MESFER AL SHAHRANI, REEM GAHTANI, MOHAMMAD ABOHASSAN, MOHAMMAD ALSHAHRANI, YASSER ALRAEY, AYED DERA, MOHAMMAD RAJEH ASIRI, PRASANNA RAJAGOPALAN^*

Oncology Research, Vol.32, No.2, pp. 251-259, 2024, DOI:10.32604/or.2023.043139

Abstract Gastric cancers are caused primarily due to the activation and amplification of the EGFR or HER2 kinases resulting in cell proliferation, adhesion, angiogenesis, and metastasis. Conventional therapies are ineffective due to the intra-tumoral heterogeneity and concomitant genetic mutations. Hence, dual inhibition strategies are recommended to increase potency and reduce cytotoxicity. In this study, we have conducted computational high-throughput screening of the ChemBridge library followed by in vitro assays and identified novel selective inhibitors that have a dual impediment of EGFR/HER2 kinase activities. Diversity-based High-throughput Virtual Screening (D-HTVS) was used to screen the whole ChemBridge small molecular library against EGFR and… More > Graphic Abstract

Jianing Yi^*, Shuai Chen^*, Pingyong Yi^†, Jinlin Luo^*, Meng Fang^*, Yang Du^*, Lianhong Zou^*, Peizhi Fan^*

Oncology Research, Vol.28, No.5, pp. 519-831, 2020, DOI:10.3727/096504020X15960154585410

Abstract 5-Fluorouracil (5-FU) is a widely used chemotherapeutic agent for breast cancer. However, acquired chemoresistance leads to a loss of its efficacy; methods to reverse are urgently needed. Some studies have shown that pyrotinib, an ErbB receptor tyrosine kinase inhibitor, is effective against HER2+ breast cancer. However, whether pyrotinib sensitizes 5-FU-resistant breast cancer cells to 5-FU is unknown. We hypothesized that the combination of pyrotinib and 5-FU would show synergistic antitumor activity, and pyrotinib could reverse 5-FU resistance in HER2+ breast cancer cells in vitro and in vivo. Our data showed that pyrotinib inhibited the growth of 5-FU-resistant SKBR-3/FU and MDA-MB-453/FU… More >

Keiichi Kontani^1,*, Kana Kuraishi¹, Shin-ichiro Hashimoto¹, Shoko Norimura², Nozomi Hashimoto¹, Masahiro Ohtani³, Naomi Fujiwara-Honjo⁴, Manabu Date⁵, Koji Teramoto⁶, Hiroyasu Yokomise¹

Oncologie, Vol.23, No.2, pp. 229-239, 2021, DOI:10.32604/Oncologie.2021.016277

Abstract The prognosis of patients with human epidermal growth factor receptor-2 (HER2)-overexpressed metastatic breast cancer (MBC) has improved drastically following the development of anti-HER2 therapies. We question what factors are involved in the improved outcome by the treatment. One hundred and two MBC patients who received chemotherapy were classified into groups according to breast cancer subtype: luminal/HER2-negative (n = 50), HER2 (n = 26), and triple-negative subtypes (n = 26). Clinicopathologic features and clinical outcomes of the groups were compared. Disease-free intervals in the triple-negative group were significantly shorter than those in the other two groups. Age, tumor grade, the number… More >

YANFEI LI¹, LULU DAI², KE CAI², YINGKUI SONG², XIQING LIU^3,*

BIOCELL, Vol.45, No.3, pp. 685-694, 2021, DOI:10.32604/biocell.2021.013612

Abstract RPA3 (Replication Protein A3) (14 kD) is a part of the canonical heterotrimeric replication protein A complex (RPA/RP-A). This study aimed to explore the functional role of RPA3 and the mechanisms of its dysregulation in breast cancer. Data from the Cancer Genome Atlas (TCGA)-breast cancer patients and GSE75688 were utilized for gene expression and survival analysis. Breast cancer cell lines MDA-MB-231 and SK-BR-3 were used for in-vitro cell studies. Clonogenic assay and immunofluorescent staining of γ-H2AX were performed to examine radiation-induced cytotoxicity. Systemic correlation analysis was performed to identify potential transcription factors (TFs) regulating RPA3 expression. ChIP-qPCR and dual-luciferase assay… More >

ZHIXIONG WANG^1,2, NA RISU², JIAYU FU², HUI LIU³, GUOMIN ZHOU³, QIAN LIU³, YAN ZOU⁴, JIAXING TANG⁴, LONG LI⁴, XUEKAI ZHU^4,*

BIOCELL, Vol.45, No.1, pp. 157-165, 2021, DOI:10.32604/biocell.2021.010261

Abstract Chimeric antigen receptor (CAR) T-cell therapy is mostly limited to hematological malignancies and has a poor effect on solid tumors. CAR T cells as a kind of immune cell may be affected by some immunomodulatory drugs such as pomalidomide, so the use of pomalidomide may improve the effect of CAR T cells on solid tumors. In this study, CD133- or HER2-specific CAR T cells were chosen to investigate whether pomalidomide can regulate the function of CAR T cells in vitro. We found that pomalidomide can significantly enhance the ability of CD133-CAR T cells and HER2-CAR T cells to kill tumor… More >