Malignancy Spectrum最新文献

{"title":"Mirdametinib (Gomekli) wins FDA approval, bringing relief to NF-1 patients with surgically inoperable plexiform neurofibromatosis worldwide","authors":"Memuna J. Zeb","doi":"10.1002/msp2.70020","DOIUrl":"https://doi.org/10.1002/msp2.70020","url":null,"abstract":"<p>Neurofibromatosis type 1 (NF-1) is an autosomal dominant, complex multi-system disorder that primarily affects the skin and nervous system. It is characterized by mutations in the <i>NF1</i> gene on chromosome 17, leading to abnormal production of neurofibromin protein. Common symptoms include café au lait spots, Lisch nodules, neurofibromas, plexiform neurofibromas, scoliosis, vision disorders, and learning and mental disabilities [<span>1</span>]. Managing NF-1 can be challenging because it is a lifelong disorder in which chronic pain is a prominent feature; consequently, opioids are prescribed and somnolence is frequently reported. Surgical interventions to remove tumors can also result in long-term physical impairments [<span>2</span>]. In recent years, new treatments like Selumetinib (Koselugo) have been approved. However, its effectiveness is mainly limited to children, and it can cause adverse effects like vomiting, raised creatinine phosphokinase, dry skin, and diarrhea [<span>3</span>]. A new development is the U.S. Food and Drug Administration's (FDA) approval on February 11, 2025 of mirdametinib (Gomekli), a mitogen-activated protein kinase kinase (MEK) inhibitor, for the treatment of adults and pediatric patients aged 2 years and older with NF-1-associated surgically inoperable plexiform neurofibromas. [<span>4</span>].</p><p>Loss of neurofibromin protein in NF-1 patients causes Ras signaling dysregulation. This results in MEK hyperactivation, driving uncontrolled cell growth and tumor formation. Mirdametinib, a specific noncompetitive MEK inhibitor (MEKi), blocks MEK activity, reducing hyperactivation of Ras and shrinkage of surgically inoperable plexiform neurofibromatosis. A Phase II trial assessed the safety and efficacy of mirdametinib in adolescents and adults of age ≥ 16 years with <i>NF1</i>-related plexiform neurofibromas. The results showed that mirdametinib is well-tolerated and effective, with a 42% partial response rate and at least 20% tumor shrinkage by volume [<span>5</span>].</p><p>The ReNeu trial, a pivotal Phase IIb study, evaluated the efficacy of mirdametinib in 114 patients. The results demonstrated a substantial confirmed objective response rate, durable reductions in plexiform neurofibromas volume, and clinically meaningful improvements in pain and health-related quality of life [<span>6</span>]. Crucially, mirdametinib stands out as a treatment distinct from traditional approaches like selumetinib, as it has been proved to be effective in the treatment for both children and adults.</p><p>Although mirdametinib represents a breakthrough for plexiform neurofibromas in NF-1, it carries a broad side-effect profile. Most commonly, cutaneous toxicities, including acneiform rash, eczema, seborrheic dermatitis, paronychia, and xerosis, have been reported [<span>7</span>], along with fatigue, profound changes in bile acid metabolism leading to nausea, vomiting, diarrhea [<span>8</span>], as well as MEKi-associated re","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"171-172"},"PeriodicalIF":0.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197086","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}

{"title":"Chemotherapy + immunotherapy + anti-vascular therapy and firmonertinib + capmatinib prolong OS in EGFR-mutated and MET amplification following disease progression on osimertinib plus savolitinib: A case report of NSCLC","authors":"Ting Xu,&nbsp;Xiaohua Wang,&nbsp;Wanlin Shen,&nbsp;Mingxia Yang","doi":"10.1002/msp2.70018","DOIUrl":"https://doi.org/10.1002/msp2.70018","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Backgound</h3>\u0000 \u0000 <p>The combination of osimertinib and savolitinib as second-line treatment after epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance can significantly improve median progression-free survival (mPFS), objective response rate (ORR), and duration of remission (DOR). The combination therapy is safe and controllable, with no new safety signals or unexpected toxicity. However, the mechanism of drug resistance for tumor progression after dual-targeted therapy is currently unclear, and there is no clinical data reference for treatment after drug resistance. This case suggests some treatment options for lung adenocarcinoma patient after dual-targeted therapy with osimertinib and savolitinib.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case presentation</h3>\u0000 \u0000 <p>A patient with <i>EGFR</i>-mutated lung adenocarcinoma developed mesenchymal–epithelial transition factor (<i>MET</i>) amplification-related resistance after first-line almonertinib. Subsequent sequential regimens—osimertinib plus savolitinib, chemo-immuno-antiangiogenesis therapy, and finally furmonertinib plus capmatinib—each yielded transient benefit.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The report shows that the combination of chemotherapy and immunotherapy, as well as the dual-targeted therapy of firmonertinib and capmatinib, prolonged the overall survival of the patient.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This case suggests some treatment options for lung adenocarcinoma patient after dual-targeted therapy with osimertinib and savolitinib. The results indicated that traditional treatment or the combination of MET-TKI with another targeted therapy may improve the prognosis of patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"151-158"},"PeriodicalIF":0.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197085","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}

{"title":"Immune infiltration in TP53 missense mutant contributes to poor prognosis in hepatocellular carcinoma, unlike CTNNB1 mutations","authors":"Durgadevi Veeraiyan,&nbsp;Vishnu Kurpad,&nbsp;Vinayak Munirathnam,&nbsp;Chaitra V.,&nbsp;Sonal Asthana,&nbsp;Akhileshwar Namani,&nbsp;Tapas Patra","doi":"10.1002/msp2.70015","DOIUrl":"https://doi.org/10.1002/msp2.70015","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Hepatocellular carcinoma (HCC) is one of the deadliest cancer over the world. In this study, we aimed to determine the most critical molecular event in HCC patients with tumor protein p53 (<i>TP53</i>) or catenin beta 1 (<i>CTNNB1</i>) mutations, and to explore how these two mutations differ in their impact on HCC prognostication.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We performed an integrated comparative analysis of exome and transcriptome data from The Cancer Genome Atlas (TCGA) for HCC patients. Patient prognosis and correlation with the immune infiltration characteristics were performed. HCC cell line based in vitro experiments were also performed to validate the mechanistic insights.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The 3-year progression-free survival (PFS) analysis of HCC patients with <i>TP53</i> mutations indicated a significantly poorer clinical outcome compared to those with <i>CTNNB1</i> mutations. Functional annotation of the <i>TP53</i> mutant cohort revealed a substantial upregulation of genes associated with immune regulation, while the <i>CTNNB1</i> mutant cohort displayed a prominent activation of metabolic pathways. Further comparative analysis and in vitro experiments showed that <i>TP53</i> missense mutations activated the signal transducer and activator of transcription 3 (STAT3) signaling pathway, which fostered neutrophil infiltration and enhanced the enrichment of regulatory T (Treg) cells by secreting specific inflammatory molecules in the tumor microenvironment. Notably, treatment with a an STAT3 inhibitor suppressed the expression of these inflammatory molecules, underscoring how an immunosuppressive tumor microenvironment in the <i>TP53</i> mutant cohort contributes to a poor prognosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our study provides valuable insights, revealing that HCC patients with <i>TP53</i> missense mutations exhibit a distinct immune profile associated with poorer clinical outcome compared to those with <i>CTNNB1</i> mutations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"117-127"},"PeriodicalIF":0.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197084","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}

{"title":"Fetuin-A:adiponectin ratio (FAR) as a critical biomarker in obesity-induced colorectal cancer?","authors":"Chandrani Fouzder,&nbsp;Subhadip Mukhopadhyay,&nbsp;Aditi Banerjee,&nbsp;Suprabhat Mukherjee","doi":"10.1002/msp2.70021","DOIUrl":"https://doi.org/10.1002/msp2.70021","url":null,"abstract":"&lt;p&gt;Obesity is one of the burning lifestyle-related health problems of the current generation, affecting more than one-third of the global population. Obese individuals face a severe risk of various cancers, particularly concerning colorectal cancer (CRC), which has an extremely low survival rate among affected patients [&lt;span&gt;1&lt;/span&gt;]. In fact, obesity is linked to 4%–8% of global cancer cases, and obese cancer patients face a 17% higher risk of mortality [&lt;span&gt;2&lt;/span&gt;]. A recent report examined the relationship between obesity and four obesity-related cancers, namely cancers of the colon, rectum, pancreas, and kidney [&lt;span&gt;2&lt;/span&gt;]. The study analyzed cancer incidence data from 42 countries and found positive correlation coefficients of 0.27 and 0.33 for colon cancer and rectal cancer, respectively [&lt;span&gt;2&lt;/span&gt;]. Obesity-related CRC is associated with chronic low-grade inflammation, which may promote the progression of colorectal neoplasia through the inflammation–dysplasia–tumor sequence, particularly in early-onset cases. [&lt;span&gt;3&lt;/span&gt;]. The risk of CRC in overweight/obese women under 50 years old has doubled, and a high-fat diet (HFD) consumed by a mother can lead to CRC in both mother and foetus [&lt;span&gt;4&lt;/span&gt;]. Obesity modulates the CRC microenvironment, where the fat components are readily taken up by the tumor but not the CD8&lt;sup&gt;+&lt;/sup&gt; T cells, thereby blocking tumor infiltration and blunting cancer immunotherapy [&lt;span&gt;5&lt;/span&gt;]. In fact, HFD causes metabolic dysregulation by gut microbiota, increases the levels of lysophosphatidic acid, and promotes colorectal tumorigenesis [&lt;span&gt;6, 7&lt;/span&gt;]. Similarly, the increase in the levels of palmitic acid in the blood caused by an HFD, which then leads to the activation of Toll-like receptor 4 (TLR4) in the colonic tissue, promotes growth, inflammatory pathogenesis, and CRC metastasis, and is directly associated with poor survival rates in patients with CRC [&lt;span&gt;8&lt;/span&gt;]. Among the events, obesity-induced and/or obesity-associated pro-inflammatory milieu is majorly signaled by the adipokine, called fetuin-A or alpha-2-Heremans-Schmid glycoprotein (AHSG), whose serum level is positively correlated with visceral adipose tissue mass and body mass index (BMI, &gt;30 kg/m&lt;sup&gt;2&lt;/sup&gt;). Fetuin-A binds to TLR4 to induce inflammation-mediated fatty colon, interacts with membrane annexins (II and VI), and activates the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway to promote the proliferation of CRC cells. In contrast, adiponectin, a 30-kDa adipokine secreted by the adipocytes, prevents obesity through anti-inflammatory and hypolipidemic actions, and low adiponectin levels are associated with obesity, other inflammatory diseases, and poor prognosis across multiple cancer subtypes, including CRC [&lt;span&gt;8&lt;/span&gt;]. Individuals with the highest serum levels of adiponectin possess around 60% less risk of CRC. Exogeneous adiponectin treatment was found to restric","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"167-170"},"PeriodicalIF":0.0,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197037","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}

{"title":"Multimodal management and outcome of pediatric and adolescent malignant central nervous system tumors: A single-center retrospective study","authors":"Priyadharshini Veeralakshmanan,&nbsp;Wesley M. Jose,&nbsp;Suhas Udayakumaran,&nbsp;M. R. Bindhu,&nbsp;Debnarayan Dutta,&nbsp;Kannan Rajesh,&nbsp;Sruthi Kavalagunta,&nbsp;Renjitha Bhaskaran,&nbsp;Nikhil K. Haridas,&nbsp;M. P. Rakesh,&nbsp;Keechilat Pavithran","doi":"10.1002/msp2.70019","DOIUrl":"https://doi.org/10.1002/msp2.70019","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>There is a paucity of real-world evidence in the Indian context to address the outcome of primary brain tumors (PBTs) in children. This study aimed to describe the demographic profile, clinical characteristics, and histological features of PBTs based on the 2016 World Health Organization classification, assess the efficacy of treatment methods, and identify the factors that influence the outcome.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methodology</h3>\u0000 \u0000 <p>This is a single-institution, hospital-based study. Data were collected for pediatric patients aged 0−19 years, from September 2001 to May 2023 (22 years), who were diagnosed with malignant PBTs. Patients with radiologically or histologically proven tumors were included. Those with metastatic disease to the central nervous system were excluded. The overall survival (OS) and recurrence-free survival (RFS) were estimated using the Kaplan–Meier method.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 251 patients with pediatric brain tumors were included in this analysis. The mean age was 9.10 ± 5.54 years. The male-to-female ratio was 1.20:1. In this cohort, the most common histologies were medulloblastoma and astrocytoma. The mean survival of all patients with PBTs was 141.00 ± 7.90 months with 1-, 3-, and 8-year OS rates of 79.00%, 67.00%, and 60.00%, respectively. Medulloblastoma had 1-, 3-, and 8-year OS rates of 81.00%, 72.00%, and 65.00%, respectively. The 1-year OS rates for glioblastoma and brainstem glioma were 46.00% and 45.00%, respectively. Complete tumoral resection showed longer survival than lesser degrees of resection (<i>p</i> = 0.001). Embryonal tumors (ETs) had a better RFS of 133.60 ± 12.70 months (<i>p</i> ≤ 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>ETs have a better prognosis than glial tumors. With an improved OS, the surgical resection extent has a favorable outcome. As a chemosensitive tumor, medulloblastoma benefits most from systemic treatment and responds well to a multimodal approach.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"128-139"},"PeriodicalIF":0.0,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197038","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}

{"title":"Clinical efficacy of Xiaoyao San combined with Bazhen Decoction in the treatment of insomnia in postoperative breast cancer patients","authors":"Feifei Lv,&nbsp;Xin Zhang,&nbsp;Liang Wang,&nbsp;Shaodan Li,&nbsp;Fagen Li","doi":"10.1002/msp2.70016","DOIUrl":"https://doi.org/10.1002/msp2.70016","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aimed to evaluate the effects of Xiaoyao San combined with Bazhen Decoction on insomnia in patients following breast cancer surgery.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 86 patients experiencing insomnia after breast cancer surgery were randomly assigned to either the treatment group or the control group. The treatment group received Xiaoyao San combined with Bazhen Decoction, while the control group was treated with estazolam tablets. The treatment duration was 4 weeks. Pittsburgh Sleep Quality Index (PSQI) scores were assessed before and after treatment. The overall efficacy and incidence of adverse reactions were compared between the two groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>PSQI scores in both groups significantly decreased after treatment (<i>p</i> &lt; 0.05). Total effective rate in the treatment group (93.02%) was higher than that in the control group (86.05%), although the difference was not statistically significant (<i>p</i> &gt; 0.05). The incidence of adverse reactions in the treatment group (4.65%) was significantly lower than that in the control group (20.93%) (<i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Xiaoyao San combined with Bazhen Decoction can effectively improve sleep quality in patients with insomnia following breast cancer surgery, demonstrating good clinical efficacy and fewer adverse reactions. Further studies are needed to confirm these findings and explore broader clinical applications.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"145-150"},"PeriodicalIF":0.0,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145196845","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}

{"title":"Primary mediastinal synovial sarcoma in an infant: A case report","authors":"Şule Çalışkan Kamış,&nbsp;Begül Yağcı","doi":"10.1002/msp2.70017","DOIUrl":"https://doi.org/10.1002/msp2.70017","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Primary mediastinal synovial sarcoma (PMSS) is an uncommon and aggressive soft tissue tumor, particularly rare in infants. Its diagnosis is challenging due to overlapping features with other thoracic neoplasms and requires integration of histopathology, immunohistochemistry, and molecular genetics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case presentation</h3>\u0000 \u0000 <p>We present a case of a 4-month-old girl admitted with respiratory distress and found to have a large posterior mediastinal mass. Histopathology and immunohistochemistry were compatible with biphasic synovial sarcoma. However, molecular confirmation via detection of <i>SS18-SSX</i> fusion was not performed. Despite multimodal chemotherapy, the tumor progressed, and complete surgical resection was unachievable. The patient died during follow-up in the pediatric intensive care unit.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Accurate diagnosis is critically dependent on <i>SS18-SSX</i> molecular testing, particularly in infants. Incomplete resection and lack of genetic confirmation may contribute to poor prognosis. Literature supports that complete resection is the only consistent predictor of survival. This case illustrates the limitations and consequences of managing PMSS without molecular confirmation or complete resection. A multidisciplinary approach with current diagnostic standards is essential in these high-risk pediatric tumors.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"163-166"},"PeriodicalIF":0.0,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145196797","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}

{"title":"Pleural cavitations and pneumothorax following axitinib therapy in metastatic renal cell carcinoma: A case report","authors":"Feride Yılmaz,&nbsp;Serkan Yaşar,&nbsp;Figen Demirkazık,&nbsp;Zafer Arık,&nbsp;Mustafa Erman","doi":"10.1002/msp2.70014","DOIUrl":"https://doi.org/10.1002/msp2.70014","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Tumor cavitation and pneumothorax are uncommon yet serious complications of antiangiogenic therapies. These risks are particularly significant in patients with metastatic renal cell carcinoma (mRCC). Axitinib, a selective inhibitor of vascular endothelial growth factor receptors (VEGFRs), is generally used as a second-line treatment for mRCC. However, rare cases of lung metastases with cavitary lesions and pneumothorax have been reported after the use of axitinib. Therefore, we decided to report one of these rare cases.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case presentation</h3>\u0000 \u0000 <p>A 46-year-old male with mRCC developed pleural cavitations and secondary pneumothorax after starting axitinib therapy. Despite intensive management, his condition worsened with recurrent pneumothorax, ultimately leading to sepsis and multiorgan failure.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This case underscores the potential risks of tumor cavitation-induced pneumothorax in patients receiving axitinib. Close radiological monitoring and timely intervention are essential for reducing morbidity and mortality in such cases. Clinicians should remain vigilant for this rare but serious complication during axitinib therapy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"159-162"},"PeriodicalIF":0.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145197015","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}

{"title":"A follow-up study of 25 patients with pancreatic cancer receiving gemcitabine and cisplatin and 21-h infusional 5-fluorouracil","authors":"Mozaffar Aznab,&nbsp;Arash Golpazir Sorkheh,&nbsp;Kiumars Eslsm Pia,&nbsp;Sayed Javad Hossini,&nbsp;Fatemeh Heydarpour","doi":"10.1002/msp2.70013","DOIUrl":"https://doi.org/10.1002/msp2.70013","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The purpose of this study was to assess clinical characteristics and survival of patients with advanced pancreatic cancer who were treated with gemcitabine, cisplatin, and 21-h infusional 5-fluorouracil (5-FU).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study was a prospective, observational study at a medical center in Western Iran. The clinical and survival data from 25 patients treated with gemcitabine, cisplatin, and 21-h infusional 5-FU at our center were prospectively assessed. Patients received chemotherapy consisting of cycles of continuous infusion of 5-FU (650 mg/m²) for 21 h on Days 1, 2, 3, and 4. Gemcitabine was administered at a dose of 1 g/m² on Days 1 and 8, and cisplatin was administered at a dose of 60 mg/m² on Day 1, with granulocyte colony-stimulating factor (G-CSF) support. Each cycle was repeated every 21 days for 5−6 cycles.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 25 patients with an age range of 39−73 years were studied. One out of the two patients with stage Ⅱ cancer survived for more than 43 months. Four out of the 14 patients with stage Ⅲ cancer survived for more than 15 months. Seventeen patients died, and eight subjects were alive at the end of the study. The mean and median of overall survival (OS) rates for the 25 patients were 20 and 12 months, respectively. The median progression-free survival (PFS) was 6 months.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>It seems that the triple therapy with gemcitabine, cisplatin, and infusional 5-FU afforded significant PFS and OS benefits in patients with advanced pancreatic cancer.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 3","pages":"140-144"},"PeriodicalIF":0.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145196931","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}

{"title":"The result of maintenance therapy with rituximab in extra nodal lymphoma","authors":"Mozaffar Aznab,&nbsp;Fatemeh Heydarpur,&nbsp;Amirmasoud Rahimi,&nbsp;Sayed Javad Hossini,&nbsp;Kiumrs Eslampia","doi":"10.1002/msp2.70011","DOIUrl":"https://doi.org/10.1002/msp2.70011","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Maintenance treatment with rituximab has been used in some nodal lymphomas, such as follicular and diffuse large cell lymphoma. The aim of this study was to evaluate the survival of extra nodal lymphoma patients under maintenance treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and methods</h3>\u0000 \u0000 <p>From July 2008 to December 2017, after induction treatment in patients with extra nodal lymphoma, if the patients consented and the drug was available, they were treated with rituximab every 3 months for 2 years.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 112 patients with extra nodal lymphoma met the inclusion criteria. Among them, 89 patients had high-grade lymphomas and 23 patients were in the group of low-grade lymphomas. The group of patients with high-grade lymphoma who received the rituximab-containing regimen as a maintenance treatment had lower rates of recurrence and death compared to the group that received rituximab only in the induction phase. In patients with low-grade lymphoma, the recurrence rate and mortality were also lower in the group receiving maintenance treatment compared to other groups, but the difference was not statistically significant.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The use of rituximab in patients with extra nodal lymphoma as maintenance can increase the survival of the patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100882,"journal":{"name":"Malignancy Spectrum","volume":"2 2","pages":"95-102"},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/msp2.70011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144519800","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}