Long-Term Remission of a Spinal Atypical Teratoid Rhabdoid Tumor in Response to Intensive Multimodal Therapy by Fahd Refai, Haneen Al-Maghrabi, Hassan Al Trabolsi, Jaudah Al-Maghrabi

“…Provided clinical and diagnostic suspicion is high, the histopathological diagnosis is relatively straightforward to secure by testing for the characteristic loss of the tumor suppressor protein SMARCB1/INI1. Here, we describe a case of thoracic spinal ATRT in a three-year-old boy that showed characteristic aggressive progression until managed with intensive multimodal therapy to achieve durable long-term remission. …”
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Tumor Suppressor Function of CYLD in Nonmelanoma Skin Cancer by K. C. Masoumi, Gina Shaw-Hallgren, Ramin Massoumi

“…In basal cell carcinoma, the tumor suppressor protein CYLD is repressed at the transcriptional levels through hedgehog signaling pathway. …”
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Dual EMCV-IRES-integrated dengue virus can express an exogenous gene and cellular Mdm2 integration suppresses the dengue viral replication by Tadahisa Teramoto

“…It was also revealed that a cellular gene, Mdm2, which antagonizes tumor suppressor protein p53 (TP53), could terminate the viral replication in BHK21 cells. …”
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Placental Maspin Gene Expression Pattern May Be Used to Distinguish Between Preeclampsia and Intrauterine Growth Restriction by Gogsen Onalan, Yunus Kasim Terzi, Yusuf Aytac Tohma, Erkan Yurtcu, Esra Kuscu, Feride Iffet Sahin, Hulusi Bulent Zeyneloglu

“… Objective: Maspin is one of the members of serin protease inhibitor superfamily, and acts as a tumor suppressor protein. Here we report maspin expression in placental tissues of preeclampsia or intrauterine growth retardation pregnancies. …”
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Elucidating Molecular Interactions of Natural Inhibitors with HPV-16 E6 Oncoprotein through Docking Analysis by Satish Kumar, Lingaraja Jena, Sneha Galande, Sangeeta Daf, Kanchan Mohod, Ashok K. Varma

“…In the present study, we explored these natural inhibitors against E6 oncoprotein of high-risk HPV-16, which is known to inactivate the p53 tumor suppressor protein. A robust homology model of HPV-16 E6 was built to anticipate the interaction mechanism of E6 oncoprotein with natural inhibitory molecules using a structure-based drug designing approach. …”
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Loss of p53 Expression in Gastric Epithelial Cells of Helicobacter pylori-Infected Jordanian Patients by Mohammad A. Abu-Lubad, Ghada F. Helaly, Weliam J. Haddadin, Dua’a A. K. Jarajreh, Amin A. Aqel, Munir A. Al-Zeer

“…H. pylori induces the production of reactive oxygen species, DNA damage, and accelerates the degradation of the tumor suppressor protein p53, which may lead to cancer development. …”
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Differences in phenotypes of normal and malignant cells concerning chromosomal fragility and ganglioside expression by Iskra Sainova, Vera Kolyovska, Desislava Drenska, Dimitar Maslarov, Dimitrina Dimitrova-Dikanarova, Tzvetanka Markova

“…Of particular interest were interactions involving gangliosides, the reduced form of tri-peptide glutathione (GSH) and/or of tumor-suppressor protein HACE1. The average titers of gangliosides and of anti-ganglioside antibodies in extracts from experimental in vitro models of laboratory-incubated cultures of mouse embryonic 3T3 fibroblasts, of mouse malignant myeloma cells, as well as of mixed cultures of both cellular types, were determined after previous passing of each one through GSH-agarose columns about the “selection” of the molecules in each one of the described samples, possessing affinity to GSH. …”
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E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescence. by Alicia Avenhaus, Milica Velimirović, Julia Bulkescher, Martin Scheffner, Felix Hoppe-Seyler, Karin Hoppe-Seyler

“…The formation of a trimeric complex between the HPV E6 oncoprotein, the cellular ubiquitin ligase E6AP and the p53 tumor suppressor protein leads to proteolytic p53 degradation and plays a central role for HPV-induced cell transformation. …”
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Fragile Histidine Triad (FHIT) Suppresses Proliferation and Promotes Apoptosis in Cholangiocarcinoma Cells by Blocking PI3K-Akt Pathway by Qiang Huang, Zhen Liu, Fang Xie, Chenhai Liu, Feng Shao, Cheng-lin Zhu, Sanyuan Hu

“…Fragile histidine triad (FHIT) is a tumor suppressor protein that regulates cancer cell proliferation and apoptosis. …”
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HPV16E6-Dependent c-Fos Expression Contributes to AP-1 Complex Formation in SiHa Cells by Feixin Liang, Shinichiro Kina, Hiroyuki Takemoto, Akira Matayoshi, Thongsavanh Phonaphonh, Nao Sunagawa, Keiichi Arakaki, Akira Arasaki, Hai Kuang, Hajime Sunakawa

“…To date, the major role of HPV16E6 in cancer has been considered to be its ability to inhibit the p53 tumor-suppressor protein, thereby thwarting p53-mediated cytotoxic responses to cellular stress signals. …”
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APC orchestrates microtubule dynamics by acting as a positive regulator of KIF2A and a negative regulator of CLASPs by Yong Wang, Xinping Liu, Zheng Liu, Shasha Hua, Kai Jiang

“…Tumor suppressor protein Adenomatous polyposis coli protein (APC) is an EB-binding and microtubule (MT) plus end-tracking protein; however, how exactly APC regulates MT dynamics remains elusive. …”
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Discovery of a sushi domain-containing protein 2-positive phenotype in circulating tumor cells of metastatic breast cancer patients by Kai Bartkowiak, Parinaz Mossahebi Mohammadi, Paula Nissen, Stefan Werner, David Agorku, Antje Andreas, Maria Geffken, Sven Peine, Karl Verpoort, Thomas M. Deutsch, Laura L. Michel, Andreas Schneeweiss, Verena Thewes, Andreas Trumpp, Olaf Hardt, Volkmar Müller, Sabine Riethdorf, Hartmut Schlüter, Klaus Pantel

“…This resulted in upregulation of ER-alpha, the tumor progression protein GRP78 (78-kDa glucose-regulated protein) and downregulation of the tumor suppressor protein PDCD4 (programmed cell death protein 4). …”
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Identification of novel pQTL‐SNPs associated with lung adenocarcinoma risk: A multi‐stage study by Yutong Wu, Huiwen Xu, Liping Mao, Rongrong Zhao, Junfeng Chu, Lili Huang, Wendi Zhang, Yiran Liu, Qiong Chen, Xiaobo Tao, Siqi Li, Shenxuan Zhou, Anhui Ning, Zhenyu Li, Tian Tian, Lei Zhang, Jiahua Cui, Guangyu Tian, Minjie Chu

“…Meanwhile, the expression of their corresponding target proteins were all decreased in both plasma and tumor tissues of LUAD cases, which may play a role of tumor suppressor proteins. After mutation of 3 pQTL‐SNPs (rs7683000, rs73224660, and rs2776937), the expression of corresponding target proteins BST1 and NRP1 decreased, and as potential tumor suppressor proteins, which may promote tumorigenesis and further increasing the risk of developing LUAD (OR >1, p < 0.05); while after mutation the other pQTL‐SNP rs62069916, the corresponding target protein APOH expression was increased, while as a potential tumor suppressor protein, which may inhibit tumorigenesis and further reduced the risk of developing LUAD (OR <1, p < 0.05). …”
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Post-Translational Modifications of Proteins Orchestrate All Hallmarks of Cancer by Pathea Shawnae Bruno, Aneeta Arshad, Maria-Raluca Gogu, Natalie Waterman, Rylie Flack, Kimberly Dunn, Costel C. Darie, Anca-Narcisa Neagu

“…On the other hand, PTMs of proteins can enhance anticancer mechanisms in the tumoral ecosystem or sustain the beneficial effects of oncologic therapies through degradation or inactivation of carcinogenic proteins or/and activation of tumor-suppressor proteins. In this review, we summarized and analyzed a wide spectrum of PTMs of proteins involved in all regulatory mechanisms that drive tumorigenesis, genetic instability, epigenetic reprogramming, all events of the metastatic cascade, cytoskeleton and extracellular matrix (ECM) remodeling, angiogenesis, immune response, tumor-associated microbiome, and metabolism rewiring as the most important hallmarks of cancer. …”
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The Function of SUMOylation and Its Role in the Development of Cancer Cells under Stress Conditions: A Systematic Review by Qi Zhao, Ying Ma, Zugui Li, Kexin Zhang, Minying Zheng, Shiwu Zhang

“…This review focused on SUMOylation in tumor cells to discuss its effects on tumor suppressor proteins and oncoproteins as well as classical tumor pathways to identify new insights for cancer clinical therapy.…”
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High Glucose with Insulin Induces Cell Cycle Progression and Activation of Oncogenic Signaling of Bladder Epithelial Cells Cotreated with Metformin and Pioglitazone by Daejin Kim, Byul-Nim Ahn, YeongSeok Kim, Dae Young Hur, Jae Wook Yang, Ga Bin Park, Jung Eun Jang, Eun Ju Lee, Min Jeong Kwon, Tae Nyun Kim, Mi Kyung Kim, Jeong Hyun Park, Byoung Doo Rhee, Soon Hee Lee

“…Prolonged exposure to high glucose and insulin enhanced cyclin D, cyclin-dependent kinase 4 (Cdk4), and Cdk2 expression and suppressed cyclin-dependent kinase inhibitors p21 and p15/16 in HBlEpC cotreated with pioglitazone and metformin. Levels of tumor suppressor proteins p53 and cav-1 were downregulated while those of the oncogenic protein as c-Myc were upregulated under high glucose and insulin supplementation in HBlEpC cotreated with pioglitazone and metformin. …”
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