Pub Date : 2023-10-04eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.589
Filip Barbarewicz, Kai-Olaf Henkel, Florian Dudde
{"title":"Diagnosis and management of postoperative wound infections in the head and neck region.","authors":"Filip Barbarewicz, Kai-Olaf Henkel, Florian Dudde","doi":"10.18632/oncoscience.589","DOIUrl":"10.18632/oncoscience.589","url":null,"abstract":"","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"10 ","pages":"56-58"},"PeriodicalIF":0.0,"publicationDate":"2023-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10549770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41174703","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 : 2023-10-02eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.588
Peeter Karihtala
{"title":"The mutational signatures of cancer: can passengers set a direction for prognosis?","authors":"Peeter Karihtala","doi":"10.18632/oncoscience.588","DOIUrl":"https://doi.org/10.18632/oncoscience.588","url":null,"abstract":"","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"10 ","pages":"54-55"},"PeriodicalIF":0.0,"publicationDate":"2023-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10545096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41125376","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 : 2023-09-20eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.587
Mohamed A Gouda, Maria A Zarzour, Ara A Vaporciyan, Kalevi Kairemo, Hubert H Chuang, Vivek Subbiah
Pazopanib is a multi-kinase inhibitor that is currently approved for treatment of advanced renal cell carcinoma and chemotherapy-refractory soft tissue sarcoma. In this case report, we discuss the case of a patient with a EWSR1-NFATC2 fusion positive bone sarcoma who had exceptional tumor control through using pazopanib and surgery for an overall duration exceeding 5 years. We also review the literature on EWSR1-NFATC2 translocation-associated sarcomas and use of pazopanib in bone sarcomas.
{"title":"Activity of pazopanib in <i>EWSR1-NFATC2</i> translocation-associated bone sarcoma.","authors":"Mohamed A Gouda, Maria A Zarzour, Ara A Vaporciyan, Kalevi Kairemo, Hubert H Chuang, Vivek Subbiah","doi":"10.18632/oncoscience.587","DOIUrl":"https://doi.org/10.18632/oncoscience.587","url":null,"abstract":"<p><p>Pazopanib is a multi-kinase inhibitor that is currently approved for treatment of advanced renal cell carcinoma and chemotherapy-refractory soft tissue sarcoma. In this case report, we discuss the case of a patient with a <i>EWSR1-NFATC2</i> fusion positive bone sarcoma who had exceptional tumor control through using pazopanib and surgery for an overall duration exceeding 5 years. We also review the literature on <i>EWSR1-NFATC2</i> translocation-associated sarcomas and use of pazopanib in bone sarcomas.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"10 ","pages":"44-53"},"PeriodicalIF":0.0,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10511123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41143758","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 : 2023-09-20eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.586
Mohamed A Gouda, Filip Janku, Neeta Somaiah, Kelly K Hunt, Sireesha Yedururi, Vivek Subbiah
Ripretinib is a tyrosine kinase inhibitor that was approved by the United States FDA in 2020 for treatment of advanced gastrointestinal stromal tumor (GIST) in patients who received prior treatment with three or more tyrosine kinase inhibitors. In this case report, we show the durable clinical benefit achieved in a patient with GIST by using ripretinib and repeated timely surgical resection of limited disease progression. The total time on ripretinib was 43 months which is longer than the current reported data from ripretinib clinical trials. Such approach for using multi-disciplinary disease management can improve the durability of response to tyrosine kinase inhibitors, including ripretinib, and associated clinical outcomes.
{"title":"Multi-disciplinary management of recurrent gastrointestinal stromal tumor harboring KIT exon 11 mutation with the switch-control kinase inhibitor ripretinib and surgery.","authors":"Mohamed A Gouda, Filip Janku, Neeta Somaiah, Kelly K Hunt, Sireesha Yedururi, Vivek Subbiah","doi":"10.18632/oncoscience.586","DOIUrl":"https://doi.org/10.18632/oncoscience.586","url":null,"abstract":"<p><p>Ripretinib is a tyrosine kinase inhibitor that was approved by the United States FDA in 2020 for treatment of advanced gastrointestinal stromal tumor (GIST) in patients who received prior treatment with three or more tyrosine kinase inhibitors. In this case report, we show the durable clinical benefit achieved in a patient with GIST by using ripretinib and repeated timely surgical resection of limited disease progression. The total time on ripretinib was 43 months which is longer than the current reported data from ripretinib clinical trials. Such approach for using multi-disciplinary disease management can improve the durability of response to tyrosine kinase inhibitors, including ripretinib, and associated clinical outcomes.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"10 ","pages":"38-43"},"PeriodicalIF":0.0,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10511119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41158950","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 : 2022-05-09DOI: 10.18632/oncoscience.557
Long Jiang, F. Wermeling
CRISPR/Cas9-based tools are anticipated to transform the gene therapy field by facilitating the correction of disease-causing mutations. However, CRISPR/Cas9 generates DNA damage, which triggers a DNA damage response centered around the tumor-suppressor p53. In this research perspective, we discuss implications of this and describe a CRISPR-p53 interactome with cancer-related genes that, if mutated, can give cells a selective advantage following exposure to CRISPR/Cas9. We propose that the genes in the CRISPR-p53 interactome should be monitored in the clinical setting and describe that transient p53 inhibition could be used to limit the enrichment of cells with such mutations.
{"title":"A CRISPR-p53 interactome with potential implications for clinical CRISPR/Cas9 use","authors":"Long Jiang, F. Wermeling","doi":"10.18632/oncoscience.557","DOIUrl":"https://doi.org/10.18632/oncoscience.557","url":null,"abstract":"CRISPR/Cas9-based tools are anticipated to transform the gene therapy field by facilitating the correction of disease-causing mutations. However, CRISPR/Cas9 generates DNA damage, which triggers a DNA damage response centered around the tumor-suppressor p53. In this research perspective, we discuss implications of this and describe a CRISPR-p53 interactome with cancer-related genes that, if mutated, can give cells a selective advantage following exposure to CRISPR/Cas9. We propose that the genes in the CRISPR-p53 interactome should be monitored in the clinical setting and describe that transient p53 inhibition could be used to limit the enrichment of cells with such mutations.","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"51 1","pages":"27 - 29"},"PeriodicalIF":0.0,"publicationDate":"2022-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84455461","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 : 2022-04-22eCollection Date: 2022-01-01DOI: 10.18632/oncoscience.554
Daolin Tang, Rui Kang
Immunotherapy, especially the use of immune checkpoint inhibitors, has improved overall survival in cancer patients. However, a large proportion of patients initially do not respond to treatment or relapse after a period of response. Heat shock protein 90 (HSP90) is a conserved molecular chaperone that promotes the maturation and folding of substrate proteins involved in many different cellular pathways. Our recent drug screen and functional assay identified HSP90 as a universal control of the protein stability of nuclear transcription factor STAT1 in a variety of different cancer cells, thereby promoting subsequent gene expression of immune checkpoint molecules (IDO1 and PD-L1). In vivo, we used different mouse models of pancreatic cancer and demonstrated that targeting HSP90 enhanced the efficacy of PD-1 blockade therapy. These findings establish HSP90 as a targetable vulnerability in immune therapy.
{"title":"HSP90 as an emerging barrier to immune checkpoint blockade therapy.","authors":"Daolin Tang, Rui Kang","doi":"10.18632/oncoscience.554","DOIUrl":"10.18632/oncoscience.554","url":null,"abstract":"<p><p>Immunotherapy, especially the use of immune checkpoint inhibitors, has improved overall survival in cancer patients. However, a large proportion of patients initially do not respond to treatment or relapse after a period of response. Heat shock protein 90 (HSP90) is a conserved molecular chaperone that promotes the maturation and folding of substrate proteins involved in many different cellular pathways. Our recent drug screen and functional assay identified HSP90 as a universal control of the protein stability of nuclear transcription factor STAT1 in a variety of different cancer cells, thereby promoting subsequent gene expression of immune checkpoint molecules (IDO1 and PD-L1). <i>In vivo</i>, we used different mouse models of pancreatic cancer and demonstrated that targeting HSP90 enhanced the efficacy of PD-1 blockade therapy. These findings establish HSP90 as a targetable vulnerability in immune therapy.</p>","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"1 1","pages":"20-22"},"PeriodicalIF":0.0,"publicationDate":"2022-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9033023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78037362","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 : 2022-04-22DOI: 10.18632/oncoscience.556
Han Yang, Xuesen Dong
{"title":"Crosstalk between KIF15 and AR in castrate-resistant prostate cancers","authors":"Han Yang, Xuesen Dong","doi":"10.18632/oncoscience.556","DOIUrl":"https://doi.org/10.18632/oncoscience.556","url":null,"abstract":"","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"48 1","pages":"25 - 26"},"PeriodicalIF":0.0,"publicationDate":"2022-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89082102","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 : 2022-04-22DOI: 10.18632/oncoscience.555
I. Jordan, K. K. Lee, J. McDonald, L. Mariño-Ramírez
{"title":"Epigenetics and cancer disparities: when nature might be nurture","authors":"I. Jordan, K. K. Lee, J. McDonald, L. Mariño-Ramírez","doi":"10.18632/oncoscience.555","DOIUrl":"https://doi.org/10.18632/oncoscience.555","url":null,"abstract":"","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"28 1","pages":"23 - 24"},"PeriodicalIF":0.0,"publicationDate":"2022-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75145272","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 : 2022-04-21DOI: 10.18632/oncoscience.553
K. Nichols, I. Sánchez-García
B-cell acute lymphoblastic leukemia (B-ALL) is the most common childhood cancer and leading cause of pediatric cancer death. In childhood B-ALL, a mutation (hereditary or de novo) leads to appearance of preleukemic cells that are capable of normal lymphoid differentiation; however, upon acquisition of one or more second hit mutations, these preleukemic cells transform into full-blown leukemic blasts. While identification of the specific events that trigger the malignant evolution of preleukemic cells has remained elusive in humans, it has long been hypothesized that (delayed) exposure to infection promotes an immune response that then spurs the acquisition of additional genetic lesions [1]. Recently, independent studies using different genetically predisposed mice have demonstrated the occurrence of such an infection-triggered leukemogenic mechanism, collectively showing that several types of stress in the immune system can promote clonal evolution of preleukemic cells in a significant proportion of mice [2–4]. Interestingly, the immune stress does not act by selecting a preleukemic clone that already harbors the second hit; on the contrary, the infection acts by promoting acquisition of the second hit itself, therefore leading to full-blown B-ALL [1]. Together, these observations support the idea that by eliminating preleukemic cells, childhood B-ALL might be preventable [1–5]. Nevertheless, it has remained unclear how to target preleukemic cells as a means to prevent the development of B-ALL. To address this question, we took advantage of the Pax5+/− mice [2, 4]. Similar to children who harbor heterzygous germline PAX5 mutations, B-ALL develops in up to 25% of Pax5+/− mice, but only when these animals experience an immune stress, such as exposure to infection [2]. The leukemias that develop in this model acquire various types of second hit mutations which resemble those observed in human B-ALL, including activating mutations affecting the Janus Kinases (JAKs) [2]. We previously observed that pro-B cells in Pax5+/− mice are particularly dependent on the cytokine interleukin-7 (IL-7) for their survival, and that blocking IL-7-induced signaling using the JAK1/2 inhibitor ruxolitnib led to increased cell death in vitro [2]. Based on these findings, we used Pax5+/− mice to explore whether treatment with Editorial
{"title":"Towards the prevention of childhood leukemia","authors":"K. Nichols, I. Sánchez-García","doi":"10.18632/oncoscience.553","DOIUrl":"https://doi.org/10.18632/oncoscience.553","url":null,"abstract":"B-cell acute lymphoblastic leukemia (B-ALL) is the most common childhood cancer and leading cause of pediatric cancer death. In childhood B-ALL, a mutation (hereditary or de novo) leads to appearance of preleukemic cells that are capable of normal lymphoid differentiation; however, upon acquisition of one or more second hit mutations, these preleukemic cells transform into full-blown leukemic blasts. While identification of the specific events that trigger the malignant evolution of preleukemic cells has remained elusive in humans, it has long been hypothesized that (delayed) exposure to infection promotes an immune response that then spurs the acquisition of additional genetic lesions [1]. Recently, independent studies using different genetically predisposed mice have demonstrated the occurrence of such an infection-triggered leukemogenic mechanism, collectively showing that several types of stress in the immune system can promote clonal evolution of preleukemic cells in a significant proportion of mice [2–4]. Interestingly, the immune stress does not act by selecting a preleukemic clone that already harbors the second hit; on the contrary, the infection acts by promoting acquisition of the second hit itself, therefore leading to full-blown B-ALL [1]. Together, these observations support the idea that by eliminating preleukemic cells, childhood B-ALL might be preventable [1–5]. Nevertheless, it has remained unclear how to target preleukemic cells as a means to prevent the development of B-ALL. To address this question, we took advantage of the Pax5+/− mice [2, 4]. Similar to children who harbor heterzygous germline PAX5 mutations, B-ALL develops in up to 25% of Pax5+/− mice, but only when these animals experience an immune stress, such as exposure to infection [2]. The leukemias that develop in this model acquire various types of second hit mutations which resemble those observed in human B-ALL, including activating mutations affecting the Janus Kinases (JAKs) [2]. We previously observed that pro-B cells in Pax5+/− mice are particularly dependent on the cytokine interleukin-7 (IL-7) for their survival, and that blocking IL-7-induced signaling using the JAK1/2 inhibitor ruxolitnib led to increased cell death in vitro [2]. Based on these findings, we used Pax5+/− mice to explore whether treatment with Editorial","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"2 1","pages":"17 - 19"},"PeriodicalIF":0.0,"publicationDate":"2022-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88776304","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 : 2022-03-23DOI: 10.18632/oncoscience.551
M. Belleri, M. Presta
Sphingolipids, a class of compounds composed by a sphingoid base backbone, represent major components of biological membranes, and play a pivotal role in a variety of subcellular signaling processes. Abnormal sphingolipid metabolism sets the basis for the pathogenesis of variety of genetic diseases known collectively as sphingolipidosis, or sphingolipodystrophy. Among them, globoid cell leukodystrophy (also named Krabbe disease; OMIM #245200), is an autosomal recessive sphingolipidosis characterized by degeneration of oligodendroglia and progressive demyelination due to the genetic deficiency of β-galactosylceramidase (GALC; EC 3.2.1.46) [1], a lysosomal acid hydrolase that catalyzes the removal of β-galactose from β-galactosylceramide (GalCer) and other terminal β-galactose-containing sphingolipids. Based on a long-held and recently confirmed “psychosine hypothesis” [2], Krabbe disease may manifest as a consequence of the accumulation of the neurotoxic GALC substrate β-galactosylsphingosine (psychosine) in the central and peripheral nervous system [3]. Thus, most of the studies concerning the biological role of GALC have been performed on Krabbe patients and Galc-deficient twitcher mice (an authentic animal model of the disease [4]), leading to the envision that the major biological function of GALC may consist in its psychosine “scavenging” activity. However, experimental evidence indicates that GALC may act not only as a psychosine scavenger, but its modulation also exerting a series of psychosineindependent effects [5, 6]. For instance, GALC deficiency affects neovascularization in in vitro and in vivo in the presence of negligible, if any changes in psychosine levels [7, 8]. In addition, knock-down of the human GALC ortholog galcb in zebrafish embryos affects cell survival and neuronal differentiation in the absence of any significant accumulation of this metabolite [9]. In this frame, a recent study has shown that Galc knockdown in murine melanoma B16 cells causes a significant increase of the levels of the oncosuppressive sphingolipid ceramide mirrored by a decrease of sphingomyelins, phosphatidylethanolamines and cholesteryl esters, paralleled by an increased concentration of diacylglycerols [10]. These alterations of the lipidomic profile resulted in the inhibition of the tumorigenic activity of murine melanoma B16 cells. Increased levels of ceramide were observed also in GALC-silenced human melanoma A2058 cells and tumor xenografts, with a consequent decrease of their tumorigenic potential [10]. In keeping with these observations, a progressive increase of GALC expression occurs during tumor progression in human pathological skin specimens ranging from common nevi to stage IV melanoma. Again, the levels of GALC expression were inversely related to the levels of ceramide immunoreactivity in the same tumor samples [5, 10]. Together, these findings indicate that GALC might act as an oncogenic enzyme during melanoma progression by decreasin
{"title":"β-Galactosylceramidase in cancer: more than a psychosine scavenger","authors":"M. Belleri, M. Presta","doi":"10.18632/oncoscience.551","DOIUrl":"https://doi.org/10.18632/oncoscience.551","url":null,"abstract":"Sphingolipids, a class of compounds composed by a sphingoid base backbone, represent major components of biological membranes, and play a pivotal role in a variety of subcellular signaling processes. Abnormal sphingolipid metabolism sets the basis for the pathogenesis of variety of genetic diseases known collectively as sphingolipidosis, or sphingolipodystrophy. Among them, globoid cell leukodystrophy (also named Krabbe disease; OMIM #245200), is an autosomal recessive sphingolipidosis characterized by degeneration of oligodendroglia and progressive demyelination due to the genetic deficiency of β-galactosylceramidase (GALC; EC 3.2.1.46) [1], a lysosomal acid hydrolase that catalyzes the removal of β-galactose from β-galactosylceramide (GalCer) and other terminal β-galactose-containing sphingolipids. Based on a long-held and recently confirmed “psychosine hypothesis” [2], Krabbe disease may manifest as a consequence of the accumulation of the neurotoxic GALC substrate β-galactosylsphingosine (psychosine) in the central and peripheral nervous system [3]. Thus, most of the studies concerning the biological role of GALC have been performed on Krabbe patients and Galc-deficient twitcher mice (an authentic animal model of the disease [4]), leading to the envision that the major biological function of GALC may consist in its psychosine “scavenging” activity. However, experimental evidence indicates that GALC may act not only as a psychosine scavenger, but its modulation also exerting a series of psychosineindependent effects [5, 6]. For instance, GALC deficiency affects neovascularization in in vitro and in vivo in the presence of negligible, if any changes in psychosine levels [7, 8]. In addition, knock-down of the human GALC ortholog galcb in zebrafish embryos affects cell survival and neuronal differentiation in the absence of any significant accumulation of this metabolite [9]. In this frame, a recent study has shown that Galc knockdown in murine melanoma B16 cells causes a significant increase of the levels of the oncosuppressive sphingolipid ceramide mirrored by a decrease of sphingomyelins, phosphatidylethanolamines and cholesteryl esters, paralleled by an increased concentration of diacylglycerols [10]. These alterations of the lipidomic profile resulted in the inhibition of the tumorigenic activity of murine melanoma B16 cells. Increased levels of ceramide were observed also in GALC-silenced human melanoma A2058 cells and tumor xenografts, with a consequent decrease of their tumorigenic potential [10]. In keeping with these observations, a progressive increase of GALC expression occurs during tumor progression in human pathological skin specimens ranging from common nevi to stage IV melanoma. Again, the levels of GALC expression were inversely related to the levels of ceramide immunoreactivity in the same tumor samples [5, 10]. Together, these findings indicate that GALC might act as an oncogenic enzyme during melanoma progression by decreasin","PeriodicalId":94164,"journal":{"name":"Oncoscience","volume":"4 1","pages":"11 - 12"},"PeriodicalIF":0.0,"publicationDate":"2022-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79502067","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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