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6 results on '"De-Dong Cao"'

1. Case report: Innovative treatment for one metastatic thyroid-like follicular carcinoma of the kidney with ATM and POLE mutations

Author

Jin-Ju Lei, Jie Rao, Hong-Yan Feng, De-Dong Cao, Hong-Lin Yan, Jing-Ping Yuan, Zhen-Min Jiang, and Yi-Qiao Zhang

Subjects
metastatic thyroid-like follicular carcinoma of the kidney, ATM and POLE mutations, programmed death 1 receptor inhibitor, pazopanib, radiotherapy, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Thyroid-like follicular renal cell carcinoma (TLFRCC), also known as thyroid-like follicular carcinoma of the kidney or thyroid follicular carcinoma like renal tumor, is an exceedingly rare variant of renal cell carcinoma that has only recently been acknowledged. This neoplasm exhibits a distinct follicular morphology resembling that of the thyroid gland. Immunohistochemical analysis reveals positive expression of PAX8, Vimentin, and EMA, while thyroid-specific markers TG and TTF1 are consistently absent. Furthermore, there is a notable absence of any concurrent thyroid pathology on clinical evaluation. Previous reports have suggested that TLFRCC is an indolent, slow-growing malignancy with infrequent metastatic potential. In this report, we present a case of TLFRCC characterized by remarkable ossification and widespread metastasis, including multifocal pulmonary lesions, involvement of the abdominal wall, and infiltration into the psoas muscle. To our knowledge, this represents only the third documented instance of distant metastasis in thyroid follicular renal carcinoma. The current case demonstrates a therapeutic approach that combines radiotherapy with the utilization of toripalimab, a programmed cell death 1 (PD-1) receptor inhibitor, and pazopanib. This treatment regimen was tailored based on comprehensive genomic profiling, which identified mutations in the POLE (catalytic subunit of DNA polymerase epsilon) and ATM (ataxia-telangiectasia mutated) genes, both of which have been implicated in the pathogenesis of various malignant tumors. These findings represent a novel discovery, as such mutations have never been reported in association with TLFRCC. Thus far, this therapeutic approach has proven to be the most efficacious option for treating metastatic TLFRCC among previously reported, and it also marks the first mention of the potential benefits of radiotherapy in managing this particular subtype of renal cell carcinoma.

Published
2024
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3. Autophagic cell death induced by reactive oxygen species is involved in hyperthermic sensitization to ionizing radiation in human hepatocellular carcinoma cells

Author

Ximing Xu, Jun-Jian Deng, Lei Shi, Guangjin Yuan, Xin Chen, De-Dong Cao, and Jinju Lei

Subjects
0301 basic medicine, Hyperthermia, Ionizing radiation, Programmed cell death, Carcinoma, Hepatocellular, Hepatocellular carcinoma, Cell Survival, Apoptosis, 03 medical and health sciences, 0302 clinical medicine, Radiation, Ionizing, medicine, Autophagy, Humans, Sensitization, chemistry.chemical_classification, Reactive oxygen species, Chemistry, Liver Neoplasms, Gastroenterology, RNA-Binding Proteins, General Medicine, Hep G2 Cells, Hyperthermia, Induced, Basic Study, medicine.disease, Cell biology, Acetylcysteine, 030104 developmental biology, medicine.anatomical_structure, Autophagic cell death, 030220 oncology & carcinogenesis, Reactive Oxygen Species, Microtubule-Associated Proteins
Abstract

AIM To investigate whether autophagic cell death is involved in hyperthermic sensitization to ionizing radiation in human hepatocellular carcinoma cells, and to explore the underlying mechanism. METHODS Human hepatocellular carcinoma cells were treated with hyperthermia and ionizing radiation. MTT and clonogenic assays were performed to determine cell survival. Cell autophagy was detected using acridine orange staining and flow cytometric analysis, and the expression of autophagy-associated proteins, LC3 and p62, was determined by Western blot analysis. Intracellular reactive oxygen species (ROS) were quantified using the fluorescent probe DCFH-DA. RESULTS Treatment with hyperthermia and ionizing radiation significantly decreased cell viability and surviving fraction as compared with hyperthermia or ionizing radiation alone. Cell autophagy was significantly increased after ionizing radiation combined with hyperthermia treatment, as evidenced by increased formation of acidic vesicular organelles, increased expression of LC3II and decreased expression of p62. Intracellular ROS were also increased after combined treatment with hyperthermia and ionizing radiation. Pretreatment with N-acetylcysteine, an ROS scavenger, markedly inhibited the cytotoxicity and cell autophagy induced by hyperthermia and ionizing radiation. CONCLUSION Autophagic cell death is involved in hyperthermic sensitization of cancer cells to ionizing radiation, and its induction may be due to the increased intracellular ROS.

Published
2017

4. Endostar enhances the antitumor effects of radiation by affecting energy metabolism and alleviating the tumor microenvironment in a Lewis lung carcinoma mouse model

Author

Liang Liu, Yong‑Fa Zheng, De‑Dong Cao, Hui‑Lin Xu, Ze‑Zhang Tao, Chang‑Hu Li, Wei Ge, Ping‑Po Ming, Xi‑Ming Xu, and Wei‑Ping Tao

Subjects
Cancer Research, Tumor microenvironment, Pathology, medicine.medical_specialty, Oncogene, Cancer, Lewis lung carcinoma, Articles, Cell cycle, Biology, medicine.disease, Molecular medicine, chemistry.chemical_compound, Oncology, chemistry, Lactate dehydrogenase, Cancer research, medicine, Lung cancer
Abstract

Lung cancer is a leading cause of morbidity and mortality. Previous studies have identified that an improvement in treatment efficacy was achieved using Endostar; however, the role of Endostar in lung cancer remains poorly understood. The present study investigated whether the enhanced antitumor effects of Endostar in combination with radiation involved changes in the metabolism and microenvironment in non-small cell lung cancer. A Lewis lung carcinoma mouse model was used, including the control, Endostar (ES), radiotherapy (RT) and Endostar plus radiotherapy (ES + RT) groups. The tumor inhibition rates and growth were described based on changes in tumor volume. In addition, ultraviolet enzymatic analysis was performed to determine the lactate level and reverse transcription-polymerase chain reaction was used to measure the mRNA expression of lactate dehydrogenase (LDH). A Meph-3 pH meter was used to detect the ranges of tumor interstitial tissue pH, and immunohistochemical analysis was adopted to examine hypoxia within the tumor microenvironment. The tumor inhibition rate of the ES + RT group was significantly higher compared with the other three groups (P

Published
2015

5. Endostar combined with chemotherapy versus chemotherapy alone for advanced NSCLCs: a meta-analysis

Author

Wei, Ge, De-dong, Cao, Hui-min, Wang, Fang-fang, Jie, Yong-fa, Zheng, and Yu, Chen

Subjects
Lung Neoplasms, Vomiting, Nausea, Leukopenia, Combined Modality Therapy, Thrombocytopenia, Recombinant Proteins, Endostatins, Treatment Outcome, Carcinoma, Non-Small-Cell Lung, Antineoplastic Combined Chemotherapy Protocols, Humans, Drug Therapy, Combination, Platinum, Randomized Controlled Trials as Topic
Abstract

Use of recombinant human endostatin combined with conventional cytotoxic therapy to treat tumors has been growing because of evidence of increased efficacy. However, whether antiangiogenic therapy combined with chemotherapy really benefits patients with advanced non-small cell lung cancers (NSCLCs) remains unclear.This study was conducted to evaluate the clinical efficacy and safety of rh-endostatin (Endostar) combined with chemotherapy in the treatment of NSCLC patients.We selected data from the Cochrane Library, EMBASE, Medline, SCI,CBM, CNKI, to obtain all clinical controlled trials, including the addition of endostar to chemotherapy in advanced NSCLC patients. Fifteen trials with 1335 patients were included according to the inclusion criteria. All were randomized controlled trials, and two trials were adequate in reporting randomization. Seventeen trials did not mention the blinding methods.Meta-analysis indicated that the NPE arm (Vinorelbine+cisplatin+Endostar) had a different response rate compared with NP(Vinorelbine+cisplatin) arm (OR2.16, 95%CI 1.57 to 2.99). The incidences of severe leukopenia (OR0.94, 95%CI 0.66 to 1.32) and severe thrombocytopenia (OR 1.00, 95%CI 0.64 to 1.57) and nausea and vomiting (OR 0.85, 95%CI 0.61 to 1.20) were similar in the two arms. The NPE plus radiotherapy (RT) arm had a similar response rate compared with NP plus RT arm (OR 2.39, 95%CI 0.99 to 5.79), as were the incidences of leukopenia (OR0.83, 95%CI 0.35 to 1.94), thrombocytopenia (OR 0.78, 95%CI 0.19 to 3.16) and radiation esophagitis (OR 1.00, 95%CI 0.40 to 2.49).Our results suggested that in the treatment of advanced NSCLC, endostar in combination with platinum-based chemotherapy could improve the response rate without obviously increasing side effects.

Published
2012

6. Endostar enhances the antitumor effects of radiation by affecting energy metabolism and alleviating the tumor microenvironment in a Lewis lung carcinoma mouse model.

Author

YONG-FA ZHENG, WEI GE, HUI-LIN XU, DE-DONG CAO, LIANG LIU, PING-PO MING, CHANG-HU LI, XI-MING XU, WEI-PING TAO, and ZE-ZHANG TAO

Subjects
LUNG cancer patients, LUNG cancer treatment, MEDICAL technology, METABOLIC regulation, BIOCHEMISTRY
Abstract

Lung cancer is a leading cause of morbidity and mortality. Previous studies have identified that an improvement in treatment efficacy was achieved using Endostar; however, the role of Endostar in lung cancer remains poorly understood. The present study investigated whether the enhanced antitumor effects of Endostar in combination with radiation involved changes in the metabolism and microenvironment in non-small cell lung cancer. A Lewis lung carcinoma mouse model was used, including the control, Endostar (ES), radiotherapy (RT) and Endostar plus radiotherapy (ES + RT) groups. The tumor inhibition rates and growth were described based on changes in tumor volume. In addition, ultraviolet enzymatic analysis was performed to determine the lactate level and reverse transcription-polymerase chain reaction was used to measure the mRNA expression of lactate dehydrogenase (LDH). A Meph-3 pH meter was used to detect the ranges of tumor interstitial tissue pH, and immunohistochemical analysis was adopted to examine hypoxia within the tumor microenvironment. The tumor inhibition rate of the ES + RT group was significantly higher compared with the other three groups (P<0.05). Following treatment, the lactate levels decreased in all three treatment groups compared with the control, particularly in the ES + RT group (P<0.05). Reduced LDH expression and hypoxic fraction in the tumor microenvironment were also observed in the ES + RT group (P<0.05). Furthermore, changes from acidic to alkaline pH in the tumor microenvironment were detected in the ES + RT group. The present study suggested that Endostar is involved in the regulation of metabolism and tumor microenvironment hypoxia, which may be responsible for the enhanced antitumor effect of Endostar in combination with radiotherapy. [ABSTRACT FROM AUTHOR]

Published
2015
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