Geothermal resources in Egypt are useful as a promising source of renewable energy. Little attempts have been carried out to expansively investigate the geothermal potentiality in the Western Desert. The present study is focused on the investigation of geothermal resources in the Northern Western Desert. To achieve this objective, the available aeromagnetic data is firstly reduced to the pole (RTP), then filtered using tilt derivative (TDR) and Butterworth low and high pass methods. The major trends of the different predominant detected local and regional lineaments (probably basement structures) have been determined and correlated with surface structures. To delineate the basement depth configuration, power spectral analysis of aeromagnetic data, as well as constructing 2D modeling (verified by drilled wells data) were applied. The results have been used to estimate the Curie point depth (CPD), geothermal 

The Precambrian Homrit–Waggat granite is a post‐orogenic batholithic intrusion located in the northern region of the Nubian Shield, characterized by a typical annular morphology and significant secondary alteration. This study aims to elucidate the processes that have shaped the intrusion in both macroscopic and microscopic perspectives, employing a combination of field observation and petrographic analysis alongside major and trace element compositions of minerals. Within the central region of the pluton, biotite and amphibole are observed sporadically, while the predominant crystallization of anhydrous oligoclase in the outer regions has led to a progressive increase in volatile components within the residual melt, ultimately resulting in a volatile‐saturated aluminosilicate melt. The exsolved fluids subsequently interacted with the previously crystallized mineral assemblage, producing metasomatic 

The post-collisional Homrit Waggat ring pluton exposed in southeastern Egypt preserves a record of events in the magma plumbing system at mid-crustal depths (c. 11 km). The pluton consists of two successive granite rings: an inner syeno-granite ring (c. 630–626 Ma) and an outer alkali granite ring (c. 635 Ma). High-resolution aeromagnetic data for the total magnetic intensity were used to construct vertical cross-sections through the pluton to configure its subsurface geometry and internal structure. A reduction-to-pole filter was applied to the total magnetic intensity data to position the magnetic anomalies directly above their sources. Several derivation techniques were applied to the reduction-to-pole data, including the tilt derivation filter to highlight the subsurface structural contacts and faults, the analytical signal technique to delineate the concentric magnetic rings, and both 3D Euler deconvolution and 2D

Glioma is a type of aggressive and incurable brain tumor. Patients with glioma are highly resistant to all types of therapies, including immunotherapies. Epigenetic reprogramming is a key molecular hallmark in tumors across cancer types, including glioma. Mounting evidence highlights a pivotal role of epigenetic regulation in shaping tumor biology and therapeutic responses through mechanisms involving both glioma cells and immune cells, as well as their symbiotic interactions in the tumor microenvironment (TME). In this review, we discuss the molecular mechanisms of epigenetic regulation that impacts glioma cell biology and tumor immunity in both a cell-autonomous and non-cell-autonomous manner. Moreover, we provide an overview of potential therapeutic approaches that can disrupt epigeneticregulated tumor-immune symbiosis in the glioma TME.

Abundant macrophage infiltration and altered tumor metabolism are two key hallmarks of glioblastoma. By screening a cluster of metabolic small-molecule compounds, we show that inhibiting glioblastoma cell glycolysis impairs macrophage migration and lactate dehydrogenase inhibitor stiripentol emerges as the top hit. Combined profiling and functional studies demonstrate that lactate dehydrogenase A (LDHA)-directed extracellular signalregulated kinase (ERK) pathway activates yes-associated protein 1 (YAP1)/ signal transducer and activator of transcription 3 (STAT3) transcriptional coactivators in glioblastoma cells to upregulate C-C motif chemokine ligand 2 (CCL2) and CCL7, which recruit macrophages into the tumor microenvironment. Reciprocally, infiltrating macrophages produce LDHA-containing extracellular vesicles to promote glioblastoma cell glycolysis, proliferation, and survival. Genetic and pharmacological inhibition of LDHA-mediated tumor-macrophage symbiosis markedly suppresses tumor progression and macrophage infiltration in glioblastoma mouse models. Analysis of tumor and plasma samples of glioblastoma patients confirms that LDHA and its downstream signals are potential biomarkers correlating positively with macrophage density. Thus, LDHA-mediated tumor-macrophage symbiosis provides therapeutic targets for glioblastoma.

Glioblastoma (GBM) is an aggressive and lethal type of brain tumor in human adults. The standard of care offers minimal clinical benefit, and most GBM patients experience tumor recurrence after treatment. In recent years, significant advancements have been made in the development of novel immunotherapies or other therapeutic strategies that can overcome immunotherapy resistance in many advanced cancers. However, the benefit of immune-based treatments in GBM is limited because of the unique brain immune profiles, GBM cell heterogeneity, and immunosuppressive tumor microenvironment. In this review, we present a detailed overview of current immunotherapeutic strategies and discuss the challenges and potential molecular mechanisms underlying immunotherapy resistance in GBM. Furthermore, we provide an in-depth discussion regarding the strategies that can overcome immunotherapy resistance in GBM, which will likely require combination therapies.

Tumor-associated macrophages (TAMs) are the predominant immune cells in the tumor microenvironment that promote breast cancer brain metastasis (BCBM). Here, we identify TANK-binding kinase (TBK1) as a critical signaling molecule enriched and activated in TAMs of BCBM tumors, playing an indispensable role in BCBM development and metastatic outgrowth in the brain. Mechanistically, BCBM cell-secreted matrix metalloproteinase 1 binds to protease-activated receptor 1 and integrin αVβ5 on macrophages, leading to TBK1 activation mediated by the nuclear factor-kappa B pathway. Reciprocally, TBK1-regulated TAMs produce granulocyte-macrophage colony-stimulating factor (GM-CSF) to drive breast cancer cell epithelial–mesenchymal transition, migration, and invasion, ultimately contributing to BCBM development and brain metastatic outgrowth. Inhibition of TBK1 signaling in TAMs or GM-CSF receptor in cancer cells impedes BCBM development and brain metastatic outgrowth. Correspondingly, the TBK1–GM-CSF signaling axis correlates with lower overall survival in patients with BCBM. Thus, TBK1-mediated tumor-TAM symbiotic interaction provides a promising therapeutic target for patients with BCBM.

The CHEK2 gene serves a canonical role in the DNA damage response (DDR) pathway encoding the regulatory kinase CHK2 in the homologous recombination (HR) repair of double-strand breaks (DSB). Although CHEK2 is traditionally considered a tumor suppressor gene, recent studies suggest additional functions. Across several cohort studies, CHEK2 expression was negatively correlated with the efficacy of immune checkpoint inhibitors (ICI), which target the interaction between effector immune and tumor cells. This review explores two possible explanations for this observed phenomenon: the first relating to the canonical role of CHEK2, and the second introducing a novel role of the CHEK2 gene in immunomodulation of the tumor microenvironment (TME). DDR mutations have been implicated in increased levels of tumor mutation burden (TMB), often manifesting as neoepitope expression on the tumor cell surface recognized by effector immune cells. As a result, impaired DNA repair due to CHEK2 loss of function, either from germline deleterious variants or acquired mutations, results in the recruitment of CD8+ cytotoxic T-cells and subsequent efficacy of ICI treatment. However, functional loss of CHEK2 may be directly involved in potentiating the immune response through canonical inflammatory and anti-tumor pathways, acting through the cGAS-STING pathway. Although the exact mechanism by which CHEK2 modulates immune responses is still under investigation, combination therapy with CHEK1/2 inhibition and ICI immunotherapy has shown benefit in preclinical studies of several solid tumors.