New advances in the research of clinical treatment and novel anticancer agents in tumor angiogenesis

Li, Xin; Zhou, Jianbo; Xue, Wei; Li, Chunxi; Ma, Zifan; Wan, Qiaoling; Peng, Fu

doi:10.1016/j.biopha.2023.114806

Cited by 12 publications

(2 citation statements)

References 353 publications

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“…Nintedanib, an oral tyrosine kinase inhibitor targeting VEGFR1-3, FGFR1-3, and PDGFR, is approved for the treatment of idiopathic pulmonary fibrosis and lung cancer [ 56 , 57 , 58 ]. Nintedanib showed an unexpected effect on cancer cells, stimulating their growth in some of NSCLC cultures at lower concentrations, while inhibiting it at higher concentrations.…”

Section: Discussionmentioning

confidence: 99%

Multidrug-Resistant Profiles in Non-Small Cell Lung Carcinoma Patient-Derived Cells: Implications for Personalized Approaches with Tyrosine Kinase Inhibitors

Dinić,

Dragoj,

Jovanović Stojanov

et al. 2024

Cancers

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The impact of tyrosine kinase inhibitors (TKIs) on multidrug resistance (MDR) in non-small cell lung carcinoma (NSCLC) is a critical aspect of cancer therapy. While TKIs effectively target specific signaling pathways of cancer cells, they can also act as substrates for ABC transporters, potentially triggering MDR. The aim of our study was to evaluate the response of 17 patient-derived NSCLC cultures to 10 commonly prescribed TKIs and to correlate these responses with patient mutational profiles. Using an ex vivo immunofluorescence assay, we analyzed the expression of the MDR markers ABCB1, ABCC1, and ABCG2, and correlated these data with the genetic profiles of patients for a functional diagnostic approach. NSCLC cultures responded differently to TKIs, with erlotinib showing good efficacy regardless of mutation burden or EGFR status. However, the modulation of MDR mechanisms by erlotinib, such as increased ABCG2 expression, highlights the challenges associated with erlotinib treatment. Other TKIs showed limited efficacy, highlighting the variability of response in NSCLC. Genetic alterations in signaling pathways associated with drug resistance and sensitivity, including TP53 mutations, likely contributed to the variable responses to TKIs. The relationships between ABC transporter expression, gene alterations, and response to TKIs did not show consistent patterns. Our results suggest that in addition to mutational status, performing functional sensitivity screening is critical for identifying appropriate treatment strategies with TKIs. These results underscore the importance of considering drug sensitivity, off-target effects, MDR risks, and patient-specific genetic profiles when optimizing NSCLC treatment and highlight the potential for personalized approaches, especially in early stages.

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Section: Discussionmentioning

confidence: 99%

Multidrug-Resistant Profiles in Non-Small Cell Lung Carcinoma Patient-Derived Cells: Implications for Personalized Approaches with Tyrosine Kinase Inhibitors

Dinić,

Dragoj,

Jovanović Stojanov

et al. 2024

Cancers

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“…These molecules can be secreted by the tumor and/or stromal cells, or mobilized from the extracellular matrix (Tuxhorn et al, 2001;Van Moorselaar and Voest, 2002;Condon, 2005). The vascular endothelial growth factor (VEGF), which is considered the most potent mediator of angiogenesis and endothelial cell functions, stimulates endothelial cell proliferation, differentiation and migration, and promotes increased vascular permeability (Van Moorselaar and Voest, 2002;Montico et al, 2013;Li et al, 2023).…”

Section: Introductionmentioning

confidence: 99%

Differential Tempol effects in prostatic cancer: angiogenesis and short- and long- term treatments

Santos,

Rossetto,

Montico

et al. 2023

Preprint

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Prostate cancer (PCa) is the second cause of cancer death among men worldwide. Several processes are involved in the development and progression of PCa such as angiogenesis, inflammation and oxidative stress. The present study investigated the effect of short- or long-term Tempol treatment at different stages of prostate adenocarcinoma progression, focusing on angiogenic, proliferative, and stromal remodeling processes in TRAMP mice. The dorsolateral lobe of the prostate of TRAMP mice were evaluated at two different stages of PCa progression; early and late stages. Early stage was again divided into, short- or long-term. 50mg/kg Tempol dose was administered orally. The results demonstrated that Tempol mitigated the prostate histopathological lesion progressions in the TRAMP mice in all treated groups. However, Tempol increased molecules involved in the angiogenic process such as CD31 and VEGFR2 relative frequencies, particularly in long-term treatment. In addition, Tempol upregulated molecule levels involved in angiogenesis and stromal remodeling process VEGF, TGF-β1, VE-cadherin and vimentin, particularly, in T8-16 group. Thus, it was concluded that Tempol treatment delayed prostatic lesion progression in the dorsolateral lobe of the TRAMP mice. However, Tempol also led to pro-angiogenic effects and glandular stromal microenvironment imbalance, especially, in the long-term treatment.

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Differential tempol effects in prostatic cancer: angiogenesis and short- and long-term treatments

Santos,

Rossetto,

Montico

et al. 2024

J Mol Histol

View full text Add to dashboard Cite

Prostate cancer (PCa) is the second cause of cancer death among men worldwide. Several processes are involved in the development and progression of PCa such as angiogenesis, in ammation and oxidative stress. The present study investigated the effect of short-or long-term Tempol treatment at different stages of prostate adenocarcinoma progression, focusing on angiogenic, proliferative, and stromal remodeling processes in TRAMP mice. The dorsolateral lobe of the prostate of TRAMP mice were evaluated at two different stages of PCa progression; early and late stages. Early stage was again divided into, short-or long-term. 50mg/kg Tempol dose was administered orally. The results demonstrated that Tempol mitigated the prostate histopathological lesion progressions in the TRAMP mice in all treated groups. However, Tempol increased molecules involved in the angiogenic process such as CD31 and VEGFR2 relative frequencies, particularly in long-term treatment. In addition, Tempol upregulated molecule levels involved in angiogenesis and stromal remodeling process VEGF, TGF-β1, VE-cadherin and vimentin, particularly, in T8-16 group. Thus, it was concluded that Tempol treatment delayed prostatic lesion progression in the dorsolateral lobe of the TRAMP mice. However, Tempol also led to proangiogenic effects and glandular stromal microenvironment imbalance, especially, in the long-term treatment.

show abstract

New advances in the research of clinical treatment and novel anticancer agents in tumor angiogenesis

Cited by 12 publications

References 353 publications

Multidrug-Resistant Profiles in Non-Small Cell Lung Carcinoma Patient-Derived Cells: Implications for Personalized Approaches with Tyrosine Kinase Inhibitors

Multidrug-Resistant Profiles in Non-Small Cell Lung Carcinoma Patient-Derived Cells: Implications for Personalized Approaches with Tyrosine Kinase Inhibitors

Differential Tempol effects in prostatic cancer: angiogenesis and short- and long- term treatments

Differential tempol effects in prostatic cancer: angiogenesis and short- and long-term treatments

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