TY  - JOUR
AB  - Lung cancer, characterized by its heterogeneity, presents a significant challenge in therapeutic management, primarily due to the development of resistance to conventional drugs. This resistance is often compounded by the tumor's ability to reprogram its metabolic pathways, a survival strategy that enables cancer cells to thrive in adverse conditions. This review article explores the complex link between drug resistance and metabolic reprogramming in lung cancer, offering a detailed analysis of the molecular mechanisms and treatment strategies. It emphasizes the interplay between drug resistance and changes in metabolic pathways, crucial for developing effective lung cancer therapies. This review examines the impact of current treatments on metabolic pathways and the significance of considering metabolic factors to combat drug resistance. It highlights the different challenges and metabolic alterations in non-small-cell lung cancer and small-cell lung cancer, underlining the need for subtype-specific treatments. Key signaling pathways, including PI3K/AKT/mTOR, MAPK, and AMPK, have been discussed for their roles in promoting drug resistance and metabolic changes, alongside the complex regulatory networks involved. This review article evaluates emerging treatments targeting metabolism, such as metabolic inhibitors, dietary management, and combination therapies, assessing their potential and challenges. It concludes with insights into the role of precision medicine and metabolic biomarkers in crafting personalized lung cancer treatments, advocating for metabolic targeting as a promising approach to enhance treatment efficacy and overcome drug resistance. This review underscores ongoing advancements and hurdles in integrating metabolic considerations into lung cancer therapy strategies.
AU  - Mohanty, P.*
AU  - Pande, B.*
AU  - Acharya, R.*
AU  - Bhaskar, L.V.K.S.*
AU  - Verma, H.K.
C1  - 70754
C2  - 55731
CY  - St Alban-anlage 66, Ch-4052 Basel, Switzerland
TI  - Unravelling the triad of lung cancer, drug resistance, and metabolic pathways.
JO  - Diseases
VL  - 12
IS  - 5
PB  - Mdpi
PY  - 2024
SN  - 2079-9721
ER  - 

TY  - JOUR
AB  - Pathogenic variants in the MT-ATP6 are a well-known cause for maternally inherited mitochondrial disorders associated with a wide range of clinical phenotypes. Here, we present a 31- year old female with insulin-dependent diabetes mellitus, recurrent lactic acidosis and ketoacidosis recurrent infections with suspected immunodeficiency with T cell lymphopenia and hypogammaglobulinemia as well as proximal tetraparesis with severe muscle and limb pain and rapid physical exhaustion. Muscle biopsy and respiratory chain activities were normal. Single-exome sequencing revealed a variant in the MT-ATP6 gene: m.9143T>C. Analysis of further specimen of the index and mother (segregation studies) revealed the highest mutation load in muscle (99% level of mtDNA heteroplasmy) of the index patient. Interestingly, acute metabolic and physical decompensation during recurrent illness was documented to be a common clinical feature in patients with MT-ATP6 variants. However, it was not mentioned as a key symptom. Thus, we suggest that the clinical spectrum might be expanded in ATP6-associated diseases.
AU  - Urban, D.L.*
AU  - Scholle, L.M.*
AU  - Wagner, M.
AU  - Ludolph, A.C.*
AU  - Rosenbohm, A.*
C1  - 59358
C2  - 48756
TI  - The m.9143T>C variant: Recurrent infections and immunodeficiency as an extension of the phenotypic spectrum in MT-ATP6 mutations?
JO  - Diseases
VL  - 8
IS  - 2
PY  - 2020
SN  - 2079-9721
ER  -