&lt;p&gt;Beyond The T/C Ratio: Old And New Anticancer Activity Scores In Vivo&lt;/p&gt;

Ubezio, Paolo

doi:10.2147/cmar.s215729

Cited by 11 publications

(5 citation statements)

References 20 publications

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“…Tumour delay (T − C): This is calculated by the differences in time (in days) to reach 30% of its initial tumour volume in both groups (treated and control groups). 31 …”

Section: Methodsmentioning

confidence: 99%

Preclinical meritorious anticancer effects of Metformin against breast cancer: An In vivo trial

Rizvi

Shaukat

Azhar³

et al. 2021

Journal of Taibah University Medical Sciences

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Objective This research aims to evaluate the preclinical meritorious and anticancer effects of Metformin in a Xenograft model of breast cancer. Methods This interventional trial was conducted during a defined period of 5 months (August 2016 January 2017). We used a Xenograft model of nude BALB/c mice. A sample size of 50 mice, allocated into two groups and designated as Group A and Group B for Metformin and negative control groups, respectively. The anticancer activity of Metformin has been evaluated by comparing the tumour volume, tumour weight, tumour regression ratio, percentage regression, and survival rate. Results Compared with the control group, Metformin can significantly reduce the progression of tumour in the Xenograft model of breast cancer induced by MCF-7. This is reflected by significant differences in tumour volume at the final follow-up ( p = <0.001). Our findings are further supported by a significant reduction of the tumour growth rate ( p = <0.001) and tumour weight ( p = <0.001) in the Metformin group than in the control group. Similarly, the total survival rate and tumour regression are more significantly correlated in the Metformin group. Conclusion This study demonstrates that Metformin can significantly reduce the tumour growth and can increase the survival rate in a Xenograft model of breast cancer.

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“…Tumour delay (T − C): This is calculated by the differences in time (in days) to reach 30% of its initial tumour volume in both groups (treated and control groups). 31 …”

Section: Methodsmentioning

confidence: 99%

Preclinical meritorious anticancer effects of Metformin against breast cancer: An In vivo trial

Rizvi

Shaukat

Azhar³

et al. 2021

Journal of Taibah University Medical Sciences

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“…At the end of the experiment, mice were sacrificed, then tumours and livers were excised, measured and stored for further analysis. The treatment efficacy was calculated as the percentage of tumour growth (%Gr = 100 × ∆T/∆C, where ∆T = T − T 0 and ∆C= C − C 0 ) and the percentage of growth inhibition (%GrI = 100 − %Gr) according to [58].…”

Section: Animal Studiesmentioning

confidence: 99%

The Isoxazole Derivative of Usnic Acid Induces an ER Stress Response in Breast Cancer Cells That Leads to Paraptosis-like Cell Death

Pyrczak-Felczykowska

Reekie

Jąkalski

et al. 2022

IJMS

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Derivatives of usnic acid (UA), a secondary metabolite from lichens, were synthesized to improve its anticancer activity and selectivity. Recently we reported the synthesis and activity of an UA isoxazole derivative, named 2b, against cancer cells of different origins. Herein, the molecular mechanisms underlying its activity and efficacy in vivo were tested. The viability of breast cancer or normal cells has been tested using an MTT assay. Cell and organelle morphology was analyzed using light, electron and fluorescence microscopy. Gene expression was evaluated by RNAseq and protein levels were evaluated by Western blotting. In vivo anticancer activity was evaluated in a mice xenograft model. We found that 2b induced massive vacuolization which originated from the endoplasmic reticulum (ER). ER stress markers were upregulated both at the mRNA and protein levels. ER stress was caused by the release of Ca2+ ions from the ER by IP3R channels which was mediated, at least partly, by phospholipase C (PLC)-synthetized 1,4,5-inositol triphosphate (IP3). ER stress led to cell death with features of apoptosis and paraptosis. When applied to nude mice with xenografted breast cancer cells, 2b stopped tumour growth. In mice treated with 2b, vacuolization was observed in tumour cells, but not in other organs. This study shows that the antiproliferative activity of 2b relates to the induction of ER stress in cancer, not in healthy, cells and it leads to breast cancer cell death in vitro and in vivo.

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“…2D). Interestingly, however, in terms of tumor regression, the impact of DCF treatment was more profound in PreNAC-O than in PostNAC-O xenografts, with tumor growth inhibition rates (TGIs) 10,11 of 58.5% and 35.9%, respectively. Furthermore, even though the growth rate of PostNAC-O xenografts was signi cantly suppressed by DCF treatment, it was still comparable to that in the PreNAC-O xenograft control group (Fig.…”

Section: Resultsmentioning

confidence: 99%

Characterization of residual cancer by comparison of a pair of organoids established from a patient with ESCC before and after neoadjuvant chemotherapy

Fuchino,

Kurogi,

Tsukamoto

et al. 2023

Preprint

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Neoadjuvant chemotherapy (NAC) followed by surgery is a standard approach for management of locally advanced esophageal squamous cell carcinoma (ESCC). Patients who do not respond well to NAC have a poor prognosis. Despite extensive research, the mechanisms of chemoresistance in ESCC remain largely unknown. Here, we established paired tumor organoids – designated as PreNAC-O and PostNAC-O – from one ESCC patient before and after NAC, respectively. Although the two organoids did not exhibit significant differences in proliferation, morphology or drug sensitivity in vitro, the tumorigenicity of PostNAC-O in vivo was significantly higher than that of PreNAC-O. Xenografts from PreNAC-O tended to exhibit keratinization, while those from PostNAC-O displayed conspicuous necrotic areas. The tumorigenicity of PostNAC-O xenografts during the chemotherapy was comparable to that of PreNAC-O without treatment. Furthermore, the gene expression profiles of the xenografts suggested that expression of genes involved in the EMT and/or hypoxia response might be related to the tumorigenicity of PostNAC-O. Our data suggested that the tumorigenicity of residual cancer had been enhanced, outweighing the effects of chemotherapy, rather than being attributable to intrinsic chemoresistance. Further studies are required to clarify the extent to which residual cancers share a common mechanism similar to that revealed here.

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<p>Beyond The T/C Ratio: Old And New Anticancer Activity Scores In Vivo</p>

Cited by 11 publications

References 20 publications

Preclinical meritorious anticancer effects of Metformin against breast cancer: An In vivo trial

Preclinical meritorious anticancer effects of Metformin against breast cancer: An In vivo trial

The Isoxazole Derivative of Usnic Acid Induces an ER Stress Response in Breast Cancer Cells That Leads to Paraptosis-like Cell Death

Characterization of residual cancer by comparison of a pair of organoids established from a patient with ESCC before and after neoadjuvant chemotherapy

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