Bone marrow, besides the known functions of hematopoiesis, is an active organ of the immune system, functioning as a sanctuary for several mature immune cells. Moreover, evidence suggests that hematopoietic stem cells (the bone marrow's functional unit) are capable of directly sensing and responding to an array of exogenous stimuli. This chronic immune stimulation is harmful to normal hematopoietic stem cells, while essential for the propagation of myeloid diseases, which show a dysregulated immune microenvironment. The bone marrow microenvironment in myelodysplastic syndromes (MDS) is characterized by chronic inflammatory activity and immune dysfunction, that drive excessive cellular death and through immune evasion assist in cancer cell expansion. Acute myeloid leukemia (AML) is another example of immune response failure, with features that augment immune evasion and suppression. In this review, we will outline some of the functions of the bone marrow with immunological significance and describe the alterations in the immune landscape of MDS and AML that drive disease progression.
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http://dx.doi.org/10.3390/diseases10020033 | DOI Listing |
PLoS One
January 2025
Departamento de Bioquímica y Medicina Molecular, Universidad Autónoma de Nuevo León, Monterrey, Nuevo León, México.
Introduction: The methicillin-resistant Staphylococcus aureus (MRSA) genome varies by geographical location. This study aims to determine the genomic characteristics of MRSA using whole-genome sequencing (WGS) data from medical centers in Mexico and to explore the associations between antimicrobial resistance genes and virulence factors.
Methods: This study included 27 clinical isolates collected from sterile sites at eight centers in Mexico in 2022 and 2023.
Mol Carcinog
January 2025
Institute of Precision Medicine, The First Affiliated Hospital; Department of Pediatrics, The Seventh Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Acute myeloid leukemia (AML) is marked by the proliferation of abnormal myeloid progenitor cells in the bone marrow and blood, leading to low cure rates despite new drug approvals from 2017 to 2018. Current therapies often fail due to the emergence of drug resistance mechanisms, such as those involving anti-apoptotic pathways and immune evasion, highlighting an urgent need for novel approaches to overcome these limitations. Programmed cell death (PCD) is crucial for tissue homeostasis, with PANoptosis-a form of PCD integrating pyroptosis, apoptosis, and necroptosis-recently identified.
View Article and Find Full Text PDFDrug Dev Res
February 2025
Department of Radiation Oncology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, Fujian, China.
We aimed to elucidate the prognostic and immunological roles of B cell-related genes in colorectal cancer (CRC). This study comprehensively integrated data from single-cell RNA-sequencing, TCGA, GEO, IMvigor210, GDSC, CancerSEA, HPA, and TISIDB databases to explore prognostic implications and immunological significance of B cell-related gene signature in CRC. We identified seven prognostically significant B cell-related genes for constructing a risk score.
View Article and Find Full Text PDFSARS-CoV-2 nonstructural protein 1 (nsp1) promotes innate immune evasion by inhibiting host translation in human cells. However, the role of nsp1 in other host species remains elusive, especially in bats which are natural reservoirs of sarbecoviruses and possess a markedly different innate immune system than humans. Here, we reveal that SARS-CoV-2 nsp1 potently inhibits translation in bat cells from Rhinolophus lepidus, belonging to the same genus as known sarbecovirus reservoirs hosts.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Precision Medicine Laboratory, School of Medical Technology and Engineering, Henan University of Science and Technology, Luoyang, People's Republic of China.
Ovarian cancer (OC) remains one of the most lethal gynecological malignancies, largely due to its late-stage diagnosis and high recurrence rates. Chronic inflammation is a critical driver of OC progression, contributing to immune evasion, tumor growth, and metastasis. Inflammatory cytokines, including IL-6, TNF-α, and IL-8, as well as key signaling pathways such as nuclear factor kappa B (NF-kB) and signal transducer and activator of transcription 3 (STAT3), are upregulated in OC, promoting a tumor-promoting environment.
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