The need for the development of new cancer therapies and push for the design of new targeting techniques is on the rise, and would be useful for cancers that are resistant to current drug treatments. The understanding of the genome has significantly advanced cancer therapy, as well as prevention and earlier detection. This research highlight discusses a potential new type of cancer-targeting molecule, Sweet-P, which is the first of its kind. Sweet-P specifically targets the microRNA-144 binding site in the 3′ untranslated region (3′ UTR) of the human glucocorticoid receptor β (GRβ), which has been demonstrated to increase expression. GRβ has been shown to be highly expressed in cells from solid tumors of uroepithelial carcinomas, gliomas, osteosarcomas, and hepatocellular carcinomas, as well as in liquid tumor cells from leukemia patients. In non-cancerous diseases, GRβ has been shown to be highly expressed in glucocorticoid-resistant asthma. These maladies brought the need for the development of the Sweet-P anti-GRβ molecule. Sweet-P was shown to repress the migration of bladder cancer cells, and may serve as a new therapeutic for GRβ-related diseases.
{"title":"Sweet-P inhibition of glucocorticoid receptor β as a potential cancer therapy","authors":"Assumpta C. Nwaneri, L. McBeth, T. Hinds","doi":"10.14800/CCM.1362","DOIUrl":"https://doi.org/10.14800/CCM.1362","url":null,"abstract":"The need for the development of new cancer therapies and push for the design of new targeting techniques is on the rise, and would be useful for cancers that are resistant to current drug treatments. The understanding of the genome has significantly advanced cancer therapy, as well as prevention and earlier detection. This research highlight discusses a potential new type of cancer-targeting molecule, Sweet-P, which is the first of its kind. Sweet-P specifically targets the microRNA-144 binding site in the 3′ untranslated region (3′ UTR) of the human glucocorticoid receptor β (GRβ), which has been demonstrated to increase expression. GRβ has been shown to be highly expressed in cells from solid tumors of uroepithelial carcinomas, gliomas, osteosarcomas, and hepatocellular carcinomas, as well as in liquid tumor cells from leukemia patients. In non-cancerous diseases, GRβ has been shown to be highly expressed in glucocorticoid-resistant asthma. These maladies brought the need for the development of the Sweet-P anti-GRβ molecule. Sweet-P was shown to repress the migration of bladder cancer cells, and may serve as a new therapeutic for GRβ-related diseases.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79170520","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}
Oxidative intermediates derived from endogenous metabolism or xenobiotic stimuli are a major cause of cancer initiation. Host defense systems have evolved to cope with these oxidative stresses and prevent carcinogenesis. The basic leucine zipper transcription factor Nrf2 (Nuclear factor-erythroid derived 2-like 2, Nfe2l2) regulates the cellular defense system against oxidative stress, and governs cellular protection against chemical carcinogens. At the same time, Nrf2 enhances anti-cancer immunity in the tumor microenvironment, thereby suppressing growth and metastasis of cancer cells. These beneficial aspects of Nrf2 activities contribute to the prevention of cancer initiation, as well as its subsequent progression. On the other hand, aberrant Nrf2 activation confers malignant properties on cancer cells by enhancing proliferative ability and drug resistance. Thus, Nrf2 contributes to the prevention of carcinogenesis as well as the malignant growth of cancer cells. Increasing numbers of studies have been focusing on elucidating how these contradictory activities of Nrf2 are elicited during the multistep carcinogenic process. In this research highlight, we discuss our current understandings of Nrf2 function in cancer initiation, promotion and metastasis in a murine lung cancer model, and related topics are summarized.
{"title":"Versatile activity of the master regulator of the antioxidant response in tumor initiation, progression and metastasis","authors":"Takashi Moriguchi","doi":"10.14800/CCM.1355","DOIUrl":"https://doi.org/10.14800/CCM.1355","url":null,"abstract":"Oxidative intermediates derived from endogenous metabolism or xenobiotic stimuli are a major cause of cancer initiation. Host defense systems have evolved to cope with these oxidative stresses and prevent carcinogenesis. The basic leucine zipper transcription factor Nrf2 (Nuclear factor-erythroid derived 2-like 2, Nfe2l2) regulates the cellular defense system against oxidative stress, and governs cellular protection against chemical carcinogens. At the same time, Nrf2 enhances anti-cancer immunity in the tumor microenvironment, thereby suppressing growth and metastasis of cancer cells. These beneficial aspects of Nrf2 activities contribute to the prevention of cancer initiation, as well as its subsequent progression. On the other hand, aberrant Nrf2 activation confers malignant properties on cancer cells by enhancing proliferative ability and drug resistance. Thus, Nrf2 contributes to the prevention of carcinogenesis as well as the malignant growth of cancer cells. Increasing numbers of studies have been focusing on elucidating how these contradictory activities of Nrf2 are elicited during the multistep carcinogenic process. In this research highlight, we discuss our current understandings of Nrf2 function in cancer initiation, promotion and metastasis in a murine lung cancer model, and related topics are summarized.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75144960","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}
An important question when designing targeted therapy by modulation of stromal cells in the leukemic microenvironment is whether the stromal-derived support of tumor cell growth can be halted by drugs including originally tumor supportive agents. We recently used an in vitro system to show that either bone marrow stromal cells as a feeder layer or lipopolysaccharides (LPS) in culture medium is required for the proliferation of murine myeloid tumor cells. However, the stromal-derived support of leukemic growth is strongly suppressed when LPS is coupled in the same culture. This opposing effect of stromal cells or LPS on the myeloid leukemic growth is due, at least in part, to the rapid secretion of interleukin 12, Fas ligand and tissue inhibitor of metalloproteinases-2 from stromal cells upon LPS stimulation. These results provide a proof of principle that stromal cells can be “re-educated” by therapeutic drugs to attenuate tumor cell proliferation through re-wiring the cytokine network in the tumor microenvironment, thus diverting the disease course of myeloid leukemia in the opposite direction.
{"title":"Stromal cells and myeloid leukemic cells: Are they friends? Or foes?","authors":"Lingling Yu, Yingmin Zhao, J. F. Wang, Duonan Yu","doi":"10.14800/CCM.1348","DOIUrl":"https://doi.org/10.14800/CCM.1348","url":null,"abstract":"An important question when designing targeted therapy by modulation of stromal cells in the leukemic microenvironment is whether the stromal-derived support of tumor cell growth can be halted by drugs including originally tumor supportive agents. We recently used an in vitro system to show that either bone marrow stromal cells as a feeder layer or lipopolysaccharides (LPS) in culture medium is required for the proliferation of murine myeloid tumor cells. However, the stromal-derived support of leukemic growth is strongly suppressed when LPS is coupled in the same culture. This opposing effect of stromal cells or LPS on the myeloid leukemic growth is due, at least in part, to the rapid secretion of interleukin 12, Fas ligand and tissue inhibitor of metalloproteinases-2 from stromal cells upon LPS stimulation. These results provide a proof of principle that stromal cells can be “re-educated” by therapeutic drugs to attenuate tumor cell proliferation through re-wiring the cytokine network in the tumor microenvironment, thus diverting the disease course of myeloid leukemia in the opposite direction.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73924990","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}
Aptamers are chemically synthesized oligonucleotides that can be easily engineered for cancer immunotherapy use. So far, most of the therapeutic aptamers described are antagonistic and block the function of a receptor or its soluble ligand. Recently, aptamers have been modified to act as agonists by multimerization, with a direct application in cancer immunotherapy. Several agonistic aptamers against costimulatory receptors have been described. However, systemic costimulation, though potentially a very potent antitumor immune strategy, is not devoid of auto-inflammatory side effects. In a quest to reduce toxicity and improve efficacy - reducing the therapeutic index - the first bi-specific aptamers to target the costimulatory ligand to the tumor have been described, showing very promising results in different preclinical tumor models.
{"title":"Tumor-targeted costimulation by using bi-specific aptamers.","authors":"Fernando Pastor","doi":"10.14800/ccm.1333","DOIUrl":"https://doi.org/10.14800/ccm.1333","url":null,"abstract":"<p><p>Aptamers are chemically synthesized oligonucleotides that can be easily engineered for cancer immunotherapy use. So far, most of the therapeutic aptamers described are antagonistic and block the function of a receptor or its soluble ligand. Recently, aptamers have been modified to act as agonists by multimerization, with a direct application in cancer immunotherapy. Several agonistic aptamers against costimulatory receptors have been described. However, systemic costimulation, though potentially a very potent antitumor immune strategy, is not devoid of auto-inflammatory side effects. In a quest to reduce toxicity and improve efficacy - reducing the therapeutic index - the first bi-specific aptamers to target the costimulatory ligand to the tumor have been described, showing very promising results in different preclinical tumor models.</p>","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"3 ","pages":"e1333"},"PeriodicalIF":0.0,"publicationDate":"2016-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14800/ccm.1333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35582657","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}
Multiple myeloma (MM) is the second most commonly hematologic malignancy characterized by proliferation of monoclonal plasmas cells in bone marrow. Despite the availability of new drugs targeting the neoplastic clone and its microenvironment, MM is still an incurable disease, with patients experiencing subsequent phases of remission and relapse, eventually leading to disease resistance and patient death. In the past decades, natural products have attracted increasing attention in the field of anti-myeloma treatment by virtue of their multiple bioactivities and lower toxicity. This review focuses on the research progress and mechanisms through which these natural extracts inhibit tumor cell proliferation and normalize microenvironment in multiple myeloma. These include the induction of apoptosis, inhibition of bone injury and angiogenesis, and reversion of multidrug resistance.
{"title":"Potential therapeutic effects of natural extracts in multiple myeloma","authors":"Rong Fu, Wen-Cong Lv, Q. Guo, Zhao-Qiu Wu","doi":"10.14800/CCM.1311","DOIUrl":"https://doi.org/10.14800/CCM.1311","url":null,"abstract":"Multiple myeloma (MM) is the second most commonly hematologic malignancy characterized by proliferation of monoclonal plasmas cells in bone marrow. Despite the availability of new drugs targeting the neoplastic clone and its microenvironment, MM is still an incurable disease, with patients experiencing subsequent phases of remission and relapse, eventually leading to disease resistance and patient death. In the past decades, natural products have attracted increasing attention in the field of anti-myeloma treatment by virtue of their multiple bioactivities and lower toxicity. This review focuses on the research progress and mechanisms through which these natural extracts inhibit tumor cell proliferation and normalize microenvironment in multiple myeloma. These include the induction of apoptosis, inhibition of bone injury and angiogenesis, and reversion of multidrug resistance.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89130742","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}
Oral cancer remains one of the most common and challenging malignancies of the head and neck region. Articles were retrieved from Pubmed using specific keywords. Recent data showed that the incidence and mortality have increased over the last decades. It has poor prognosis and ranks among all cancer mortality. Tobacco smoking, alcohol, betel quid and areca nut chewing have been associated with a higher risk for oral cancers. This review summarizes the incidence, prevalence and mortality rates associated with oral cancer. We also investigated the strategies for early diagnosis, the molecular pathway of carcinogenesis, and the current treatment modalities available for oral cancer.
{"title":"Current trends in oral cancer: A systematic review","authors":"G. Corso, A. Villa, A. Tarsitano, A. Gohel","doi":"10.14800/CCM.1332","DOIUrl":"https://doi.org/10.14800/CCM.1332","url":null,"abstract":"Oral cancer remains one of the most common and challenging malignancies of the head and neck region. Articles were retrieved from Pubmed using specific keywords. Recent data showed that the incidence and mortality have increased over the last decades. It has poor prognosis and ranks among all cancer mortality. Tobacco smoking, alcohol, betel quid and areca nut chewing have been associated with a higher risk for oral cancers. This review summarizes the incidence, prevalence and mortality rates associated with oral cancer. We also investigated the strategies for early diagnosis, the molecular pathway of carcinogenesis, and the current treatment modalities available for oral cancer.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"120 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78549854","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}
Methylthioadenosine Phosphorylase is a well-known tumor suppressor and a regulator for purine and pyrimidine synthesis and metabolism. Several previous studies show MTAP could be a prognostic marker independent or coordinate with p16 in multiple cancer types. Furthermore, inhibitors of MTAP have been developed and tested in in vitro and in vivo experiment to support the selective tumor cell-killing theory of MTAP. The review aims to provide a deep understanding of the clinical role and the metabolic reprogramming regulated by MTAP in cancer as the guide to found out and solve the problems of MTAP based cancer therapy.
{"title":"Therapeutic targeting of methylthioadenosine phosphorylase","authors":"Yu-Chan Chang, Chia-Yi Su, M. Hsiao","doi":"10.14800/CCM.1322","DOIUrl":"https://doi.org/10.14800/CCM.1322","url":null,"abstract":"Methylthioadenosine Phosphorylase is a well-known tumor suppressor and a regulator for purine and pyrimidine synthesis and metabolism. Several previous studies show MTAP could be a prognostic marker independent or coordinate with p16 in multiple cancer types. Furthermore, inhibitors of MTAP have been developed and tested in in vitro and in vivo experiment to support the selective tumor cell-killing theory of MTAP. The review aims to provide a deep understanding of the clinical role and the metabolic reprogramming regulated by MTAP in cancer as the guide to found out and solve the problems of MTAP based cancer therapy.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88642311","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}
Glioblastoma (GBM)-initiating cells (GICs) are a tumorigenic subpopulation that are resistant to radio/chemotherapies and are the source of recurrence, therefore it is crucial to characterize GICs and find new therapeutic targets. We have successfully established mouse and human GICs, which retain stemness characteristics and tumorigenicity. By comparing their expression profiles with those of parental cells, we have focused on two cell surface membrane proteins, Ceacam1L and Eva1, which were prominently expressed in GICs. We demonstrated that both proteins were involved in GIC characteristics, including self-renewal, stem cell gene expression and side population, and tumorigenesis, indicating that they are potential new therapeutic targets for GBM. In this research highlight, I summarize our recent reports regarding Ceacam1L and Eva1, and then discuss about Ceacam1L and Eva1 as GBM therapeutic targets.
{"title":"Targeting the glioblastoma-initiating cell-associated antigens","authors":"T. Kondo","doi":"10.14800/CCM.1329","DOIUrl":"https://doi.org/10.14800/CCM.1329","url":null,"abstract":"Glioblastoma (GBM)-initiating cells (GICs) are a tumorigenic subpopulation that are resistant to radio/chemotherapies and are the source of recurrence, therefore it is crucial to characterize GICs and find new therapeutic targets. We have successfully established mouse and human GICs, which retain stemness characteristics and tumorigenicity. By comparing their expression profiles with those of parental cells, we have focused on two cell surface membrane proteins, Ceacam1L and Eva1, which were prominently expressed in GICs. We demonstrated that both proteins were involved in GIC characteristics, including self-renewal, stem cell gene expression and side population, and tumorigenesis, indicating that they are potential new therapeutic targets for GBM. In this research highlight, I summarize our recent reports regarding Ceacam1L and Eva1, and then discuss about Ceacam1L and Eva1 as GBM therapeutic targets.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"49 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87327395","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}
Epidermal growth factor receptor variant III (EGFRvIII) is the most common EGFR mutant found in glioblastoma (GBM). Due to a truncation of large portion of the extracellular region, EGFRvIII is unable to bind any ligand and constitutively signals to downstream effector molecules. It is tumor-specific, highly oncogenic and usually co-expressed with EGFR wild type (EGFRwt). EGFR tyrosine kinase inhibitors (TKIs) have proven ineffective in GBM and different mechanisms account for the occurrence of resistance to such inhibitors. Among these, EGFR TKIs induce a switch to platelet-derived growth factor receptor β (PDGFRβ) expression and signaling, thus rendering the tumors addicted to such receptor for continued growth and resistance to treatment. In our recent investigation, we showed the ability of a nuclease-resistant RNA aptamer, named CL4, to bind and inhibit EGFRvIII thus hampering proliferation, migration and invasion of EGFRvIII-positive GBM cells. Importantly, both CL4 and EGFR TKIs cooperate with a previously validated anti-PDGFRβ aptamer in inhibiting cell growth. Here, we highlight the potential of the EGFRvIII aptamer to hamper the EGFRvIII functional interplay with other receptor tyrosine kinases (RTKs) and cell surface proteins responsible for GBM development and progression. The utility of CL4 as targeting ligand for drug-delivery approaches is also discussed. Overall, aptamer-based molecules have significant implications for managing GBM in the near future.
{"title":"Highlighting the potential of aptamer-based strategy to treat EGFRvIII-positive glioblastoma","authors":"S. Camorani, L. Cerchia","doi":"10.14800/ccm.1314","DOIUrl":"https://doi.org/10.14800/ccm.1314","url":null,"abstract":"Epidermal growth factor receptor variant III (EGFRvIII) is the most common EGFR mutant found in glioblastoma (GBM). Due to a truncation of large portion of the extracellular region, EGFRvIII is unable to bind any ligand and constitutively signals to downstream effector molecules. It is tumor-specific, highly oncogenic and usually co-expressed with EGFR wild type (EGFRwt). EGFR tyrosine kinase inhibitors (TKIs) have proven ineffective in GBM and different mechanisms account for the occurrence of resistance to such inhibitors. Among these, EGFR TKIs induce a switch to platelet-derived growth factor receptor β (PDGFRβ) expression and signaling, thus rendering the tumors addicted to such receptor for continued growth and resistance to treatment. In our recent investigation, we showed the ability of a nuclease-resistant RNA aptamer, named CL4, to bind and inhibit EGFRvIII thus hampering proliferation, migration and invasion of EGFRvIII-positive GBM cells. Importantly, both CL4 and EGFR TKIs cooperate with a previously validated anti-PDGFRβ aptamer in inhibiting cell growth. Here, we highlight the potential of the EGFRvIII aptamer to hamper the EGFRvIII functional interplay with other receptor tyrosine kinases (RTKs) and cell surface proteins responsible for GBM development and progression. The utility of CL4 as targeting ligand for drug-delivery approaches is also discussed. Overall, aptamer-based molecules have significant implications for managing GBM in the near future.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79299556","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}
Current staging of Squamous Cell Carcinoma originating from the lip focuses on tumor size. It was thought that this American Joint Committee on Cancer (tumor–node–metastasis) staging system, whilst practical, may have shortcomings in predicting the risk of loco-regional or metastatic spread of lip tumors. This is a research highlight of a recent study performed through a rural multidisciplinary head & neck cancer unit analyzing 68 patients with primary lip SCC’s [1] . Overall 12 patients developed metastasis with increased risk of spread in patients with tumors of increased thickness (U = 103.50; degrees of freedom = 68; p < 0.001), those with a larger overall tumor size (U = 163.50; degrees of freedom = 68; p = 0.005) and patients living further from the treatment center at time of disease diagnosis (U = 199.00; degrees of freedom = 68; p = 0.018).This suggests that factors other then overall tumor size/staging have an important prognostic & staging role in patients with SCC of the lip.
{"title":"A retrospective review of lip squamous cell carcinoma characteristics as predictors of nodal spread","authors":"A. Pastuszek","doi":"10.14800/CCM.1265","DOIUrl":"https://doi.org/10.14800/CCM.1265","url":null,"abstract":"Current staging of Squamous Cell Carcinoma originating from the lip focuses on tumor size. It was thought that this American Joint Committee on Cancer (tumor–node–metastasis) staging system, whilst practical, may have shortcomings in predicting the risk of loco-regional or metastatic spread of lip tumors. This is a research highlight of a recent study performed through a rural multidisciplinary head & neck cancer unit analyzing 68 patients with primary lip SCC’s [1] . Overall 12 patients developed metastasis with increased risk of spread in patients with tumors of increased thickness (U = 103.50; degrees of freedom = 68; p < 0.001), those with a larger overall tumor size (U = 163.50; degrees of freedom = 68; p = 0.005) and patients living further from the treatment center at time of disease diagnosis (U = 199.00; degrees of freedom = 68; p = 0.018).This suggests that factors other then overall tumor size/staging have an important prognostic & staging role in patients with SCC of the lip.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"76 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72937185","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}
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