Journal of cancer biology最新文献

{"title":"Navigating alopecia: Practical guidelines for minimizing hair loss in CyberKnife stereotactic radiosurgery for calvarial or scalp tumors","authors":"David J. Park, Steven D. Chang","doi":"10.46439/cancerbiology.5.060","DOIUrl":"https://doi.org/10.46439/cancerbiology.5.060","url":null,"abstract":"","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141270129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological basis for concurrent chemoradiation in head and neck cancer: Timing matters","authors":"Allen M. Chen","doi":"10.46439/cancerbiology.5.059","DOIUrl":"https://doi.org/10.46439/cancerbiology.5.059","url":null,"abstract":"Given that the addition of cytotoxic chemotherapy to radiation has been shown to improve overall survival and local-regional control for select patients with head and neck cancer, concurrent chemoradiation constitutes a mainstay of treatment. In pre-clinical studies, platinum-based chemotherapy, when delivered concurrently with radiation, is intended to serve as a radio-sensitizer, potentiating the cytotoxic effects of radiation on proliferating squamous cell carcinoma cells. From a biological basis, it is thus advisable that patients begin chemotherapy and radiation as synchronously as possible to optimize the benefits of dual treatment. While most guidelines for concurrent chemoradiation recommend initiating concurrent chemotherapy on day 1 of radiation (with the administration of chemotherapy preceding radiation), the actual clinical practice may vary in the timing and sequencing of these treatments. This is largely because coordination can be challenging from a logisitical and social standpoint, leading to deviations from the standard. Indeed, we recently showed that variations in the timing of how concurrent chemoradiation is delivered are signficiant and may have clinical implications.","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141271187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selectively depleting the energy of cancer cells: A new therapeutic paradigm","authors":"H. Warenius","doi":"10.46439/cancerbiology.5.057","DOIUrl":"https://doi.org/10.46439/cancerbiology.5.057","url":null,"abstract":"Over the past fifty years the somatic mutation theory of cancer has emerged as the most successful explanation of the molecular phenotype of human cancer cells. Normal non-mutated genes may, however, also play a role in carcinogenesis. In particular these may contribute to aerobic glycolysis and the potential interaction of PKM2 and Cdk4 in helping the nascent cancer cell avoid apoptosis by the interaction of their respective amino acid sequences: anionic SDPTEA and cationic PRGPRP. It is proposed that cancer first occurs in normal tissues cells which, as part of the premalignant phenotype have switched from PKM1 to PKM2 expression, and this phenotype persists as cancers age and further molecular biological mechanisms to avoid apoptosis and encourage aerobic glycolysis emerge. PRGPRP and several congeners have been shown to kill a wide range of in vitro cancers by necrosis by producing a fall in ATP without harming normal diploid cells. The ATP depletion is suggested to result from inhibition of aerobic glycolysis and has resulted in the first therapeutic agent that globally selectively kills cancer cells by depriving them of energy.","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140487806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of CBL-b, c-CBL expressions in colorectal cancer patients and their relationship with clinicopathological characteristics","authors":"Reyhaneh Yarmohammadi, Minoo Pargol, Zahra Mozooni, Leyla Bahadorizadeh, Sara Minaeian, Shadi Tajvidi","doi":"10.46439/cancerbiology.4.054","DOIUrl":"https://doi.org/10.46439/cancerbiology.4.054","url":null,"abstract":"Introduction: Colorectal cancer (CRC) is the most common gastrointestinal cancer and a major cause of cancer-related mortality worldwide. Molecular indicators of pathogenic factors that regulate CRC, which are known as oncogenes, are desirable for response to treatment and improvement of CRC patient management. Several risk factors play a role in the development of this disease, which can occur genetically, familial, or sporadically. CRC tumorigenesis is stimulated by the proto-oncogene β-catenin (wnt/β-catenin). Casitas B-lineage lymphoma (c-Cbl) inhibits CRC tumor growth through an unknown mechanism that affects nuclear β-catenin. The current objective of this study is to evaluate the expression levels of Cbl-b and c-Cbl genes to determine if their transcripts can be used as suitable diagnostic indicators. Additionally, we aim to investigate the correlation between clinicopathological information of CRC patients and the levels of Cbl-b and c-Cbl. Materials and Methods: Quantitative Real-Time PCR (qRT-PCR) method was used to evaluate the expression levels of Cbl-b and c-Cbl in 45 colorectal tumor tissues and 45 adjacent control tissues. Furthermore, we analyzed the diagnostic power of Cbl-b and c-Cbl by plotting receiver operating characteristic (ROC) curves. Results: Our results showed that the expression levels of Cbl-b and c-Cbl were significantly increased in CRC patients compared to the adjacent control group (P<0.003, P<0.004). Analysis of clinicopathological features of CRC patients revealed that the expression of Cbl-b and c-Cbl was associated differently with TMN stage, LVI+ (P<0.0003, P<0.0001) (P<0.003, P<0.07). Conclusion: These results indicate that the levels of Cbl-b and c-Cbl may serve as potential diagnostic indicators for CRC.","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139289857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor evolution: The road map to future cancer therapeutics","authors":"Kambiz Afrasiabi","doi":"10.46439/cancerbiology.4.052","DOIUrl":"https://doi.org/10.46439/cancerbiology.4.052","url":null,"abstract":"","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135695818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteomic research and protein biochemistry for targeted therapy of anti-cancer drugs","authors":"Hui-Heng Lin","doi":"10.46439/cancerbiology.4.051","DOIUrl":"https://doi.org/10.46439/cancerbiology.4.051","url":null,"abstract":"","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135695542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor microenvironment: The crossroad of normal state and cancer","authors":"Kambiz Afrasiabi","doi":"10.46439/cancerbiology.4.053","DOIUrl":"https://doi.org/10.46439/cancerbiology.4.053","url":null,"abstract":"","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135695819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cyclin A2 and Ki-67 proliferation markers could be used to identify tumors with poor prognosis in African American women with breast cancer.","authors":"Desta Beyene,&nbsp;Tammey Naab,&nbsp;Victor Apprey,&nbsp;Luisel Ricks-Santi,&nbsp;Ashwini Esnakula,&nbsp;Mustafa Qasim,&nbsp;Mathew George,&nbsp;Karen G Minoza,&nbsp;Robert L Copeland,&nbsp;Carolyn Broome,&nbsp;Yasmine Kanaan","doi":"10.46439/cancerbiology.4.048","DOIUrl":"https://doi.org/10.46439/cancerbiology.4.048","url":null,"abstract":"<p><strong>Background: </strong>Diagnosed invasive breast carcinomas in African American patients are more aggressive compared with those in Caucasian patients and diagnosed at later stages of the disease with higher grade tumors. Despite advances in breast cancer systemic treatment, new prognostic and predictive biomarkers are still needed. Therefore, potential biomarkers were chosen to correlate with different subtypes, recurrence, and survival of invasive breast cancer in a cohort of African American women.</p><p><strong>Methods: </strong>Eight protein biomarkers (ER, PR, HER2, Cyclin A2, Cytokeratin 5, Vimentin, Bcl2, and Ki-67) were evaluated using tissue microarrays (TMAs) and immunohistochemistry (IHC). The IHC results from TMAs were analyzed by both supervised and unsupervised clustering methods. The predictive clusters for the supervised and unsupervised methods were compared for agreement with the empirical classification. Kappa values were used to determine the overall percent correct clusters and agreement between specific clusters. Chi-square statistics was used to examine the association between hierarchical and multinomial logistic clustering methods.</p><p><strong>Results: </strong>Five subtypes of breast tumors with distinct protein expression patterns were identified among the studied 166 breast tumors. Luminal B tumors have been distinguished from luminal A tumors by staining for cell cycle proteins Cyclin A2 and Ki-67, which promote cell proliferation. Forty-nine percent were stained positive for Cyclin A2, 39.2% positive for Ki-67, and 37% positive for both Cyclin A2 and Ki-67. The age of patients did not show any significant effect whether five (p-value= 0.576) or eight (p-value= 0.605) biomarkers were used, which indicating that age did not have any influence on the classification of the subtypes. Ninety percent of the thirty triple negative tumors were positive for Cyclin A2 or Ki-67 or both. Six-year overall survival was better for luminal A tumors (76%) than luminal B tumors (71%). Likewise, six-year relapse-free survival was better for luminal A tumors (76%) than luminal B tumors (29%).</p><p><strong>Conclusion: </strong>Discovery of molecular markers such as Cyclin A2 and Ki-67, and subtypes that are most prevalent in African Americans could lead to a better understanding of the factors contributing to higher morbidity and mortality in this group and to aid in decision-making to offer earlier treatment.</p>","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10238075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9583544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Challenges in the humanized mouse model for cancer: A commentary.","authors":"Eric Ramirez-Salazar,&nbsp;Meenhard Herlyn,&nbsp;Rajasekharan Somasundaram","doi":"10.46439/cancerbiology.2.022","DOIUrl":"https://doi.org/10.46439/cancerbiology.2.022","url":null,"abstract":"<p><p>The complexity of the tumor microenvironment has been a challenge for understanding the mechanisms of therapy resistance. The development of improved animal models that closely mimic human disease is key for understanding and treating diseases. Recently, a new humanized mouse model has been developed that enables the study of human immune cells in tumor host-cell interactions. In this commentary we highlight the critical aspects of mast cells in immune therapy resistance. These mast cells release cytokines that downmodulate HLA class I on the malignant cells making them inaccessible the cytotoxic activity of T cells.</p>","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9583711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40680588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PAK1 and PAK4 as therapeutic targets for Ewing sarcoma: a commentary.","authors":"Sydney E Parks,&nbsp;Jason T Yustein","doi":"10.46439/cancerbiology.2.032","DOIUrl":"https://doi.org/10.46439/cancerbiology.2.032","url":null,"abstract":"<p><p>Ewing sarcoma (ES) is an aggressive pediatric bone tumor that is prone to metastasis. Due to low five-year survival rates and limited therapeutic options for metastatic disease, there is a dire clinical need for improved ES treatments. Targeting p21-activated kinases (PAKs) may be key. PAK1 and PAK4 are associated with aggressive ES and poor patient outcomes, although their molecular mechanisms remain largely uncharacterized in this disease. This commentary aims to highlight the recent advancements made to the understanding of PAK1 and PAK4 in ES in the paper \"p21-activated kinases as viable therapeutic targets for the treatment of high-risk Ewing sarcoma\" by Qasim et al.</p>","PeriodicalId":73632,"journal":{"name":"Journal of cancer biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9802585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10467948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}