells results in the successful eradication of tumors in vivo by promoting the function and expansion of TIL.

Elevated levels of HMGB1 in the bone marrow and serum of MPN patients demonstrate a correlation with biochemical indices related to AS. This finding may serve as a valuable reference for predicting AS complications in MPN patients.

HMGA2, along with other HMG family members, emerges as a potential prognostic biomarker and therapeutic target in HCC. This study provides new insights into the role of HMG proteins in HCC progression.

To corroborate these findings, cellular experiments were conducted, confirming HMGN1's crucial involvement in homologous recombination repair and its potential to enhance the sensitivity of LUAD cells to standard chemotherapeutic drugs. This study proposes HMGN1 as a novel prognostic biomarker and a promising target for chemotherapy in lung adenocarcinoma.

The combination of these three drugs altered the TME and promoted an increase in anti-tumor immune components. This may provide a promising new treatment strategy for colon cancer.

Our study has identified several genes in different immune cells that were associated with cervical cancer. However, further research is necessary to confirm these findings and provide more comprehensive insights into the association between these gene expressions and cervical cancer risk.

These results suggest that CLP may binds to the paraprotein produced by heavy chain MM in the blood and therefore its blood levels are found to be low. Additionally, low levels of HMGN1, which is involved in DNA repair, suggest that HMGN1 may contribute to the complex genetic abnormalities found in MM.

This study highlighted the potential of HMGN1 as a biomarker for pan- - cancer analysis.

The cells in the model group were treated with 500 ng/mL HMGN1, while the antagonist group was treated with 500 ng/mL TAK-242 (resatorvid), a Toll-like receptor 4 (TLR4) antagonist, in addition to HMGN1...The results of Western blot suggested that the protein expression levels of iNOS, TLR4, MyD88, NF-κB p65 and IKK-β decreased significantly in the antagonist group. Conclusion HMGN1 may induce the activation of BV2 microglial cells by upregulating pro-inflammatory mediators through activating the TLR4/MyD88/NF-κB p65/IKK-β signaling pathway.

Thus, MSN@TheraVac provides a timely release of TheraVac for the curative treatment of colon tumors and holds potential for translation into a clinical therapy for patients with immunologically "cold" colorectal cancers. This ROS-responsive MSN platform may also be tailored for the selective delivery of other cancer vaccines for effective immunotherapy.

The resultant tumor-free mice were resistant to subsequent re-challenge with the same tumors, indicating the generation of long-term tumor specific protective immunity. Since the immune-activating arm also induces full maturation of human DCs, and anti-PDL-1 or anti-CTLA4 have been FDA-approved, this combinational immunotherapy has the potential to be an effective clinical therapy for patients with solid tumors.