Pub Date : 2021-12-29DOI: 10.33696/cancerbiology.2.024
A. Marin, Gabriela Silva Soares, D. Zanette, M. Aoki
Chronic Myeloid Leukemia (CML) is a clonal disorder originated by a pluripotent hematopoietic stem cell, which presents the translocation t(9;22) (q34;q11) in 90% of the cases. This genetic abnormality is a balanced translocation between Abelson Murine Leukemia (ABL) located in chromosome 9 with the Breakpoint Cluster Region (BCR) gene at chromosome 22, generating Philadelphia chromosome (Ph) or BCR-ABL1, which codes an oncoprotein of 210 kDa [1-4]. This alteration represents a hallmark in oncology and for CML research, diagnosis, and prognosis. The standard treatment of CML patients is with Tyrosine Kinase Inhibitors (TKIs), and the first line is Imatinib [5]. This drug was developed in 1990s by Brian Druker and Nicholas Lydon and in 1998 a phase 1 clinical trial was conducted, causing cancer regression in most patients with CML in chronic phase. Five years later, 98% of patients from this trial were still in remission. In 2001, this drug was approved by FDA, revolutionizing the treatment of CML. Imatinib is quite selective for BCRABL1 onco-protein, so it does not inhibit other tyrosine kinase enzymes, so far representing one of the pioneers in oncological targeted therapy [6].
{"title":"Molecular Biology for BCR-ABL1 Quantification for Chronic Myeloid Leukemia Monitorization and Evaluation","authors":"A. Marin, Gabriela Silva Soares, D. Zanette, M. Aoki","doi":"10.33696/cancerbiology.2.024","DOIUrl":"https://doi.org/10.33696/cancerbiology.2.024","url":null,"abstract":"Chronic Myeloid Leukemia (CML) is a clonal disorder originated by a pluripotent hematopoietic stem cell, which presents the translocation t(9;22) (q34;q11) in 90% of the cases. This genetic abnormality is a balanced translocation between Abelson Murine Leukemia (ABL) located in chromosome 9 with the Breakpoint Cluster Region (BCR) gene at chromosome 22, generating Philadelphia chromosome (Ph) or BCR-ABL1, which codes an oncoprotein of 210 kDa [1-4]. This alteration represents a hallmark in oncology and for CML research, diagnosis, and prognosis. The standard treatment of CML patients is with Tyrosine Kinase Inhibitors (TKIs), and the first line is Imatinib [5]. This drug was developed in 1990s by Brian Druker and Nicholas Lydon and in 1998 a phase 1 clinical trial was conducted, causing cancer regression in most patients with CML in chronic phase. Five years later, 98% of patients from this trial were still in remission. In 2001, this drug was approved by FDA, revolutionizing the treatment of CML. Imatinib is quite selective for BCRABL1 onco-protein, so it does not inhibit other tyrosine kinase enzymes, so far representing one of the pioneers in oncological targeted therapy [6].","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"235 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75574832","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}
Pub Date : 2021-12-29DOI: 10.33696/cancerbiology.2.022
Ajda Altinoz, A. Abdel-Aziz, M. Ameri
This commentary refers to our published article, as highlighted in this article most common gene causing breast cancer in the population living in the United Arab Emirates is BRCA2 followed by BRCA1 [1]. This is the first publication discussing about clinical and pathological features of breast cancer in woman with a positive genetic mutation in the United Arab Emirates. The UAE has a rising population of a mixed ethnic population with predominantly Arabic background. Breast cancer (BC) is the most common cancer in the UAE according to GLOBOCAN statistics in 2020 [2]. Despite the rise in cancer, there is less published data about genetic predisposition in breast cancer in this part of the world.
{"title":"Genetic Predisposition of Breast Cancer in the United Arab Emirates","authors":"Ajda Altinoz, A. Abdel-Aziz, M. Ameri","doi":"10.33696/cancerbiology.2.022","DOIUrl":"https://doi.org/10.33696/cancerbiology.2.022","url":null,"abstract":"This commentary refers to our published article, as highlighted in this article most common gene causing breast cancer in the population living in the United Arab Emirates is BRCA2 followed by BRCA1 [1]. This is the first publication discussing about clinical and pathological features of breast cancer in woman with a positive genetic mutation in the United Arab Emirates. The UAE has a rising population of a mixed ethnic population with predominantly Arabic background. Breast cancer (BC) is the most common cancer in the UAE according to GLOBOCAN statistics in 2020 [2]. Despite the rise in cancer, there is less published data about genetic predisposition in breast cancer in this part of the world.","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"34 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85076231","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}
Pub Date : 2021-12-29DOI: 10.33696/cancerbiology.2.026
Hussein Al-Akhrass, Nicolas Pasquier, J. Ivaska
Tyrosine kinase-type cell surface receptor HER2targeted therapies have dramatically improved breast cancer patients’ outcome compared to conventional chemotherapies. In the clinic, HER2 monoclonal antibody trastuzumab with chemotherapy represent the gold standard treatment of HER2-positive breast cancer [1]. In the advanced metastatic setting, other Federation of Drug Administration (FDA)-approved HER2-based therapeutic options are used such as HER2 small molecule tyrosine kinase inhibitor neratinib [2]. Metastatic tumors are often therapy-resistant due to drug resistance mechanisms leading to sustained cancer progression most notably with regard to brain metastatic breast cancer, the most challenging medical-oncology situation [3]. 50% of brain metastatic HER2-positive breast cancer samples exhibit enriched HER3 expression compared to their matched primary tumors [4]. Elevated HER3 levels is one of the most reported therapy-resistance mechanisms in breast cancer [5]. HER3 lacks a fully active intracellular kinase domain, however, upon ligand binding the receptor heterodimerizes with its favorite partner HER2 that adopts constitutively the open conformation required for receptor dimerization [6]. The HER2-HER3 heterodimer is a unique and powerful signaling unit facilitating signaling such that even a residual HER2 activation is sufficient to trans-phosphorylate HER3 that bears at least six direct docking sites for the p85 adaptor subunit of phosphoinositide 3-kinase [5,6]. This enables HER3 to compensate for HER2 inhibition and renders HER2-HER3 the most signaling-effective component among all the different heterodimers within the HER family [6,7]. HER3 inhibition is an unmet clinical need since the extensive preclinical and clinical efforts targeting this receptor have thus far failed to lead to FDA approval in any cancer type. This is partly owing to the fact that targeting HER3 using classic tyrosine kinase inhibitors is not an option [5].
{"title":"SorLA Targeting - A Method to Overcome Therapy Resistance in Breast Cancer","authors":"Hussein Al-Akhrass, Nicolas Pasquier, J. Ivaska","doi":"10.33696/cancerbiology.2.026","DOIUrl":"https://doi.org/10.33696/cancerbiology.2.026","url":null,"abstract":"Tyrosine kinase-type cell surface receptor HER2targeted therapies have dramatically improved breast cancer patients’ outcome compared to conventional chemotherapies. In the clinic, HER2 monoclonal antibody trastuzumab with chemotherapy represent the gold standard treatment of HER2-positive breast cancer [1]. In the advanced metastatic setting, other Federation of Drug Administration (FDA)-approved HER2-based therapeutic options are used such as HER2 small molecule tyrosine kinase inhibitor neratinib [2]. Metastatic tumors are often therapy-resistant due to drug resistance mechanisms leading to sustained cancer progression most notably with regard to brain metastatic breast cancer, the most challenging medical-oncology situation [3]. 50% of brain metastatic HER2-positive breast cancer samples exhibit enriched HER3 expression compared to their matched primary tumors [4]. Elevated HER3 levels is one of the most reported therapy-resistance mechanisms in breast cancer [5]. HER3 lacks a fully active intracellular kinase domain, however, upon ligand binding the receptor heterodimerizes with its favorite partner HER2 that adopts constitutively the open conformation required for receptor dimerization [6]. The HER2-HER3 heterodimer is a unique and powerful signaling unit facilitating signaling such that even a residual HER2 activation is sufficient to trans-phosphorylate HER3 that bears at least six direct docking sites for the p85 adaptor subunit of phosphoinositide 3-kinase [5,6]. This enables HER3 to compensate for HER2 inhibition and renders HER2-HER3 the most signaling-effective component among all the different heterodimers within the HER family [6,7]. HER3 inhibition is an unmet clinical need since the extensive preclinical and clinical efforts targeting this receptor have thus far failed to lead to FDA approval in any cancer type. This is partly owing to the fact that targeting HER3 using classic tyrosine kinase inhibitors is not an option [5].","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"79 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83126077","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}
Pub Date : 2021-12-29DOI: 10.33696/cancerbiology.2.025
A. Fütterer, Amaia Talavera-Gutiérrez, C. Martínez-A
Each of these cell types displays specific characteristics. Epithelial cells have apicobasal polarity, are connected by cell junctions, and can form epithelial layers that cover many tissues, whereas mesenchymal cells lack apicobasal polarity, are less connected, but are more motile [2]. Both cell types can nonetheless undergo highly connected mutual transitions. EMT and its reverse process MET are thus well-studied in embryonic development, and several rounds of EMT and MET are described for the generation of various organs throughout their differentiation and development. Molecular studies to analyze these transitions show the involvement of several regulatory networks of transcriptional and translational regulators, linked to post-transcriptional and posttranslational modifications. Gene and protein regulation participate in cellular processes such as cell-cell contact, cell adhesion, cell polarity, cytoskeletal organization (which implies cell migration), all of which are responsible for successful, correct transitions [3-5].
{"title":"The Impact of Dido on the Epithelial-Mesenchymal Transition","authors":"A. Fütterer, Amaia Talavera-Gutiérrez, C. Martínez-A","doi":"10.33696/cancerbiology.2.025","DOIUrl":"https://doi.org/10.33696/cancerbiology.2.025","url":null,"abstract":"Each of these cell types displays specific characteristics. Epithelial cells have apicobasal polarity, are connected by cell junctions, and can form epithelial layers that cover many tissues, whereas mesenchymal cells lack apicobasal polarity, are less connected, but are more motile [2]. Both cell types can nonetheless undergo highly connected mutual transitions. EMT and its reverse process MET are thus well-studied in embryonic development, and several rounds of EMT and MET are described for the generation of various organs throughout their differentiation and development. Molecular studies to analyze these transitions show the involvement of several regulatory networks of transcriptional and translational regulators, linked to post-transcriptional and posttranslational modifications. Gene and protein regulation participate in cellular processes such as cell-cell contact, cell adhesion, cell polarity, cytoskeletal organization (which implies cell migration), all of which are responsible for successful, correct transitions [3-5].","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"109 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77340299","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}
Pub Date : 2021-06-29DOI: 10.33696/cancerbiology.2.018
A. Morales
Peripheral nerves have been shown to modulate the growth and spread of tumours in the prostate, feeding both cancer cells and the stroma in the tumour environment. Several in vitro and in vivo studies have reported the effect of botulinum toxin (BT) on tumour tissue in the prostate. BT in humans has been observed to cause increased apoptosis of cancer cells, with morphological changes characterized by extensive degenerative and atrophic areas of cancer, reduced cytoplasm, and pyknotic nuclei, compared to the characteristics of cancer tissues injected with saline solution. Based on this set of physiological and pathogenic knowledge, experimental, epidemiological, and clinical evidences have been generated that demonstrates the effect of BT on the control of prostate cancer, which represents a powerful therapeutic tool that would reduce mortality from prostate cancer.
{"title":"Botulinum Toxin: The Promising Future of Prostate Cancer Treatment","authors":"A. Morales","doi":"10.33696/cancerbiology.2.018","DOIUrl":"https://doi.org/10.33696/cancerbiology.2.018","url":null,"abstract":"Peripheral nerves have been shown to modulate the growth and spread of tumours in the prostate, feeding both cancer cells and the stroma in the tumour environment. Several in vitro and in vivo studies have reported the effect of botulinum toxin (BT) on tumour tissue in the prostate. BT in humans has been observed to cause increased apoptosis of cancer cells, with morphological changes characterized by extensive degenerative and atrophic areas of cancer, reduced cytoplasm, and pyknotic nuclei, compared to the characteristics of cancer tissues injected with saline solution. Based on this set of physiological and pathogenic knowledge, experimental, epidemiological, and clinical evidences have been generated that demonstrates the effect of BT on the control of prostate cancer, which represents a powerful therapeutic tool that would reduce mortality from prostate cancer.","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"159 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75737131","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}
Pub Date : 2021-06-29DOI: 10.33696/cancerbiology.2.016
M. Lieber
Various types of forces, such as cohesive and adhesive forces, are involved in physical and biological processes. Many of these processes appear to have developmental features through different scales of nature, and such processes may reflect a universal dynamic of accommodation involving the universal dimensional constants. A particular avenue of plant tissue culture research, utilizing the process of electronic desaturation, might very well point to such a subsuming, universal process. Through the process of electronic desaturation of proteins in living cells, cohesive and adhesive forces are generated and regenerated between cellular proteins and between structured water and the proteins throughout and between mammalian cells. Those forces stabilize cells and tissues and prevent carcinogenesis [1,2]. In electronic desaturation, methylglyoxal-ascorbic acid complexes attach to particular protein regions, which enable or promote the conduction or movement of outer electrons of the proteins via methylglyoxal-ascorbic acid to oxygen. When such cohesive forces cease to exist in cells due to the conversion of methylglyoxal (MG) to D-lactic acid by glyoxalase, carcinogenesis ensues. Glyoxalase is an enzyme that can actively exist in cells. As noted by SzentGyorgyi [1,2], the presence of oxygen, MG, and ascorbic acid enabled the evolution of organisms with high levels of development and a general capability of preventing dedifferentiation that could lead to carcinogenesis.
{"title":"Forces, Chromosomal Configurations, and Carcinogenesis: Towards Another Therapeutic Approach","authors":"M. Lieber","doi":"10.33696/cancerbiology.2.016","DOIUrl":"https://doi.org/10.33696/cancerbiology.2.016","url":null,"abstract":"Various types of forces, such as cohesive and adhesive forces, are involved in physical and biological processes. Many of these processes appear to have developmental features through different scales of nature, and such processes may reflect a universal dynamic of accommodation involving the universal dimensional constants. A particular avenue of plant tissue culture research, utilizing the process of electronic desaturation, might very well point to such a subsuming, universal process. Through the process of electronic desaturation of proteins in living cells, cohesive and adhesive forces are generated and regenerated between cellular proteins and between structured water and the proteins throughout and between mammalian cells. Those forces stabilize cells and tissues and prevent carcinogenesis [1,2]. In electronic desaturation, methylglyoxal-ascorbic acid complexes attach to particular protein regions, which enable or promote the conduction or movement of outer electrons of the proteins via methylglyoxal-ascorbic acid to oxygen. When such cohesive forces cease to exist in cells due to the conversion of methylglyoxal (MG) to D-lactic acid by glyoxalase, carcinogenesis ensues. Glyoxalase is an enzyme that can actively exist in cells. As noted by SzentGyorgyi [1,2], the presence of oxygen, MG, and ascorbic acid enabled the evolution of organisms with high levels of development and a general capability of preventing dedifferentiation that could lead to carcinogenesis.","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72572580","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}
Pub Date : 2021-06-29DOI: 10.33696/cancerbiology.2.020
Matthew T. Hey, Hans E Drawbert, Francisco A. Tarrazzi, M. Block, S. Razi
Lung cancer remains the leading cause of cancer related death in the United States with mortality rates surpassing breast, prostate, brain, and colorectal cancers combined [1,2]. Recent data shows that susceptibility for both men and women for developing invasive lung and bronchogenic carcinoma peak after the age of 70 years [2]. As the generation of baby boomers age, those older than 65 years will nearly double and the number of elderly population older than 85 years will triple from 2020 to 2050 [3]. These shifting demographics are an early sign of the improvements and advancements in overall care of the elderly population. It therefore remains imperative that lung cancer treatment and selection criteria evolves accordingly in elderly and high-risk population. Some of the challenges facing the elderly and high-risk population relates to comorbidities, limited cardiac and pulmonary function reserve, decreased decision-making capacity, quality of life issues and lack of social support among others [4,5].
{"title":"Surgery Versus Radiation Therapy for Early-Stage Lung Cancer: Patient Selection is Crucial","authors":"Matthew T. Hey, Hans E Drawbert, Francisco A. Tarrazzi, M. Block, S. Razi","doi":"10.33696/cancerbiology.2.020","DOIUrl":"https://doi.org/10.33696/cancerbiology.2.020","url":null,"abstract":"Lung cancer remains the leading cause of cancer related death in the United States with mortality rates surpassing breast, prostate, brain, and colorectal cancers combined [1,2]. Recent data shows that susceptibility for both men and women for developing invasive lung and bronchogenic carcinoma peak after the age of 70 years [2]. As the generation of baby boomers age, those older than 65 years will nearly double and the number of elderly population older than 85 years will triple from 2020 to 2050 [3]. These shifting demographics are an early sign of the improvements and advancements in overall care of the elderly population. It therefore remains imperative that lung cancer treatment and selection criteria evolves accordingly in elderly and high-risk population. Some of the challenges facing the elderly and high-risk population relates to comorbidities, limited cardiac and pulmonary function reserve, decreased decision-making capacity, quality of life issues and lack of social support among others [4,5].","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89544429","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}
Exosomes are nanosized, organelle-like membranous vesicles secreted from various cell types, including normal cells and cancer cells. Exosomes contain abundant bioactive molecules, including nucleic acids, lipids, and proteins and dynamically participate in intercellular communications. By shuttling the functional molecules into the recipient cells, exosomes secreted by cancerous cells can alter the cellular environment to favor tumor growth and metastasis. In this review, we focus on exosomes to promote cancer progression via their various bioactive cargoes through different mechanisms/pathways. By recognizing these pathways, we can design efficient therapeutic strategies to control cancer progression.
{"title":"Exosome to Promote Cancer Progression via Its Bioactive Cargoes.","authors":"Austin McMasters, Kelly M McMasters, Hongying Hao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Exosomes are nanosized, organelle-like membranous vesicles secreted from various cell types, including normal cells and cancer cells. Exosomes contain abundant bioactive molecules, including nucleic acids, lipids, and proteins and dynamically participate in intercellular communications. By shuttling the functional molecules into the recipient cells, exosomes secreted by cancerous cells can alter the cellular environment to favor tumor growth and metastasis. In this review, we focus on exosomes to promote cancer progression via their various bioactive cargoes through different mechanisms/pathways. By recognizing these pathways, we can design efficient therapeutic strategies to control cancer progression.</p>","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"2 2","pages":"29-34"},"PeriodicalIF":0.0,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8277159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39185142","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}
Pub Date : 2021-06-01DOI: 10.33696/cancerbiology.2.021
Austin McMasters, K. McMasters, H. Hao
Exosomes are nanosized, organelle-like membranous vesicles secreted from various cell types, including normal cells and cancer cells. Exosomes contain abundant bioactive molecules, including nucleic acids, lipids, and proteins and dynamically participate in intercellular communications. By shuttling the functional molecules into the recipient cells, exosomes secreted by cancerous cells can alter the cellular environment to favor tumor growth and metastasis. In this review, we focus on exosomes to promote cancer progression via their various bioactive cargoes through different mechanisms/pathways. By recognizing these pathways, we can design efficient therapeutic strategies to control cancer progression.
{"title":"Exosome to Promote Cancer Progression via Its Bioactive Cargoes","authors":"Austin McMasters, K. McMasters, H. Hao","doi":"10.33696/cancerbiology.2.021","DOIUrl":"https://doi.org/10.33696/cancerbiology.2.021","url":null,"abstract":"Exosomes are nanosized, organelle-like membranous vesicles secreted from various cell types, including normal cells and cancer cells. Exosomes contain abundant bioactive molecules, including nucleic acids, lipids, and proteins and dynamically participate in intercellular communications. By shuttling the functional molecules into the recipient cells, exosomes secreted by cancerous cells can alter the cellular environment to favor tumor growth and metastasis. In this review, we focus on exosomes to promote cancer progression via their various bioactive cargoes through different mechanisms/pathways. By recognizing these pathways, we can design efficient therapeutic strategies to control cancer progression.","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"18 10 1","pages":"29 - 34"},"PeriodicalIF":0.0,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78101810","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}
Pub Date : 2020-12-31DOI: 10.33696/cancerbiology.1.014
Dora Jericevic, Jacob Taylor, William C. Huang
Background: We recently published our multi-institutional experience performing primary robot-assisted retroperitoneal lymph node dissection (RA-RPLND) for men with non-seminomatous germ cell tumor (NSGCT). We concluded that primary RA-RPLND for NSGCT can be performed safely with low complication rates, acceptable early oncologic outcomes, and lower overall theoretical chemotherapy burden. In this commentary, we explore outcomes in clinical stage I patients stratified by clinical risk factors (RF) and estimate reductions in chemotherapy burden. Methods: In our original study, we included clinical stage I and highly select clinical stage II patients. Clinical risk factors were defined as lymphovascular invasion (LVI) and/or predominance of embryonal carcinoma (EC) (>40%) in the orchiectomy specimen. Results: 72% (28/39) of stage I patients that underwent RA-RPLND could be classified as belonging to the RF+ group (Figure 1). Among the RF+ group, 36% (10/28) had both LVI and EC (LVI+EC+). Of the LVI+EC+ patients, 70% had positive nodes (N+), whereas the rate was much lower in the LVI only (LVI+EC-) and EC only (LVI-EC+) groups (17% for both). Primary RA-RPLND allowed for accurate pathologic staging and avoidance of chemotherapy in the 90% and 64% of pN0 patients in the RF-and RF+ groups, respectively. Overall node positive rates were 36% and 9% for men with and without clinical risk factors, respectively. The majority of these node positive patients had pN1 disease and were thus candidates for post RPLND surveillance, thus reducing therapeutic burden and exposure to long-term toxicity. Conclusion : Primary RA-RPLND can be safely performed with low complication rates and acceptable short term oncologic outcomes. Assessing clinical risk factors when deciding on treatment may further improve outcomes by helping to identify clinical stage I patients who are more likely to be stage II and thus benefit most from adjuvant treatment with RPLND.
{"title":"Influence of Clinical Risk Factors on Outcomes in Men with Stage I Non-Seminomatous Germ Cell Tumor Undergoing Robot-Assisted Retroperitoneal Lymph Node Dissection","authors":"Dora Jericevic, Jacob Taylor, William C. Huang","doi":"10.33696/cancerbiology.1.014","DOIUrl":"https://doi.org/10.33696/cancerbiology.1.014","url":null,"abstract":"Background: We recently published our multi-institutional experience performing primary robot-assisted retroperitoneal lymph node dissection (RA-RPLND) for men with non-seminomatous germ cell tumor (NSGCT). We concluded that primary RA-RPLND for NSGCT can be performed safely with low complication rates, acceptable early oncologic outcomes, and lower overall theoretical chemotherapy burden. In this commentary, we explore outcomes in clinical stage I patients stratified by clinical risk factors (RF) and estimate reductions in chemotherapy burden. Methods: In our original study, we included clinical stage I and highly select clinical stage II patients. Clinical risk factors were defined as lymphovascular invasion (LVI) and/or predominance of embryonal carcinoma (EC) (>40%) in the orchiectomy specimen. Results: 72% (28/39) of stage I patients that underwent RA-RPLND could be classified as belonging to the RF+ group (Figure 1). Among the RF+ group, 36% (10/28) had both LVI and EC (LVI+EC+). Of the LVI+EC+ patients, 70% had positive nodes (N+), whereas the rate was much lower in the LVI only (LVI+EC-) and EC only (LVI-EC+) groups (17% for both). Primary RA-RPLND allowed for accurate pathologic staging and avoidance of chemotherapy in the 90% and 64% of pN0 patients in the RF-and RF+ groups, respectively. Overall node positive rates were 36% and 9% for men with and without clinical risk factors, respectively. The majority of these node positive patients had pN1 disease and were thus candidates for post RPLND surveillance, thus reducing therapeutic burden and exposure to long-term toxicity. Conclusion : Primary RA-RPLND can be safely performed with low complication rates and acceptable short term oncologic outcomes. Assessing clinical risk factors when deciding on treatment may further improve outcomes by helping to identify clinical stage I patients who are more likely to be stage II and thus benefit most from adjuvant treatment with RPLND.","PeriodicalId":92985,"journal":{"name":"Archives of cancer biology and therapy","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90805602","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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