Pub Date : 2024-02-07DOI: 10.18632/oncoscience.594
Richard E. Kast
{"title":"IPIAD- an augmentation regimen added to standard treatment of pancreatic ductal adenocarcinoma using already-marketed repurposed drugs irbesartan, pyrimethamine, itraconazole, azithromycin, and dapsone","authors":"Richard E. Kast","doi":"10.18632/oncoscience.594","DOIUrl":"https://doi.org/10.18632/oncoscience.594","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139796880","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 : 2024-02-07DOI: 10.18632/oncoscience.594
Richard E. Kast
{"title":"IPIAD- an augmentation regimen added to standard treatment of pancreatic ductal adenocarcinoma using already-marketed repurposed drugs irbesartan, pyrimethamine, itraconazole, azithromycin, and dapsone","authors":"Richard E. Kast","doi":"10.18632/oncoscience.594","DOIUrl":"https://doi.org/10.18632/oncoscience.594","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139856917","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 : 2023-08-17eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.583
Elzbieta Izbicka, Robert T Streeper
The “war on cancer” [1] began with the National Cancer Act, a United States federal law intended “to amend the Public Health Service Act so as to strengthen the National Cancer Institute in order to more effectively carry out the national effort against cancer” that was signed by President Richard Nixon on December 23, 1971. As the 50th anniversary is now two years gone, the war has not been necessarily a blitzkrieg. To paraphrase Charles Dickens, today “it is the best of times, it is the worst of times” for cancer drugs. Great progress in cancer therapy has been made thanks to the combined impact of better supportive care, ever improving drugs and earlier cancer detection. On the other hand, the Anthropocene era brings new challenges due to increased human impact of environmental factors, which along with changes in diet and lifestyle may contribute to a worrisome increase in early-onset cancers, a situation viewed as a potential emerging global epidemic [2]. Conventional chemotherapy, one of the oldest anticancer weapons brought in late 1940s, encompasses alkylating agents, antimetabolites, natural products, hormones and steroids. Chemotherapy relies on the concept of eliminating the fast growing cancer cells [1] but adversely affects other fast growing normal cells in the body and lacks specificity. Despite these limitations, cytotoxic chemotherapy is widely used today. Targeted therapies that emerged in the late 1980s are based on the assumption that cancer cells express and rely on the use of various unique targets for their survival. A success story of a targeted BCR-ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec) spurred development of other targeted therapies, many of which effectively eradicated human cancers in animal models but failed to show clinical efficacy. Immunotherapy with monoclonal antibodies is a variation on the theme of targeted therapy. In particular, immune-checkpoint inhibitors do not kill cancer cells directly but instead mobilize the immune system to do the killing. In some cases, high success rates have been noted even in metastatic cancer [3] but substantial concerns remain regarding long-term toxicity [4]. Chimeric antigen receptor (CAR-T) targeted cell therapy has produced remarkable clinical responses with some hematological malignancies but is less effective in solid tumors and is limited by serious toxicities, antigen escape and restricted trafficking [5]. Targeted gene editing using CRISPR (clustered regularly interspaced palindromic repeat) with the bacterial RNA-guided CRISPR-Cas9 system has opened a new chapter in the drug development [6]. Several CRISPR-based products are undergoing clinical trials in patients with leukemias, lymphomas, solid tumors, and other diseases [7]. Whilst the bacterial CRISPR-Cas9 suffers from limited delivery to cells and tissues, a recent discovery of a CRISPR-like eukaryotic system based on the Fanzor protein, which uses RNA for precise DNA targeting, is expected to fa
{"title":"Cancer drug development yesterday, today and tomorrow.","authors":"Elzbieta Izbicka, Robert T Streeper","doi":"10.18632/oncoscience.583","DOIUrl":"10.18632/oncoscience.583","url":null,"abstract":"The “war on cancer” [1] began with the National Cancer Act, a United States federal law intended “to amend the Public Health Service Act so as to strengthen the National Cancer Institute in order to more effectively carry out the national effort against cancer” that was signed by President Richard Nixon on December 23, 1971. As the 50th anniversary is now two years gone, the war has not been necessarily a blitzkrieg. To paraphrase Charles Dickens, today “it is the best of times, it is the worst of times” for cancer drugs. Great progress in cancer therapy has been made thanks to the combined impact of better supportive care, ever improving drugs and earlier cancer detection. On the other hand, the Anthropocene era brings new challenges due to increased human impact of environmental factors, which along with changes in diet and lifestyle may contribute to a worrisome increase in early-onset cancers, a situation viewed as a potential emerging global epidemic [2]. Conventional chemotherapy, one of the oldest anticancer weapons brought in late 1940s, encompasses alkylating agents, antimetabolites, natural products, hormones and steroids. Chemotherapy relies on the concept of eliminating the fast growing cancer cells [1] but adversely affects other fast growing normal cells in the body and lacks specificity. Despite these limitations, cytotoxic chemotherapy is widely used today. Targeted therapies that emerged in the late 1980s are based on the assumption that cancer cells express and rely on the use of various unique targets for their survival. A success story of a targeted BCR-ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec) spurred development of other targeted therapies, many of which effectively eradicated human cancers in animal models but failed to show clinical efficacy. Immunotherapy with monoclonal antibodies is a variation on the theme of targeted therapy. In particular, immune-checkpoint inhibitors do not kill cancer cells directly but instead mobilize the immune system to do the killing. In some cases, high success rates have been noted even in metastatic cancer [3] but substantial concerns remain regarding long-term toxicity [4]. Chimeric antigen receptor (CAR-T) targeted cell therapy has produced remarkable clinical responses with some hematological malignancies but is less effective in solid tumors and is limited by serious toxicities, antigen escape and restricted trafficking [5]. Targeted gene editing using CRISPR (clustered regularly interspaced palindromic repeat) with the bacterial RNA-guided CRISPR-Cas9 system has opened a new chapter in the drug development [6]. Several CRISPR-based products are undergoing clinical trials in patients with leukemias, lymphomas, solid tumors, and other diseases [7]. Whilst the bacterial CRISPR-Cas9 suffers from limited delivery to cells and tissues, a recent discovery of a CRISPR-like eukaryotic system based on the Fanzor protein, which uses RNA for precise DNA targeting, is expected to fa","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10434997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10050587","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 : 2023-06-28eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.581
Florian Dudde, Kai-Olaf Henkel, Filip Barbarewicz
Head and neck tumors are among the most common malignancies [1]. In this anatomical region, squamous cell carcinoma (SCC) is the most common malignant entity [1]. However, there are also other malignant tumors that, unlike SCC, originate in the salivary glands of the head and neck region, such as mucoepidermoid carcinoma or adenoid cystic carcinoma (ACC) [2]. In general, tumors originating from the minor salivary glands often show a higher degree of malignancy than tumors of the major salivary glands (parotid gland, submandibular gland, sublingual gland) [2]. Consequently, the ACC in particular is often localized in the area of the hard palate (small salivary glands). In rare cases, ACC has also been described in other regions of the head and neck region, such as the paranasal sinuses or the tongue [3, 4]. The clinical features of ACC in the head and neck region are often variable. Typically, a swelling of the respective facial region that progresses quickly or slowly, depending on the growth pattern, is often associated with diffuse pain [5]. Furthermore, signs of paralysis and reduced sensitivity in the facial region are possible due to the perineural and perivascular pattern of ACC spread [5]. Most ACC usually show a slow growth pattern with a histologically highly differentiated cell picture, but markedly infiltrative growth behavior [5]. Histologically, the ACC often does not show any increased mitotic rates, which leads in particular to a lack of sensitivity towards chemotherapeutic agents [6]. In advanced ACC, even conventional radiation therapy can sometimes only achieve limited improvement with regard to the long-term outcome of ACC given the low mitotic aspect [6]. Diagnostically, three-dimensional imaging such as computed tomography and/or magnetic resonance imaging offer advantages with regard to tumor spread and the presence of metastases in the sense of tumor staging and provide important information in the context of therapy planning. Typically, ACC can show increased uptake of contrast medium agent with an infiltrative spread pattern in the respective anatomical region (Figure 1) [3].
{"title":"Adenoid cystic carcinoma of the head and neck - treatment strategies of a highly malignant tumor with variable localizations.","authors":"Florian Dudde, Kai-Olaf Henkel, Filip Barbarewicz","doi":"10.18632/oncoscience.581","DOIUrl":"10.18632/oncoscience.581","url":null,"abstract":"Head and neck tumors are among the most common malignancies [1]. In this anatomical region, squamous cell carcinoma (SCC) is the most common malignant entity [1]. However, there are also other malignant tumors that, unlike SCC, originate in the salivary glands of the head and neck region, such as mucoepidermoid carcinoma or adenoid cystic carcinoma (ACC) [2]. In general, tumors originating from the minor salivary glands often show a higher degree of malignancy than tumors of the major salivary glands (parotid gland, submandibular gland, sublingual gland) [2]. Consequently, the ACC in particular is often localized in the area of the hard palate (small salivary glands). In rare cases, ACC has also been described in other regions of the head and neck region, such as the paranasal sinuses or the tongue [3, 4]. The clinical features of ACC in the head and neck region are often variable. Typically, a swelling of the respective facial region that progresses quickly or slowly, depending on the growth pattern, is often associated with diffuse pain [5]. Furthermore, signs of paralysis and reduced sensitivity in the facial region are possible due to the perineural and perivascular pattern of ACC spread [5]. Most ACC usually show a slow growth pattern with a histologically highly differentiated cell picture, but markedly infiltrative growth behavior [5]. Histologically, the ACC often does not show any increased mitotic rates, which leads in particular to a lack of sensitivity towards chemotherapeutic agents [6]. In advanced ACC, even conventional radiation therapy can sometimes only achieve limited improvement with regard to the long-term outcome of ACC given the low mitotic aspect [6]. Diagnostically, three-dimensional imaging such as computed tomography and/or magnetic resonance imaging offer advantages with regard to tumor spread and the presence of metastases in the sense of tumor staging and provide important information in the context of therapy planning. Typically, ACC can show increased uptake of contrast medium agent with an infiltrative spread pattern in the respective anatomical region (Figure 1) [3].","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10115518","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 : 2023-06-27eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.580
Patricia M Gomez Barila, Jan Paul Medema
{"title":"Kinase-targeted therapy in subsets of colorectal cancer.","authors":"Patricia M Gomez Barila, Jan Paul Medema","doi":"10.18632/oncoscience.580","DOIUrl":"10.18632/oncoscience.580","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10295670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9727479","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 : 2023-06-14eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.579
Deepak Bhamidipati, Vivek Subbiah
Neuroendocrine tumors (NETs) encompass a variety of neoplasms which display a wide spectrum of biologic behavior, ranging from the aggressive neuroendocrine carcinoma (NEC) to often indolent well-differentiated NETs. For well-differentiated NETs, somatostatin analogs (SSAs) are widely accepted as an effective frontline therapy for progressive or symptomatic disease; however, subsequent therapy options such as capecitabine/ temozolomide, sunitinib, everolimus, and radionuclide therapy in selected cases are associated with variable response rates (typically less than 20%) and limited progression-free survival. NECs can respond to platinum-based chemotherapy, but responses are typically short lived. There is evidence to suggest that neuroendocrine neoplasms such as small-cell lung cancer (SCLC) and pancreatic NETs are responsive to DNA alkylators such as temozolomide [1, 2]. Recently, lurbinectedin a DNA minor groove inhibitor and marine derivative was shown to inhibit oncogenic transcription through binding to CG-rich sequences near the promoters of protein-coding genes to promote apoptosis and cell-death [3]. Encouraging results from a phase II basket study of lurbinectedin as a second-line treatment for patients with SCLC, which demonstrated a 35% response rate, resulted in the FDA-approval of lurbinectedin in pre-treated patients with SCLC [4]. Moreover, in a subset analysis lurbinectedin was shown to effective treatment for platinum-sensitive relapsed SCLC, especially in patients with chemotherapy-free interval (CTFI) ≥180 days with an objective response rate of over 60% [5]. It was shown to be active in BRCA1/2 germline mutated breast cancer [6]. In addition
{"title":"Lurbinectedin, a DNA minor groove inhibitor for neuroendocrine neoplasms beyond small cell lung cancer.","authors":"Deepak Bhamidipati, Vivek Subbiah","doi":"10.18632/oncoscience.579","DOIUrl":"10.18632/oncoscience.579","url":null,"abstract":"Neuroendocrine tumors (NETs) encompass a variety of neoplasms which display a wide spectrum of biologic behavior, ranging from the aggressive neuroendocrine carcinoma (NEC) to often indolent well-differentiated NETs. For well-differentiated NETs, somatostatin analogs (SSAs) are widely accepted as an effective frontline therapy for progressive or symptomatic disease; however, subsequent therapy options such as capecitabine/ temozolomide, sunitinib, everolimus, and radionuclide therapy in selected cases are associated with variable response rates (typically less than 20%) and limited progression-free survival. NECs can respond to platinum-based chemotherapy, but responses are typically short lived. There is evidence to suggest that neuroendocrine neoplasms such as small-cell lung cancer (SCLC) and pancreatic NETs are responsive to DNA alkylators such as temozolomide [1, 2]. Recently, lurbinectedin a DNA minor groove inhibitor and marine derivative was shown to inhibit oncogenic transcription through binding to CG-rich sequences near the promoters of protein-coding genes to promote apoptosis and cell-death [3]. Encouraging results from a phase II basket study of lurbinectedin as a second-line treatment for patients with SCLC, which demonstrated a 35% response rate, resulted in the FDA-approval of lurbinectedin in pre-treated patients with SCLC [4]. Moreover, in a subset analysis lurbinectedin was shown to effective treatment for platinum-sensitive relapsed SCLC, especially in patients with chemotherapy-free interval (CTFI) ≥180 days with an objective response rate of over 60% [5]. It was shown to be active in BRCA1/2 germline mutated breast cancer [6]. In addition","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10266487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10029380","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 : 2023-06-09eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.578
Elinor Nemlander, Marcela Ewing, Axel C Carlsson, Andreas Rosenblad
Cancer remains a significant global health burden, and early detection plays a crucial role in improving patient outcomes. Primary care settings serve as frontline gatekeepers, providing an opportunity for early detection through symptom assessment and targeted screening. However, detecting early-stage cancer and identifying individuals at high risk can be challenging due to the complexity and subtlety of symptoms [1]. The challenging nature of early detection is revealed by diagnostic errors in primary care, with cancer being one of the most frequently missed or delayed diagnoses [2]. In recent years, the emergence of machine learning (ML) techniques has shown promise in revolutionizing early detection efforts [3]. This editorial explores the potential of ML in enhancing early cancer detection in primary care.
{"title":"Transforming early cancer detection in primary care: harnessing the power of machine learning.","authors":"Elinor Nemlander, Marcela Ewing, Axel C Carlsson, Andreas Rosenblad","doi":"10.18632/oncoscience.578","DOIUrl":"10.18632/oncoscience.578","url":null,"abstract":"Cancer remains a significant global health burden, and early detection plays a crucial role in improving patient outcomes. Primary care settings serve as frontline gatekeepers, providing an opportunity for early detection through symptom assessment and targeted screening. However, detecting early-stage cancer and identifying individuals at high risk can be challenging due to the complexity and subtlety of symptoms [1]. The challenging nature of early detection is revealed by diagnostic errors in primary care, with cancer being one of the most frequently missed or delayed diagnoses [2]. In recent years, the emergence of machine learning (ML) techniques has shown promise in revolutionizing early detection efforts [3]. This editorial explores the potential of ML in enhancing early cancer detection in primary care.","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10254750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9673645","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 : 2023-05-11eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.575
Melisa Husein, Patrick Petignat, Marie Cohen
{"title":"UPR-induced ovarian cancer cell fusion: a mechanism favoring drug resistance?","authors":"Melisa Husein, Patrick Petignat, Marie Cohen","doi":"10.18632/oncoscience.575","DOIUrl":"10.18632/oncoscience.575","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10174630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10290144","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 : 2023-03-23eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.573
David Rubio-Mangas, Mariano García-Arranz, Javier Suela, Damian García-Olmo
Colorectal cancer (CRC) is a heterogeneous disease that occurs in the colon and the rectum, parts of the gastrointestinal system [1]. CRC is the third leading cause of cancer-related death worldwide [2]. The incidence and mortality of CRC is expected to increase significantly in the future, with more than 2.2 million new cases and 1.1 million deaths expected by 2030 [3]. Metastasis is the leading cause of death in CRC patients, especially liver metastasis. According to previous studies, about 25% of CRC cases are clinically diagnosed with liver metastases in early stages, and about 50% of CRC patients experience symptoms of liver metastases throughout the course of the disease [4–6]. Differential presence of exons (DPE) by nextgeneration sequencing (NGS) is an innovative method to analyze the complete exome sequence and can be used as a stratification and predictive tool in patients with colorectal cancer (CRC) [7, 8]. CRC is one of the most common neoplasms worldwide, and often presents at advanced stages, making it difficult to treat and decreasing survival rates [9].
{"title":"New method of clustering colorectal cancer patients using differential presence of exons (DPE) sequencing.","authors":"David Rubio-Mangas, Mariano García-Arranz, Javier Suela, Damian García-Olmo","doi":"10.18632/oncoscience.573","DOIUrl":"10.18632/oncoscience.573","url":null,"abstract":"Colorectal cancer (CRC) is a heterogeneous disease that occurs in the colon and the rectum, parts of the gastrointestinal system [1]. CRC is the third leading cause of cancer-related death worldwide [2]. The incidence and mortality of CRC is expected to increase significantly in the future, with more than 2.2 million new cases and 1.1 million deaths expected by 2030 [3]. Metastasis is the leading cause of death in CRC patients, especially liver metastasis. According to previous studies, about 25% of CRC cases are clinically diagnosed with liver metastases in early stages, and about 50% of CRC patients experience symptoms of liver metastases throughout the course of the disease [4–6]. Differential presence of exons (DPE) by nextgeneration sequencing (NGS) is an innovative method to analyze the complete exome sequence and can be used as a stratification and predictive tool in patients with colorectal cancer (CRC) [7, 8]. CRC is one of the most common neoplasms worldwide, and often presents at advanced stages, making it difficult to treat and decreasing survival rates [9].","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10037527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9559554","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 : 2023-01-30eCollection Date: 2023-01-01DOI: 10.18632/oncoscience.572
Nidhi Garg, Mangesh A Thorat
{"title":"HER2 expression should be routinely evaluated in DCIS to avoid under or overtreatment!","authors":"Nidhi Garg, Mangesh A Thorat","doi":"10.18632/oncoscience.572","DOIUrl":"10.18632/oncoscience.572","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9890724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9198012","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}
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