{"title":"Neoadjuvant Chemotherapy for Adults with Osteogenic Sarcoma.","authors":"Michael J Robinson, Elizabeth J Davis","doi":"10.1007/s11864-024-01269-2","DOIUrl":"10.1007/s11864-024-01269-2","url":null,"abstract":"<p><strong>Opinion statement: </strong>Osteosarcoma is the most common primary malignant bone tumor in adolescents and adults. The 5-year survival rate is 65% when localized; however, survival drops dramatically to 10-20% in cases of metastatic disease. Therapy for osteosarcoma saw its first significant advancement in the 1970-80's, with the introduction of our current standard of care, consisting of the neo/adjuvant treatment regimen methotrexate, doxorubicin (Adriamycin), and cisplatin (collectively referred to as MAP) and surgical resection. Since MAP, development of a better therapeutic approach has stalled, creating a plateau in patient outcomes that has persisted for 40 years. Despite substantial research into a variety of pathways for novel treatment options, clinical trials have not produced sizeable improvements in outcomes. In this article, we discuss our current neoadjuvant standard of care therapy, followed by a review of contemporary therapeutic options, including tyrosine kinase inhibitors (TKIs), immune checkpoint inhibitors (ICIs), monoclonal antibodies (mAbs), and chimeric antigen receptor (CAR) T cells. Lastly, we consider the challenges hindering the success of novel treatment options and future research directions.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1366-1373"},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tarlatamab-dlle: A New Hope for Patients with Extensive-Stage Small-Cell Lung Cancer.","authors":"Parveen Kumar Goyal, Kavita Sangwan","doi":"10.1007/s11864-024-01268-3","DOIUrl":"10.1007/s11864-024-01268-3","url":null,"abstract":"<p><strong>Opinion statement: </strong>Lung cancer is expected to contribute to about 0.234 million new cases and about 0.125 million mortalities in the United States in the year 2024. Small cell lung cancer (SCLC), a neuroendocrine carcinoma, has lesser prevalence but is more aggressive at an extensive stage where the tumor is not only confined to hemithorax, mediastinum, and supraclavicular region but spread beyond the supraclavicular region. The prognosis of SCLC, irrespective of the limited or extensive stage, is very poor. Only a 5-10% overall survival rate in five years is expected and with extensive-stage SCLC, long-term disease-free survival is rare. In May 2024, the USFDA approved Tarlatamab-dlle, a DLL3 targeted bi-specific T-cell engager, for treating extensive-stage SCLC in adult patients, on or after platinum-based chemotherapy or on progression. Before the approval of Tarlatamab-dlle, only a few drugs, such as Atezolizumab and Durvalumab, received FDA approval for treating extensive-stage SCLC. It might be possible that Tarlatamab-dlle received accelerated FDA approval for extensive-stage SCLC, leaving some questions unanswered at this stage. This manuscript is focused on clinical, pre-clinical, and other pharmacological aspects of Tarlatamab-dlle for extensive-stage SCLC.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1337-1344"},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142401860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Acquired Bortezomib Resistance in Multiple Myeloma: From Mechanisms to Strategy.","authors":"Fangfang Li, Jing Liu, Yunfeng Fu","doi":"10.1007/s11864-024-01273-6","DOIUrl":"10.1007/s11864-024-01273-6","url":null,"abstract":"<p><strong>Opinion statement: </strong>Multiple myeloma (MM) is a heterogeneous plasma cell tumor with a survival period of several months to over ten years. Despite the development of various new drugs, MM is still incurable and recurs repeatedly. Bortezomib, a landmark event in the history of MM treatment, has dramatically improved the prognosis of patients with MM. Although proteasome inhibitors (PIs) represented by bortezomib, have greatly prolonged MM survival, unfortunately, almost all MM will develop bortezomib resistance, leading to relapse with a shorter survival. It has been reported that both the tumor microenvironment and myeloma cells drive bortezomib resistance. Multiple treatment methods have been attempted to overcome bortezomib resistance, but unfortunately, there has been no breakthrough. It is believed that the key resistance mechanism has not yet been discovered. A deeper understanding of the mechanism of bortezomib resistance and strategies to overcome it can help identify key resistance mechanisms and further improve the prognosis of MM.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1354-1365"},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Immunotherapy in the Fight Against Bone Metastases: A Review of Recent Developments and Challenges.","authors":"Zhonghui Peng, Wei Huang, Ziyu Xiao, Jinge Wang, Yongzhe Zhu, Fudou Zhang, Dongqiang Lan, Fengjiao He","doi":"10.1007/s11864-024-01256-7","DOIUrl":"10.1007/s11864-024-01256-7","url":null,"abstract":"<p><strong>Opinion statement: </strong>Bone metastasis, a frequent and detrimental complication of advanced cancers, often triggers bone deterioration events that severely compromise patient quality of life and prognosis. The past few years have witnessed the emergence and continuous advancements in immunotherapy, ushering in innovative therapeutic prospects for bone metastasis. These advancements include not only the use of immune checkpoint inhibitors (ICIs), both as standalone and combined treatments, but also the investigation of novel targets within immune cells residing in bone metastases. These breakthroughs have instilled fresh optimism for effectively managing patients with bone metastasis. This article endeavors to present an exhaustive review of the recent progress made across a spectrum of immunotherapeutic strategies and targeted therapies specifically designed for individuals battling bone metastasis from malignant tumors. By doing so, it seeks to offer insights that can inform clinical practices and guide further medical research in this domain.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1374-1389"},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chunxiao He, Zilong Wang, Jiaying Yu, Shuang Mao, Xi Xiang
{"title":"Current Drug Resistance Mechanisms and Treatment Options in Gastrointestinal Stromal Tumors: Summary and Update.","authors":"Chunxiao He, Zilong Wang, Jiaying Yu, Shuang Mao, Xi Xiang","doi":"10.1007/s11864-024-01272-7","DOIUrl":"10.1007/s11864-024-01272-7","url":null,"abstract":"<p><strong>Opinion statement: </strong>Gastrointestinal stromal tumor (GIST) is characterized by well-defined oncogenes. Despite the significant improvement in treatment outcomes with adjuvant imatinib therapy for patients, drug resistance remains a major challenge for GIST therapy. This review focuses on the mechanisms contributing to drug resistance phenotype in GIST, such as primary imatinib-resistant mutants, secondary mutations, non-covalent binding of TKI to its target, tumor heterogeneity, re-activation of pro-survival/proliferation pathways through non-KIT/PDGFRA kinases, and loss of therapeutic targets in wild-type GIST. Corresponding suggestions are proposed to overcome drug-resistance phenotype of GIST. This review also summarizes the suitability of currently approved TKIs on different KIT/PDGFRA mutations and updates related clinical trials. Recent potent drugs and emerging strategies against advanced GISTs in clinical trials are presented. Additionally, metabolic intervention offers a new avenue for clinical management in GIST. A landscape of metabolism in GIST and metabolic changes under imatinib treatment are summarized based on currently published data. The OXPHOS pathway is a promising therapeutic target in combination with TKI against sensitive KIT/PDGFRA mutants. Comprehensive understanding of the above resistance mechanisms, experimental drugs/strategies and metabolic changes is critical to implement the proper therapy strategy and improve the clinical therapy outcomes for GIST.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1390-1405"},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142512324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Respiratory Depression Associated with Opioids: A Narrative Review.","authors":"Mellar P Davis, Sandra DiScala, Amy Davis","doi":"10.1007/s11864-024-01274-5","DOIUrl":"10.1007/s11864-024-01274-5","url":null,"abstract":"<p><strong>Opinion: </strong>All opioids have a risk of causing respiratory depression and reduced cerebral circulation. Fentanyl has the greatest risk of causing both. This is particularly a concern when combined with illicit opioids such as diamorphine (also known as heroin). Fentanyl should not be used as a frontline potent opioid due its significant risks. Buprenorphine, a schedule III opioid, morphine, or hydromorphone is preferred, followed by oxycodone, which has a significant risk of abuse relative to buprenorphine and morphine. Although all opioids were equally effective in producing analgesia, the relative safety of each opioid is no longer a secondary concern when prescribing. In the face of an international opioid epidemic, clinicians need to choose opioid analgesics safely, wisely, and carefully.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1438-1450"},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Guoxin Qu, Chunlei Zhang, Zhichao Tian, Weitao Yao
{"title":"Diagnosis and Treatment of Myxoid Liposarcoma.","authors":"Guoxin Qu, Chunlei Zhang, Zhichao Tian, Weitao Yao","doi":"10.1007/s11864-024-01262-9","DOIUrl":"10.1007/s11864-024-01262-9","url":null,"abstract":"<p><strong>Opinion statement: </strong>Myxoid liposarcoma (MLS) is a rare subtype of soft tissue sarcoma that distinguishes itself from conventional subtypes through its propensity for extrapulmonary metastasis. The distinctive magnetic resonance imaging (MRI) characteristics of MLS render it an invaluable tool for identifying primary and secondary lesions. Pathologically, MLS is characterized by the FUS-DDIT3 gene fusion. Accurate diagnosis, facilitated by MRI and pathological assessment, is critical for prognostication and the formulation of appropriate treatment strategies. Surgery remains the cornerstone of local management for MLS. The combination of surgery and radiotherapy can significantly reduce the local recurrence rate in MLS, as it is highly sensitive to both radiotherapy and chemotherapy. Additionally, for high-risk MLS cases with a large tumor diameter, chemotherapy has been shown to improve survival. The comprehensive treatment approach for MLS demonstrates superior local recurrence rates and survival rates compared to most soft tissue sarcomas. Current research focuses on developing effective therapies for unresectable or advanced disease based on genomic and phenotypic characteristics as well as the immune-tumor microenvironment.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1289-1296"},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marko Velimirovic, Matthew Brignola, Emily Chheng, Michael Smith, Khaled A Hassan
{"title":"Management of Pulmonary Toxicities Associated with Systemic Therapy in Non Small Cell Lung Cancer.","authors":"Marko Velimirovic, Matthew Brignola, Emily Chheng, Michael Smith, Khaled A Hassan","doi":"10.1007/s11864-024-01257-6","DOIUrl":"10.1007/s11864-024-01257-6","url":null,"abstract":"<p><strong>Opinion statement: </strong>Drug-induced pneumonitis is a common adverse event that may occur during lung cancer systemic therapy. The incidence/prevalence of this side effect has increased due to recent extensive use of immunotherapy. Although pneumonitis prevalence is increased with the use of immune checkpoint inhibitors, it is also associated with chemotherapy and targeted therapy. Pneumonitis can occur early after drug exposure or present after several cycles of treatment. Its severity can range from insidious to fulminant, leading to hospitalization. In most cases, the diagnosis is made based on medical history, temporal correlation with use of lung cancer systemic therapy, and computed tomography (CT) findings. In the majority of cases, stopping the offending drug and use of corticosteroids is the sufficient treatment; however, patients with more severe forms of pneumonitis require additional immunosuppressive agents. In this review, we address pneumonitis caused by chemotherapy, antibody-drug conjugates, targeted therapy, or immunotherapy, and provide a detailed management approach.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1297-1311"},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11485481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhongqi Wu, Tianxin Lyu, Leizhen Wu, Hui Yang, Wenqiang Li
{"title":"The Role of SIRT1 in Leukemia.","authors":"Zhongqi Wu, Tianxin Lyu, Leizhen Wu, Hui Yang, Wenqiang Li","doi":"10.1007/s11864-024-01265-6","DOIUrl":"10.1007/s11864-024-01265-6","url":null,"abstract":"<p><strong>Opinion statement: </strong>Leukemia is a type of hematological malignancy (HM) caused by uncontrolled proliferation, apoptosis, and differentiation of hematopoietic stem cells (HSCs). Leukemia cells proliferate greatly in the bone marrow (BM), infiltrate other tissues and organs, and affect the normal hematopoietic function. Although the emergence of new targeted agents and immune agents has improved the prognosis of patients, due to the complex pathogenic factors and heterogeneity of leukemia, there are still some patients with poor prognosis. Recent studies have shown that silent information regulator 1 (SIRT1) is involved in the proliferation, apoptosis, metabolism, and senescence of leukemia cells. As a double-edged sword in leukemia cells, SIRT1 can both promote and inhibit the growth of leukemia cells. Since its mechanism of action has not been elucidated, it is urgent to explore the regulatory mechanism of SIRT1 in leukemia. In this review, we discussed the mechanisms of SIRT1 in different aspects of leukemia, providing a theoretical basis for the treatment of patients with leukemia.</p>","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1283-1288"},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142362452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Muriel R Battaglia, Joseph Cannova, Rafael Madero-Marroquin, Anand A Patel
{"title":"Correction to: Treatment of Anemia in Lower-Risk Myelodysplastic Syndrome.","authors":"Muriel R Battaglia, Joseph Cannova, Rafael Madero-Marroquin, Anand A Patel","doi":"10.1007/s11864-024-01263-8","DOIUrl":"10.1007/s11864-024-01263-8","url":null,"abstract":"","PeriodicalId":50600,"journal":{"name":"Current Treatment Options in Oncology","volume":" ","pages":"1335"},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}