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Research Article
In-silico Study on Pharmacokinetic Properties and VEGFR-2 Binding of Quininib Through Molecular Docking
Issue:
Volume 14, Issue 1, March 2026
Pages:
1-8
Received:
15 December 2025
Accepted:
9 January 2026
Published:
29 January 2026
Abstract: Cancer growth depends on both the physiological process of angiogenesis, supported by binding of the vascular endothelial growth factor (VEGF) to endothelial cells of blood vessels, and on the interaction of angiogenic growth factors with receptors on endothelial cells, which promote angiogenesis through signaling pathways. The purpose of this in-silico study was to compare the binding of the small molecule inhibitor quininib (QNB) to the VEGFR2 receptor with the binding of the standard anti-cancer drug axitinib using AutoDock 4.2 to predict and assess docking scores; and to categorize each compound's pharmacokinetic properties using the Swiss ADME (Absorption, Distribution, Metabolism, and Excretion) online tool. The results presented here demonstrate that quininib is capable of binding to the areas of the VEGFR2 receptor corresponding to the following amino acids: LEU889, VAL898, VAL899, LEU1019, ASP1028, and ILE1044. These binding interactions involve primarily hydrophobic interactions, together with a hydrogen bond with ASP1046 and a docking score of -4.72 kcal/mol. In addition, it was found that QNB possesses a high level of gastrointestinal (GI) absorption and the ability to cross the Blood–Brain Barrier (BBB), as well as that it conforms to Lipinski's rule of five for oral administration. We can therefore conclude that quininib has the potential to inhibit angiogenesis, which could thereby suppress the growth of cancer cells by binding to VEGFR2; and that even though its inhibition of VEGFR2 is lower than that of axitinib, there is potential for QNB to be developed as an orally administered agent following appropriate formulation and subsequent validation by further in-vitro and in-vivo studies.
Abstract: Cancer growth depends on both the physiological process of angiogenesis, supported by binding of the vascular endothelial growth factor (VEGF) to endothelial cells of blood vessels, and on the interaction of angiogenic growth factors with receptors on endothelial cells, which promote angiogenesis through signaling pathways. The purpose of this in-s...
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Research Article
Cancer Antigen 15-3 and Carcinoembryonic Antigen Chemotherapeutic Response and Associated Hepato-Renal Toxicity in Cameroonian Cancer Patients
Issue:
Volume 14, Issue 1, March 2026
Pages:
9-27
Received:
22 January 2026
Accepted:
2 February 2026
Published:
26 February 2026
Abstract: Background: Chemotherapy remains central to cancer management in sub-Saharan Africa but is frequently complicated by treatment resistance and cumulative hepato-renal toxicity. Longitudinal biomarker monitoring may improve early detection of subclinical organ dysfunction and therapeutic response. This study evaluated longitudinal changes in hepatic, renal, inflammatory, and tumor-associated biomarkers to elucidate chemotherapy response and resistance patterns among cancer patients receiving systemic therapy in Cameroon. Materials and Methods: A longitudinal observational study was conducted among 120 cancer patients treated at the Cameroon Oncology Centre (February-July 2025). Serum liver enzymes (aspartate aminotransferase (AST), alanine aminotransferase (ALT)), albumin, urea, creatinine-derived estimated glomerular filtration rate (eGFR), C-reactive protein (CRP) measurement was done once at the end of the chemotherapeutic period were measured at baseline and over three follow-up time points at two-month intervals, while cancer biomarkers, namely carcinoembryonic antigen (CEA), and cancer antigen 15-3 (CA15-3) were screened within two interval periods. Non-parametric analyses (Kruskal–Wallis, Friedman tests) assessed group differences and monotonic trends, while Spearman’s correlation evaluated treatment–biomarker associations. Results: Participants were predominantly female (77.5%), with advanced-stage disease (Stage III–IV: 59.2%). Liver enzymes remained largely stable throughout follow-up, indicating preserved hepatocellular integrity. In contrast, albumin exhibited a significant monotonic decline (−1.20%, p = 0.004), reflecting cumulative metabolic and inflammatory stress. Renal function showed a modest but significant decline in eGFR (−3.77%, p = 0.044), particularly among platinum-based regimens, despite stable urea levels. Tumour marker analysis revealed a pronounced and consistent reduction in CA15-3 (−12.98%, p = 0.006), whereas CEA showed no significant longitudinal trend. Drug-specific correlations supported time-dependent renal and hepatic effects, particularly with cisplatin and combination therapies. Conclusion: Longitudinal biomarker profiling reveals subclinical renal stress, systemic metabolic burden, and differential tumour marker responsiveness during chemotherapy. CA15-3 and eGFR emerged as sensitive indicators of treatment response and toxicity, underscoring the value of integrated biomarker monitoring in resource-limited oncology settings.
Abstract: Background: Chemotherapy remains central to cancer management in sub-Saharan Africa but is frequently complicated by treatment resistance and cumulative hepato-renal toxicity. Longitudinal biomarker monitoring may improve early detection of subclinical organ dysfunction and therapeutic response. This study evaluated longitudinal changes in hepatic,...
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Research Article
Pan-cancer Analysis of Solute Carrier Family 7, Member 5 and o- [(5-Amino-2-Phenyl- 7-Benzoxazolyl) Methyl]-3, 5-Dichloro-L-Tyrosine Treatment Attempt in Rats
Meng-yu Zhang*
,
Jie-ping Wang,
Wen-guang Fu,
Ming Luo,
Shu Qin
Issue:
Volume 14, Issue 1, March 2026
Pages:
28-42
Received:
24 January 2026
Accepted:
24 February 2026
Published:
9 March 2026
Abstract: Solute Carrier Family 7, Member 5 (SLC7A5) is a member of the SLC family, which can transport large, neutral, and branched-chain amino acids. It is increasingly recognized to play an important role in human cancers. O- [(5-Amino-2-phenyl- 7-benzoxazolyl) methyl]-3, 5-dichloro-L-tyrosine (JPH203) is a SLC7A5 inhibitor. This study aims to preliminarily explore the potential role of SLC7A5 and the therapeutic effect of JPH203, providing a new direction for cancer treatment. By analyzing data from The Cancer Genome Atlas (TCGA) database and the Gene Type Tissue Expression (GTEx) database, we can elucidate the characteristics of SLC7A5 in cancers, demonstrate the association of SLC7A5 with cancer heterogeneity, and highlight its role in cancer clinical staging. Establish a rat model of hepatocellular carcinoma (HCC) and observe the changes in SLC7A5 after treatment with JPH203. SLC7A5 is highly expressed in most cancers, but has low expression in a few types. Cancers with high expression of SLC7A5 usually have poor prognosis. The mutation rate of SLC7A5 is relatively low and it is closely related to immune system. SLC7A5 is mainly positively correlated with cancer heterogeneity, and in some cancers SLC7A5 is closely related to clinical staging. After treatment with JPH203, the expression of SLC7A5 significantly decreased in HCC. Conclusion: The expression of SLC7A5 varies obviously in different cancers, leading to differential prognosis. It is closely related to immune infiltration and immune cells. JPH203 may play therapeutic role in cancers, suggesting that SLC7A5 may provide new direction and JPH203 may be helpful in the cancer treatment.
Abstract: Solute Carrier Family 7, Member 5 (SLC7A5) is a member of the SLC family, which can transport large, neutral, and branched-chain amino acids. It is increasingly recognized to play an important role in human cancers. O- [(5-Amino-2-phenyl- 7-benzoxazolyl) methyl]-3, 5-dichloro-L-tyrosine (JPH203) is a SLC7A5 inhibitor. This study aims to preliminari...
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Commentary
The Cancer Cocktail a Possible Treatment for Some Cancers
Issue:
Volume 14, Issue 1, March 2026
Pages:
43-52
Received:
18 February 2026
Accepted:
9 March 2026
Published:
30 March 2026
DOI:
10.11648/j.jctr.20261401.14
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Views:
Abstract: Many cancers are glucose-dependent and have a higher rate of glycolysis, as described by the Warburg effect. Reducing the amount of free glucose will starve cancers. Medications that control blood glucose levels, including Metformin, change the intestinal biome by increasing desirable commensal bacteria, causing a drop in A1C. With the drop in glucose, many cancers can modulate metabolism to lipids, so a low-carbohydrate diet will keep the cancer from growing. Cancer can mask the immune system, turning off PD-L1 (Programmed Death Ligand-1) and increasing the expression of CD47, the “do not eat me protein". CD47, a protein overexpressed on many cancer cells to prevent macrophages attacks. CD47 does this by binding to Signal Regulatory Protein Alpha (SIRPα) on macrophages. 4-Methylumbelliferone (4-MU) will limit the amount of masked CD47. 4-MU also has other benefits. It will protect the integrity of the B cells but also promotes insulin secretion to help cope with the degradation of B-cell function due to immune destruction. This might offset the side effects of Pembrolizumab (Keytruda), a therapeutic monoclonal antibody which targets and activates PD-1 on immune cells. PD-1 is a molecule that is found on killer T Cells and natural killer cells, which target any cell that does not display the MHC-2 cell surface molecule. These two changes, PD-L1 activation and CD-47 limitation, make cancer visible and vulnerable to Natural Killer cells, Killer T Cells, and macrophages. Pembrolizumab (Keytruda) can have toxic side effects, including a spike in blood sugar, which can damage B Cells, type 1 diabetes, and pancreatitis, though these are considered rare side effects. In Theory, Metformin and 4-MU will inhibit this occurrence with an improvement in gut bacteria and increasing insulin, and therefore lowering the risk to the pancreas and protecting B cells.
Abstract: Many cancers are glucose-dependent and have a higher rate of glycolysis, as described by the Warburg effect. Reducing the amount of free glucose will starve cancers. Medications that control blood glucose levels, including Metformin, change the intestinal biome by increasing desirable commensal bacteria, causing a drop in A1C. With the drop in gluc...
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