Cancer Innovation最新文献

{"title":"Deciphering the Chemotherapeutic Mechanism of Ferulic Acid: Insight Into the Role Against Multiple Human Cancers.","authors":"Sanzida Khatun, Md Sohel, Zitu Barman, Umme Salma, Lubatul Arbia, Md Rifat Sarker, Jasmin Akter Jame, Badhan Rani Dey, Sultana Parvin, Md Shah Poran Shuvo, Md Shahidul Islam, Tania Mannan, Snygdha Rani Das, Md Mahmudul Hasan","doi":"10.1002/cai2.70056","DOIUrl":"10.1002/cai2.70056","url":null,"abstract":"<p><p>Extensive research continues to address the challenges of developing standard cancer drugs. However, until more effective standard drugs are developed, ferulic acid (FA) may be a potential option for controlling the symptoms of cancer patients. According to our review, FA is available in natural sources and has flexible structures that possess diverse pharmacological activities. FA is effective against 16 different cancer types and has been validated in cell culture, preclinical, and clinical models. Chemotherapeutics activities of FA are regulated through varieties of mechanisms, including targeting signaling pathways, such as AKT/PI3K/mTOR/ERK/STAT NF-κB; apoptosis, such as FAS/FASL, TRADD, Bcl2, Bax, Caspases, and PARP; metastasis, such as MMPs(1,2,9), Wnt/-β catenin, angiogenesis (E&N Cadherin, vimentin, Snail, and Slug), cell proliferation (cyclin D1, E1, and CDKs(2,4,6)), inflammatory molecules (TNF-α, NF-κB,1α, IL-10, IL-8, and IL-6), regulating tumor suppressor genes (p-RB, p21, and p53), autophagy (LC3-II, p62, Beclin1, and Atg12-Atg5), glycolysis (lncRNA 495810 and PKM2), heat shock protein (Hsp60, Hsp70, and Hsp90), and some nonspecific pathways, such as oncogene suppression and antioxidant efficacies. Nanoformulation of FA increased its solubility, stability, and bioavailability, thereby enabling controlled release and making FA more effective against cancer. Additionally, FA exerted synergistic effects with other natural compounds, vitamins, radiotherapy, and chemotherapies, and reversed resistance to existing chemotherapies via diverse mechanisms, including targeting multidrug resistance proteins, apoptosis, reactive oxygen species production, hypoxia, microRNA, the β-catenin pathway, oncogene activation, and sensitizing chemotherapies and radiotherapies. Given that FA has validated the experimental model and demonstrated preliminary efficacy, these findings suggest a possible supportive role for phytochemicals pending the development of fully effective pharmaceutical therapies.</p>","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":"e70056"},"PeriodicalIF":2.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13093063/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793796","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":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148082725","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}

{"title":"Global Advances in Hepatocellular Carcinoma Research and Therapy in 2025.","authors":"Bo Hu, Qiang Gao","doi":"10.1002/cai2.70059","DOIUrl":"10.1002/cai2.70059","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains a significant global health burden, characterized by high mortality and evolving etiological patterns marked by a rise in metabolic dysfunction-associated cases. Over the past year, the therapeutic landscape has substantially evolved, driven by the maturity of clinical data regarding novel diagnostic and treatment strategies. This review synthesizes the milestone breakthroughs achieved through 2025 to provide an updated framework for the multidisciplinary management of this complex malignancy. Advances in early diagnosis have been propelled by the integration of artificial intelligence with imaging and the refinement of liquid biopsy biomarkers, significantly enhancing detection accuracy. Moreover, new findings on tumor microenvironment spatial ecosystem, metabolic reprogramming, and gut-liver axis are revealing new targets that shape these changing therapeutic modalities. Nowadays, in the clinical environment, the enhancement of resectability still gains momentum with novel conversion protocols and the least invasive approaches. One of the most notable changes is the latest development in perioperative care wherein combined systemic and locoregional interventions, such as combinations of immune checkpoint inhibitors and tyrosine kinase inhibitors, have attained previously unachieved pathological response and effectively decreased postoperative recurrence in high-risk patients. In case of progressive disease, advances in treatment models of choice have put a strong emphasis on using combination systems of regimens, which have proven better survival advantages than conventional monotherapies. All these developments highlight the shift from mono-modality therapies to more complex and individualized combination approaches, which imply that comprehensive multimodal interventions will become a standard of care and enhance patient outcomes in the long term among patients with HCC.</p>","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":"e70059"},"PeriodicalIF":2.0,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147725382","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":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148078027","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}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148062126","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}

{"title":"Oncology Health Management: From Educational Awareness to System Building.","authors":"Xinyue Bao, Bo Lan, Fei Ma","doi":"10.1002/cai2.70061","DOIUrl":"10.1002/cai2.70061","url":null,"abstract":"","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":"e70061"},"PeriodicalIF":2.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13076091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694537","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 Burden of Breast Cancer and its Attributable Risk Factors in 204 Countries and Territories, 1990–2021: Results From the Global Burden of Disease Study 2021","authors":"Jiahui Huang,&nbsp;Jiajin Li,&nbsp;Shengbin Pei,&nbsp;Cheng Zeng,&nbsp;Jiangdong Jin,&nbsp;Xun Hu,&nbsp;Jin Shi,&nbsp;Wei Dong,&nbsp;Ruimeng Wang,&nbsp;Yiqin Xia,&nbsp;Jiani Wang","doi":"10.1002/cai2.70055","DOIUrl":"10.1002/cai2.70055","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;To report the global, regional, and national burden of breast cancer (BC) and its attributable risk factors between 1990 and 2021, by age, sex, and sociodemographic index.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Using data from the Global Burden of Disease Study 2021, we analyzed BC prevalence, deaths, disability-adjusted life years (DALYs), and attributable risk factors across 204 countries and territories from 1990 to 2021. Age-standardized prevalence, deaths, and DALYs rates were estimated, and temporal trends were assessed using the estimated annual percentage change. Geographical and sociodemographic inequalities were further evaluated using decomposition analysis, concentration curves, and sociodemographic index (SDI)-based modeling. Attributable risk factors for deaths and DALYs were quantified using the comparative risk assessment framework.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Globally, BC presents a starkly diverging landscape. While the age-standardized prevalence has climbed to 239 per 100,000 (a 9.3% increase since 1990), the death and DALYs rates have actually declined by 13.7% and 9.8%, respectively. This global trend, however, masks a critical geographical shift. High-income regions maintain the highest prevalence, yet the most rapid increases in burden are now concentrated in resource-limited areas such as North Africa and the Middle East. The “triple threat” in low-SDI regions defines this transition. Decomposition analysis revealed that while population growth and aging lead to absolute mortality everywhere, high-SDI regions successfully offset this pressure through favorable epidemiological changes and advancements in screening and treatment. In contrast, low-SDI regions face a deteriorating epidemiological profile that actively contributes to rising deaths. Our inequality analysis further underscores this systemic shift; concentration curves confirm that BC mortality is becoming disproportionately concentrated in lower-SDI countries over time. Additionally, the disease follows a nonlinear, inverted U-shaped relationship with socioeconomic development, peaking at an SDI of 0.75. Finally, we identified a distinct sex-based etiological divide: while female risk patterns are multifaceted, male BC is almost singularly driven by metabolic dysregulation, with high body mass index emerging as the leading global driver of the disease.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Despite progress in reducing the BC burden, it remains a global public health challenge. The prevale","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13066758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147679939","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":"Annual Review of Systemic Medical Treatment for Colorectal Cancer in 2025","authors":"Zengzhi Cai,&nbsp;Fan Chen,&nbsp;Ying Jin,&nbsp;Feng Wang","doi":"10.1002/cai2.70057","DOIUrl":"10.1002/cai2.70057","url":null,"abstract":"<p>This review summarizes landmark advances in colorectal cancer treatment in 2025, characterizing the transition to dynamic precision oncology. Immunotherapy has revolutionized mismatch repair-deficient or microsatellite instability-high patients, becoming the standard first-line and perioperative regimen. Precision medicine expanded to patients with BRAF V600E, KRAS mutation, and HER2 amplification. While circulating tumor DNA utility was confirmed for surveillance and guiding rechallenge, its role in real-time treatment adjustment continues to be explored.</p>","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13066762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147679875","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 Novel Sensitive Technique to Detect ESR1 Hotspot Mutations in Liquid Biopsy Using Switch-Blocker–Enhanced Targeted Amplification Coupled With Pyrosequencing","authors":"Yantong Zhou,&nbsp;Wenna Wang,&nbsp;Bo Lan,&nbsp;Chunxiao Li,&nbsp;Jinsong Wang,&nbsp;Ting Wang,&nbsp;Fangzhou Sun,&nbsp;Yan Wang,&nbsp;Haili Qian,&nbsp;Fei Ma","doi":"10.1002/cai2.70054","DOIUrl":"10.1002/cai2.70054","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The detection of estrogen receptor 1 (<i>ESR1</i>) ligand-binding domain mutations in circulating tumor DNA (ctDNA) is crucial for guiding therapy in estrogen receptor-positive metastatic breast cancer. However, widespread clinical adoption of approaches for monitoring drug resistance and guiding treatment decisions is hindered by limitations of current methods regarding sensitivity, cost, and multiplexing capability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The application of switch-blocker technology, which has been patented for detecting <i>ESR1</i> hotspot mutations (Y537S/C, D538G, E380Q, and L536H/P), suppresses the amplification of wild-type alleles while allowing specific amplification of low-frequency mutant alleles. We used a switch-blocker to inhibit the amplification of a DNA target approximately 10 base pairs in length (e.g., the switch-blocker covering codon 536 of <i>ESR1</i> targets various variants at positions 536, 537, and 538). Targeted enrichment was achieved by quantitative polymerase chain reaction, followed by pyrosequencing to confirm mutation components. Next-generation sequencing and Sanger sequencing served as supplementary methods for the verification of results.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The <i>ESR1</i>-targeted DNA assay was validated for feasibility on plasmid circular templates and ctDNA linear templates. In tests using gradient-diluted <i>ESR1</i> plasmid templates, the proportion of L536H mutant copies increased from 0.0015% to 16.89% after targeted amplification, while the proportion of E380Q mutant copies increased from 0.0015% to 1.35%. In ctDNA samples previously analyzed by next-generation sequencing, the switch-blocker considerably enriched other mutant copies within the coverage range of the switch element.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This switch-blocker–enhanced pyrosequencing assay presents a targeted, multiplexed, and accessible approach for detecting <i>ESR1</i> hotspot mutations in liquid biopsies. This assay has potential for dynamic monitoring of therapeutic resistance, facilitating timely treatment decisions in advanced breast cancer management.</p>\u0000 </section>\u0000 </div>","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13053169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147641195","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":"Combining Small-Molecular Compounds With CAR T-Cell Therapy: Novel Strategies for Enhanced Cancer Immunotherapy","authors":"Rangzi Yi,&nbsp;Zijian Zhang,&nbsp;Yang Yang,&nbsp;Haichuan Zhu","doi":"10.1002/cai2.70053","DOIUrl":"https://doi.org/10.1002/cai2.70053","url":null,"abstract":"<p>Chimeric antigen receptor (CAR) T-cell therapy has been proved to be an effective cancer immunotherapy strategy against haematological malignancies, but exhaustion, limited persistence, and treatment-related toxicity have been identified as major roadblocks in solid tumour treatment. Small-molecular compounds could effectively improve CAR T-cell therapy, such as preventing exhaustion, enhancing memory formation, and enhancing the antitumor activity. Additionally, adding small molecule switches based on tetracycline-controlled gene expression system is an effective strategy to improve the safety of CAR T therapy and reduce its side effects. Despite the encouraging preclinical and clinical results, challenges still remain in optimizing dosing regimens and managing drug interactions. This review aims to summarize recent advances in combined approach and to discuss the underlying mechanisms of its potential benefits.</p>","PeriodicalId":100212,"journal":{"name":"Cancer Innovation","volume":"5 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cai2.70053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147615329","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}