Xiaoxiang Guan

Jiangsu Province Hospital

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Wenwen Zhang

Nanjing Medical University

Fang Yang

Nanjing Medical University

Longbang Chen

Nanjing General Hospital of Nanjing Military Command

Lin Tang

Zhejiang University

Weiwei Nie

Shandong Tumor Hospital

Yanru Wang

Minzu University of China

Runtian Wang

Nanjing Medical University

Yucai Wang

Mayo Clinic

Yaqin Shi

Inner Mongolia Agricultural University

Jing Xu

Nanjing Medical University

Cooperative Institutions

Nanjing Medical University

195

Nanjing University

121

Jiangsu Province Hospital

Nanjing General Hospital of Nanjing Military Command

Harbin Medical University

National Institutes of Health

The University of Texas MD Anderson Cancer Center

Chinese Academy of Medical Sciences & Peking Union Medical College

Nanjing University of Chinese Medicine

Chinese Academy of Sciences

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Comparative analyses of multi-species sequences from targeted genomic regions

Nature (2003)

James W. Thomas Jeff Touchman Robert W. Blakesley Gerard G. Bouffard Stephen M. Beckstrom‐Sternberg

Comparative Genomics

Conserved sequence

Coding region

10.1038/nature01858

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Citations (637)

Multitargeted antiangiogenic tyrosine kinase inhibitors combined to chemotherapy in metastatic breast cancer: a systematic review and meta-analysis

European Journal of Clinical Pharmacology (2014)

Zexing Wang Meiqi Wang Fei Yang Weiwei Nie Fengxia Chen

Progression-free survival

10.1007/s00228-014-1654-5

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Citations (15)

Role of Erythropoietin in Cancer-related Anaemia: A Double-edged Sword?

Journal of International Medical Research (2008)

Xiaoxiang Guan L Chen

Anaemia often occurs in cancer patients and its origin is multifactorial, resulting from either bone marrow infiltration of cancer cells or cytotoxic effects produced by chemotherapy and radiotherapy. Anaemia impacts significantly on quality of life and appears markedly to limit disease control. Erythropoietin stimulates erythrocyte formation and the human recombinant form is useful in treating anaemia in cancer patients. Over the past decade erythropoietin has been associated with amelioration of anaemia and reduced need for blood transfusions. Nevertheless, several pre-clinical and clinical trials, employing relatively high doses of erythropoietin, have been halted recently following increased mortality and morbidity, primarily due to thrombotic events and possible tumour growth stimulation. It is, therefore, too early to know whether erythropoietin is useful in controlling morbidity and mortality in cancer-related anaemia. The risk–benefit of erythropoietic agents should be studied in carefully controlled trials. This review discusses prevalent issues and addresses key questions concerning the use of erythropoietic agents for the treatment of cancer-related anaemia.

Epoetin alfa

10.1177/147323000803600101

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Citations (16)

c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment

Cell Communication and Signaling (2023)

Fangyan Gao Xin-tong Li Kun Xu Runtian Wang Xiaoxiang Guan

Abstract The MYC oncogenic family is dysregulated in diverse tumors which is generally linked to the poor prognosis of tumors. The members in MYC family are transcription factors which are responsible for the regulation of various genes expression. Among them, c-MYC is closely related to the progression of tumors. Furthermore, c-MYC aberrations is tightly associated with the prevalence of breast cancer. Tumor microenvironment (TME) is composed of many different types of cellular and non-cellular factors, mainly including cancer-associated fibroblasts, tumor-associated macrophages, vascular endothelial cells, myeloid-derived suppressor cells and immune cells, all of which can affect the diagnosis, prognosis, and therapeutic efficacy of breast cancer. Importantly, the biological processes occurred in TME, such as angiogenesis, immune evasion, invasion, migration, and the recruition of stromal and tumor-infiltrating cells are under the modulation of c-MYC. These findings indicated that c-MYC serves as a critical regulator of TME. Here, we aimed to summarize and review the relevant research, thus to clarify c-MYC is a key mediator between breast cancer cells and TME.

Crosstalk

Tumor progression

Myeloid-derived Suppressor Cell

10.1186/s12964-023-01043-1

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Citations (67)

p16 promoter hypermethylation is associated with increased breast cancer risk

Molecular Medicine Reports (2012)

Li Wang Lin Tang Ruilian Xie Weiwei Nie Longbang Chen

The current study aimed to investigate the effects of p16 hypermethylation on breast cancer quantitatively through a meta-analysis of available case-control studies (including malignant, benign and normal breast cancer tissues). The PubMed, Web of Science and EBSCO databases were searched from their inceptions to February 1, 2012. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were extracted and pooled to assess the strength of the association between p16 hypermethylation and breast cancer risk. A total of eight studies, including 691 breast cancer cases and 525 control cases, were identified for meta-analysis. Statistically significant ORs of p16 hypermethylation were obtained from the breast cancer and control groups (OR, 6.58; 95% CI, 1.15‑37.75; P=0.03). However, no significant associations between the methylation and ER and PR status in breast cancer were detected (OR, 1.24; 95% CI, 0.64‑2.41; P=0.52; OR, 1.49; 95% CI, 0.81‑2.75; P=0.20, respectively). The meta-analysis indicated that p16 hypermethylation significantly increases breast cancer risk. However, no significant associations between the methylation and ER and PR status in breast cancer were detected.

10.3892/mmr.2012.1001

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Citations (17)

[Analysis of low density lipoprotein receptor function and gene mutation in familial hypercholesterolemic patients].

PubMed (2003)

Xiaoxiang Guan Mingfang Li Leming Fan Qi Chen

To investigate low density lipoprotein receptor (LDLR) function and gene mutation in Chinese patients with familial hypercholesterolemia(FH).Lymphocytes were isolated from 10 ml anticoagulated peripheral blood of the patients, then a flow-cytometric method (FCM) with 1,1'-dioctadecyl-3,3,3', 3-tetramethylindocarbocyanine perchlorate labelled low density lipoproetin (DiI-LDL) was used to identify the function of LDLR on the surface of lymphocytes. Genomic DNA was isolated from whole blood of FH patients and analyzed by PCR-single strand conformation polymorphism (SSCP) and nucleotide sequencing methods.Defects of binding and uptaking of LDLR were identified by FCM in 2 FH patients in one family, and their parents were examined in the present study. Then they were analyzed genetically. The detected mutation was a deletion of A, which caused a frame shift in codon 297 of exon 6 and introduced a beforehand stop codon in codon 369.A novel mutation of LDL receptor gene was detected by the combination of FCM and PCR-SSCP methods.

Single-strand conformation polymorphism

genomic DNA

Stop codon

Source

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Citations (2)

A universal genotyping–microarray constructed by ligating a universal fluorescence-probe with SNP-encoded flaps cleaved from multiplex invasive reactions

Chemical Communications (2017)

Zhiyao Chen Liyan Miao Yunlong Liu Tianhui Dong Xueping Ma

The universal chip and fluorescence probe enable genotyping multiple SNPs more labor-saving and cost-saving.

Multiplex

SNP genotyping

SNP

Molecular Inversion Probe

10.1039/c7cc06649j

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Citations (6)

TAp73 and ΔNp73 Have Opposing Roles in 5-aza-2′-Deoxycytidine-Induced Apoptosis in Breast Cancer Cells

Molecules and Cells (2014)

Jing Lai Fang Yang Wenwen Zhang Yanru Wang Jing Xu

The p73 gene contains an extrinsic P1 promoter and an intrinsic P2 promoter, controlling the transcription of the pro-apoptotic TAp73 isoform and the anti-apoptotic ΔΝp73 isoform, respectively.The DNA methylation status of both promoters act equally in the epigenetic transcriptional regulation of their relevant isoforms.The aim of this study was to analyze the different effects of these p73 isoforms in 5aza-2'-deoxycytidine (5-aza-dC)-induced apoptosis in breast cancer cells.We investigated the effects of the DNA demethylation agent, 5-aza-dC, on the T-47D breast cancer cell line, and evaluated the methylation status of the p73 promoters and expression of TAp73 and ΔNp73.Furthermore, we assessed the expression of p53 and p73 isoforms in 5-aza-dC-treated T-47D cells and p53 knockout cells.5-aza-dC induced significant anti-tumor effects in T-47D cells, including inhibition of cell viability, G1 phase arrest and apoptosis.This was associated with p73 promoter demethylation and a concomitant increase in TAp73 mRNA and protein expression.In contrast, the methylation status of promoter P2 was not associated with ΔNp73 mRNA or protein levels.Furthermore, demethylation of P2 failed to inhibit the expression of ΔNp73 with 5-aza-dC in the p53 knockdown cell model.Our study suggests that demethylation of the P1 and P2 promoters has opposite effects on the expression of p73 isoforms, namely up-regulation of TAp73 and downregulation of ΔΝp73.We also demonstrate that p53 likely contributes to 5-aza-dC-induced ΔNp73 transcriptional inactivation in breast cancer cells.

DNA demethylation

Demethylation

10.14348/molcells.2014.0154

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Citations (11)

Incorporating Single-nucleotide Polymorphisms Into the Lyman Model to Improve Prediction of Radiation Pneumonitis

International Journal of Radiation Oncology*Biology*Physics (2012)

Susan L. Tucker Minghuan Li Ting Xu Daniel R. Gomez Xianglin Yuan

XRCC3

XRCC1

10.1016/j.ijrobp.2012.02.021

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