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Unlabelled: Quantitative understanding of mitochondrial heterogeneity is necessary for elucidating the precise role of these multifaceted organelles in tumor cell development. We demonstrate an early mechanistic role of mitochondria in initiating neoplasticity by performing quantitative analyses of structure-function of single mitochondrial components coupled with single cell transcriptomics. We demonstrate that the large Hyperfused-Mitochondrial-Networks (HMNs) of keratinocytes promptly get converted to the heterogenous Small-Mitochondrial-Networks (SMNs) as the stem cell enriching dose of the model carcinogen, TCDD, depolarizes mitochondria.

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Malignant gliomas are heterogeneous tumors, mostly incurable, arising in the central nervous system (CNS) driven by genetic, epigenetic, and metabolic aberrations. Mutations in isocitrate dehydrogenase (IDH1/2) enzymes are predominantly found in low-grade gliomas and secondary high-grade gliomas, with IDH1 mutations being more prevalent. Mutant-IDH1/2 confers a gain-of-function activity that favors the conversion of a-ketoglutarate (α-KG) to the oncometabolite 2-hydroxyglutarate (2-HG), resulting in an aberrant hypermethylation phenotype.

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[Adrenal tumors in pediatric patients treated with minimally invasive surgery].

Andes Pediatr

October 2024

Escuela de Medicina, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.

Unlabelled: Adrenal tumors in children are frequently neoplastic and malignant, and surgical resection is the first management option. Minimally invasive surgery (MIS) has proven to be a safe management alternative and is suggested as a preferred alternative approach.

Objective: To report the surgical outcomes of patients with adrenal tumors treated by MIS.

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Introduction: DU145 and LNCaP are classic prostate cancer cell lines. Characterizing their baseline transcriptomics profiles (without any intervention) can offer insights into baseline genetic features and oncogenic pathways that should be considered while interpreting findings after various experimental interventions such as exogenous gene transfection or drug treatment.

Methods: LNCaP and DU145 cell lines were cultured under normal conditions, followed by RNA extraction, cDNA conversion, library preparation, and RNA sequencing using the Illumina NovaSeq platform.

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Inhibiting de novo lipogenesis identifies a therapeutic vulnerability in therapy-resistant colorectal cancer.

Redox Biol

February 2025

Cell and Tumor Biology, Advanced Centre for Treatment, Research and Education in Cancer (ACTREC), Tata Memorial Centre, Kharghar, Navi Mumbai, 410210, India. Electronic address:

A significant clinical challenge in patients with colorectal cancer (CRC), which adversely impacts patient survival, is the development of therapy resistance leading to a relapse. Therapy resistance and relapse in CRC is associated with the formation of lipid droplets (LD) by stimulating de novo lipogenesis (DNL). However, the molecular mechanisms underlying the increase in DNL and the susceptibility to DNL-targeted therapies remain unclear.

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