David Haynes PhD, Jihyoun Jeon PhD, Gerard Silvestri MD, MS, Christine Lambert MD, Rafael Meza PhD, R. Adams Dudley MD, MBA, Anne Melzer MD, Arianne Baldomero MD. MS, Anne Joseph MD, Abbie Begnaud MD
Background
The utilization of lung cancer screening services is less than 20%. There are a myriad of barriers at the patient, provider, and health care system levels that account for such low uptake. One reason lung cancer screening rates remain low is that identifying who is eligible is challenging at the patient and at the population level because a quantitative estimate of smoking history (i.e., 20 pack-years of cigarette smoking exposure) is required to determine eligibility. This pack-year determination is often missing from clinical documentation and is also absent in large health survey data.
Methods
The Smoking History Generator was integrated into national cross-sectional surveys to estimate smoking exposure intensity and duration for older US adults who have smoked. National estimates, at the substate level, for the number of individuals eligible for lung cancer screening are presented.
Results
A publicly available dataset that enables researchers to estimate the population eligible for lung cancer screening at the census tract level was developed. Additionally, this approach permits exploration and description of the eligible population by age, sex, racial/ethnic groups, and current or former smoking status.
Conclusion
The dataset can be aggregated by geographic location (e.g., county, state) and filtered by age range, sex, race/ethnicity, and smoking status to estimate specific subpopulations eligible for lung cancer screening. This dataset will greatly enhance future programmatic efforts to identify and direct resources to individuals eligible for lung cancer screening.
{"title":"Who is eligible for lung cancer screening, and where are they? National subpopulation estimates of people eligible for lung cancer screening","authors":"David Haynes PhD, Jihyoun Jeon PhD, Gerard Silvestri MD, MS, Christine Lambert MD, Rafael Meza PhD, R. Adams Dudley MD, MBA, Anne Melzer MD, Arianne Baldomero MD. MS, Anne Joseph MD, Abbie Begnaud MD","doi":"10.1002/cncr.70634","DOIUrl":"10.1002/cncr.70634","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The utilization of lung cancer screening services is less than 20%. There are a myriad of barriers at the patient, provider, and health care system levels that account for such low uptake. One reason lung cancer screening rates remain low is that identifying who is eligible is challenging at the patient and at the population level because a quantitative estimate of smoking history (i.e., 20 pack-years of cigarette smoking exposure) is required to determine eligibility. This pack-year determination is often missing from clinical documentation and is also absent in large health survey data.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The Smoking History Generator was integrated into national cross-sectional surveys to estimate smoking exposure intensity and duration for older US adults who have smoked. National estimates, at the substate level, for the number of individuals eligible for lung cancer screening are presented.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A publicly available dataset that enables researchers to estimate the population eligible for lung cancer screening at the census tract level was developed. Additionally, this approach permits exploration and description of the eligible population by age, sex, racial/ethnic groups, and current or former smoking status.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The dataset can be aggregated by geographic location (e.g., county, state) and filtered by age range, sex, race/ethnicity, and smoking status to estimate specific subpopulations eligible for lung cancer screening. This dataset will greatly enhance future programmatic efforts to identify and direct resources to individuals eligible for lung cancer screening.</p>\u0000 </section>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 20","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cncr.70634","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134506","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":"Perceived risk of survivorship sexual dysfunction","authors":"Megan R. Wirtz MA, Jennifer S. Ford PhD","doi":"10.1002/cncr.70651","DOIUrl":"10.1002/cncr.70651","url":null,"abstract":"","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 20","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134397","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}
Danni Zhu MD, Zhuoran Fang MD, Guangjun Jin MD, Jiang Chen MD, Yiming Lu MD, Teng Yang MSc, Ke Shen MD, Yunfu Shi PhD, Yuansheng Zheng MD, Weiwei Xu BPharm, Xiangdong Cheng PhD, Qing Wei PhD
Background
Claudin 18.2 (CLDN18.2) is a promising therapeutic target in gastric/esophagogastric junction adenocarcinoma (GC/EGJC), but its dynamic expression during systemic therapy is unclear.
Methods
CLDN18.2 expression by immunohistochemistry in paired tumor samples from 155 patients with advanced GC/EGJC was retrospectively evaluated before and after systemic therapy. CLDN18.2-positive was defined as ≥75% of viable tumor cells exhibiting moderate-to-strong (2+ or 3+) membranous staining.
Results
Among all patients, 54 (34.84%) were CLDN18.2-positive. Following treatment, the proportion of CLDN18.2-positive patients increased significantly to 61 (39.35%) (p < .001). Among patients who were CLDN18.2-negative at baseline, 57 (56.44%) showed increased expression after treatment, including 22 (21.78%) who converted to positive status. In contrast, among those CLDN18.2-positive at baseline, expression decreased in 35 patients (64.81%), with 15 (27.78%) converting to negative status (p < .001). Among patients receiving chemotherapy alone (n = 25), 1 (4.00%) converted to negative and 5 (20.00%) converted to positive, whereas among those receiving chemotherapy combined with immunotherapy (n = 130), 14 (10.77%) converted to negative and 17 (13.08%) converted to positive (p = .45). A total of 131 patients (84.52%) demonstrated changes in CLDN18.2 expression following therapy, encompassing both conversions across the positivity threshold and fluctuations within the same classification.
Conclusion
CLDN18.2 expression in GC/EGJC is dynamic and frequently altered after systemic therapy. These findings support reassessment of CLDN18.2 status before initiating CLDN18.2-targeted therapies.
{"title":"Dynamic changes of claudin 18.2 expression after systemic therapy in gastric and esophagogastric junction cancer","authors":"Danni Zhu MD, Zhuoran Fang MD, Guangjun Jin MD, Jiang Chen MD, Yiming Lu MD, Teng Yang MSc, Ke Shen MD, Yunfu Shi PhD, Yuansheng Zheng MD, Weiwei Xu BPharm, Xiangdong Cheng PhD, Qing Wei PhD","doi":"10.1002/cncr.70632","DOIUrl":"https://doi.org/10.1002/cncr.70632","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Claudin 18.2 (CLDN18.2) is a promising therapeutic target in gastric/esophagogastric junction adenocarcinoma (GC/EGJC), but its dynamic expression during systemic therapy is unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>CLDN18.2 expression by immunohistochemistry in paired tumor samples from 155 patients with advanced GC/EGJC was retrospectively evaluated before and after systemic therapy. CLDN18.2-positive was defined as ≥75% of viable tumor cells exhibiting moderate-to-strong (2+ or 3+) membranous staining.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among all patients, 54 (34.84%) were CLDN18.2-positive. Following treatment, the proportion of CLDN18.2-positive patients increased significantly to 61 (39.35%) (<i>p</i> < .001). Among patients who were CLDN18.2-negative at baseline, 57 (56.44%) showed increased expression after treatment, including 22 (21.78%) who converted to positive status. In contrast, among those CLDN18.2-positive at baseline, expression decreased in 35 patients (64.81%), with 15 (27.78%) converting to negative status (<i>p</i> < .001). Among patients receiving chemotherapy alone (<i>n</i> = 25), 1 (4.00%) converted to negative and 5 (20.00%) converted to positive, whereas among those receiving chemotherapy combined with immunotherapy (<i>n</i> = 130), 14 (10.77%) converted to negative and 17 (13.08%) converted to positive (<i>p</i> = .45). A total of 131 patients (84.52%) demonstrated changes in CLDN18.2 expression following therapy, encompassing both conversions across the positivity threshold and fluctuations within the same classification.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>CLDN18.2 expression in GC/EGJC is dynamic and frequently altered after systemic therapy. These findings support reassessment of CLDN18.2 status before initiating CLDN18.2-targeted therapies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 20","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149100334","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}
Marius Hörner DMD, Stefan Hartmann MD, DMD, Douglas R. Adkins MD, Ravindra Uppaluri MD, PhD
Outcomes for patients with resectable head and neck squamous cell carcinoma (HNSCC) remain suboptimal despite multimodal therapy, with high rates of recurrence and patients suffering from toxicity of treatments. Immune checkpoint inhibitors, which have transformed the management of recurrent and metastatic disease, have been advanced into the perioperative and adjuvant settings. Recent phase III trials mark a turning point: the addition of adjuvant nivolumab improved disease-free survival in pathologic high-risk resected HNSCCs, while perioperative pembrolizumab significantly prolonged event-free survival in resectable locally advanced HNSCCs, supporting a shift toward integrated perioperative immunotherapy strategies. Although the former approach fits into a conventional adjuvant framework, biological insights suggest that neoadjuvant delivery enables effective immune priming extending therapeutic approaches. Together, these advances redefine therapeutic strategies in resectable HNSCC and highlight the potential of perioperative immunotherapy to improve long-term outcomes.
{"title":"Perioperative immunotherapy in head and neck squamous cell carcinoma","authors":"Marius Hörner DMD, Stefan Hartmann MD, DMD, Douglas R. Adkins MD, Ravindra Uppaluri MD, PhD","doi":"10.1002/cncr.70642","DOIUrl":"https://doi.org/10.1002/cncr.70642","url":null,"abstract":"<p>Outcomes for patients with resectable head and neck squamous cell carcinoma (HNSCC) remain suboptimal despite multimodal therapy, with high rates of recurrence and patients suffering from toxicity of treatments. Immune checkpoint inhibitors, which have transformed the management of recurrent and metastatic disease, have been advanced into the perioperative and adjuvant settings. Recent phase III trials mark a turning point: the addition of adjuvant nivolumab improved disease-free survival in pathologic high-risk resected HNSCCs, while perioperative pembrolizumab significantly prolonged event-free survival in resectable locally advanced HNSCCs, supporting a shift toward integrated perioperative immunotherapy strategies. Although the former approach fits into a conventional adjuvant framework, biological insights suggest that neoadjuvant delivery enables effective immune priming extending therapeutic approaches. Together, these advances redefine therapeutic strategies in resectable HNSCC and highlight the potential of perioperative immunotherapy to improve long-term outcomes.</p>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 20","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149100333","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}
Leptomeningeal disease (LMD) is one of the most devastating complications of advanced non–small cell lung cancer (NSCLC), historically associated with profound neurologic morbidity and poor survival. Advances in cerebrospinal fluid (CSF)-based diagnostics, improved molecular characterization, and the development of central nervous system (CNS)-penetrant targeted therapies have begun to reshape both disease assessment and treatment expectations, particularly in oncogene-driven NSCLC. Available data suggest that outcomes in LMD are highly heterogeneous and are influenced by molecular subtype, performance status, systemic disease control, and access to effective CNS-active therapies. In selected patients, especially those with epidermal growth factor receptor- or anaplastic lymphoma kinase-altered disease, contemporary targeted agents have demonstrated meaningful leptomeningeal and intracranial activity, supporting more durable and compartment-specific disease control. At the same time, diagnosis still relies on imperfect but complementary modalities, including magnetic resonance imaging and CSF cytology, whereas emerging liquid biopsy approaches may improve detection and longitudinal monitoring. Treatment failure is further shaped by the pharmacokinetic constraints of the leptomeningeal compartment, where limited drug penetration contributes to therapeutic resistance. This review highlights the evolving biology, diagnosis, prognostic determinants, and therapeutic landscape of NSCLC-associated LMD, while emphasizing persistent limitations in diagnostic standardization, response assessment, and clinical trial design. It also underscores the need for leptomeningeal-specific end points, longitudinal CSF-based biomarker integration, and more inclusive trial strategies to improve evidence generation and patient outcomes.
{"title":"Redefining leptomeningeal metastasis in non–small cell lung cancer: From terminal complication to molecularly managed disease","authors":"Kübra Canaslan MD, Kelsey Pan MD, Ticiana Leal MD","doi":"10.1002/cncr.70624","DOIUrl":"https://doi.org/10.1002/cncr.70624","url":null,"abstract":"<p>Leptomeningeal disease (LMD) is one of the most devastating complications of advanced non–small cell lung cancer (NSCLC), historically associated with profound neurologic morbidity and poor survival. Advances in cerebrospinal fluid (CSF)-based diagnostics, improved molecular characterization, and the development of central nervous system (CNS)-penetrant targeted therapies have begun to reshape both disease assessment and treatment expectations, particularly in oncogene-driven NSCLC. Available data suggest that outcomes in LMD are highly heterogeneous and are influenced by molecular subtype, performance status, systemic disease control, and access to effective CNS-active therapies. In selected patients, especially those with epidermal growth factor receptor- or anaplastic lymphoma kinase-altered disease, contemporary targeted agents have demonstrated meaningful leptomeningeal and intracranial activity, supporting more durable and compartment-specific disease control. At the same time, diagnosis still relies on imperfect but complementary modalities, including magnetic resonance imaging and CSF cytology, whereas emerging liquid biopsy approaches may improve detection and longitudinal monitoring. Treatment failure is further shaped by the pharmacokinetic constraints of the leptomeningeal compartment, where limited drug penetration contributes to therapeutic resistance. This review highlights the evolving biology, diagnosis, prognostic determinants, and therapeutic landscape of NSCLC-associated LMD, while emphasizing persistent limitations in diagnostic standardization, response assessment, and clinical trial design. It also underscores the need for leptomeningeal-specific end points, longitudinal CSF-based biomarker integration, and more inclusive trial strategies to improve evidence generation and patient outcomes.</p>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 20","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149099954","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}
Fausto Petrelli MD, Lorenzo Dottorini MD, Alberto Zaniboni MD
Pancreatic ductal adenocarcinoma (PDAC) remains among the most lethal malignancies, and activating KRAS mutations occur in more than 90% of tumors. Direct RAS targeting has moved from proof of concept to randomized clinical benefit: in previously treated metastatic PDAC, daraxonrasib improved median overall survival, progression-free survival, and objective response rate versus chemotherapy. Mutation-selective G12C and G12D inhibitors, targeted degraders, and first-line RAS(ON) combinations further broaden the landscape. Comprehensive germline and somatic profiling remains essential even with the availability of multi-selective KRAS inhibitors. KRAS alleles differ biologically, drug activity against individual alleles is not yet fully characterized, and eligibility for clinical trials often depends on the specific genotype. In addition, KRAS wild-type tumors may harbor actionable alterations, including gene fusions, amplifications, or mismatch-repair deficiency. This review synthesizes RAS biology, molecular-testing implications, clinical efficacy and toxicity data, and ongoing phase 2 and phase 3 trials. Priority questions include optimal sequencing, management of rash and mucositis, resistance, biomarker development, and integration into first-line and curative-intent therapy.
{"title":"Targeting RAS in pancreatic cancer","authors":"Fausto Petrelli MD, Lorenzo Dottorini MD, Alberto Zaniboni MD","doi":"10.1002/cncr.70640","DOIUrl":"https://doi.org/10.1002/cncr.70640","url":null,"abstract":"<div>\u0000 \u0000 <p>Pancreatic ductal adenocarcinoma (PDAC) remains among the most lethal malignancies, and activating <i>KRAS</i> mutations occur in more than 90% of tumors. Direct <i>RAS</i> targeting has moved from proof of concept to randomized clinical benefit: in previously treated metastatic PDAC, daraxonrasib improved median overall survival, progression-free survival, and objective response rate versus chemotherapy. Mutation-selective G12C and G12D inhibitors, targeted degraders, and first-line <i>RAS</i>(ON) combinations further broaden the landscape. Comprehensive germline and somatic profiling remains essential even with the availability of multi-selective <i>KRAS</i> inhibitors. <i>KRAS</i> alleles differ biologically, drug activity against individual alleles is not yet fully characterized, and eligibility for clinical trials often depends on the specific genotype. In addition, <i>KRAS</i> wild-type tumors may harbor actionable alterations, including gene fusions, amplifications, or mismatch-repair deficiency. This review synthesizes <i>RAS</i> biology, molecular-testing implications, clinical efficacy and toxicity data, and ongoing phase 2 and phase 3 trials. Priority questions include optimal sequencing, management of rash and mucositis, resistance, biomarker development, and integration into first-line and curative-intent therapy.</p>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 20","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149099955","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}
Naval G. Daver MD, Amer M. Zeidan MD, Anthony S. Stein MD, Joshua F. Zeidner MD, Keri Maher DO, Emily Curran MD, Dale Bixby MD, PhD, Wanxing Chai-Ho MD, Maximilian Stahl MD, Karen W. L. Yee MD, Don Stevens MD, Sawa Ito MD, PhD, Jana Reynolds MD, Patrick Medd MD, PhD, Emma Searle MD, PhD, Andrew Sochacki MD, Mary Lynn Savoie MD, Steven Green MD, Kazunobu Kato MD, PhD, Robert Hernandez PhD, Simon Metenou PhD, Bo Ma PhD, Lini Pandite MD, Taylor H. Schreiber MD, PhD, David A. Sallman MD
Background
This clinical trial sought to determine whether SL-172154 could be combined safely and improve the efficacy of azacitidine (AZA) in patients with higher-risk myelodysplastic syndrome (HR-MDS) or acute myeloid leukemia (AML).
Methods
Dose escalation: doses of 1, 3, and 6 mg/kg SL-172154 was evaluated as monotherapy or in combination with AZA in patients with relapsed, refractory HR-MDS or AML. Expansion: a SL-172154 dose that could be safely combined with AZA was evaluated in patients with previously untreated HR-MDS or TP53 mutant (TP53m) AML. Objectives: safety, efficacy, pharmacokinetics, pharmacodynamics, and immunogenicity.
Results
Eighty-one patients with HR-MDS (n = 33) or AML (n = 48) were enrolled in dose escalation (n = 37) or expansion (n = 44). Infusion-related reaction was the most common SL-172154-related toxicity and led to a dose limiting toxicity at 6 mg/kg. A dose of 3 mg/kg SL-172154 plus AZA was evaluated in patients with previously untreated HR-MDS (n = 21 with TP53m and n = 3 with TP53 wild type) and AML (n = 21 with TP53m). CD47 and CD40 engagement by SL-172154 was detected on leukemic blasts, myeloid, and lymphoid cells. Complete remission (CR) was achieved in 10 of 24 (43%) HR-MDS and six of 21 (29%) TP53m AML patients with median overall survival (OS) of 11.0 months (95% CI, 5.0–15.6) and 11.7 months (95% CI, 1.97–NE), respectively. Of patients in a CR, six of 10 HR-MDS and three of six TP53m AML patients achieved complete cytogenetic CR.
Conclusions
SL-172154 plus AZA was generally well tolerated with favorable CR rates in pts with TP53m HR-MDS or AML, although without substantial improvement in OS when compared to historical benchmarks for AZA or AZA/VEN, respectively.
{"title":"Phase 1 dose escalation and expansion trial of the bispecific CD47 inhibitor and CD40 agonist Fc-fusion protein SL-172154 (SIRPα-Fc-CD40L) in patients with higher-risk myelodysplastic syndrome or acute myeloid leukemia","authors":"Naval G. Daver MD, Amer M. Zeidan MD, Anthony S. Stein MD, Joshua F. Zeidner MD, Keri Maher DO, Emily Curran MD, Dale Bixby MD, PhD, Wanxing Chai-Ho MD, Maximilian Stahl MD, Karen W. L. Yee MD, Don Stevens MD, Sawa Ito MD, PhD, Jana Reynolds MD, Patrick Medd MD, PhD, Emma Searle MD, PhD, Andrew Sochacki MD, Mary Lynn Savoie MD, Steven Green MD, Kazunobu Kato MD, PhD, Robert Hernandez PhD, Simon Metenou PhD, Bo Ma PhD, Lini Pandite MD, Taylor H. Schreiber MD, PhD, David A. Sallman MD","doi":"10.1002/cncr.70626","DOIUrl":"10.1002/cncr.70626","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This clinical trial sought to determine whether SL-172154 could be combined safely and improve the efficacy of azacitidine (AZA) in patients with higher-risk myelodysplastic syndrome (HR-MDS) or acute myeloid leukemia (AML).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Dose escalation: doses of 1, 3, and 6 mg/kg SL-172154 was evaluated as monotherapy or in combination with AZA in patients with relapsed, refractory HR-MDS or AML. Expansion: a SL-172154 dose that could be safely combined with AZA was evaluated in patients with previously untreated HR-MDS or <i>TP53</i> mutant (<i>TP53</i>m) AML. Objectives: safety, efficacy, pharmacokinetics, pharmacodynamics, and immunogenicity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Eighty-one patients with HR-MDS (<i>n</i> = 33) or AML (<i>n</i> = 48) were enrolled in dose escalation (<i>n</i> = 37) or expansion (<i>n</i> = 44). Infusion-related reaction was the most common SL-172154-related toxicity and led to a dose limiting toxicity at 6 mg/kg. A dose of 3 mg/kg SL-172154 plus AZA was evaluated in patients with previously untreated HR-MDS (<i>n</i> = 21 with <i>TP53</i>m and <i>n</i> = 3 with <i>TP53</i> wild type) and AML (<i>n</i> = 21 with <i>TP53</i>m). CD47 and CD40 engagement by SL-172154 was detected on leukemic blasts, myeloid, and lymphoid cells. Complete remission (CR) was achieved in 10 of 24 (43%) HR-MDS and six of 21 (29%) <i>TP53</i>m AML patients with median overall survival (OS) of 11.0 months (95% CI, 5.0–15.6) and 11.7 months (95% CI, 1.97–NE), respectively. Of patients in a CR, six of 10 HR-MDS and three of six <i>TP53</i>m AML patients achieved complete cytogenetic CR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>SL-172154 plus AZA was generally well tolerated with favorable CR rates in pts with <i>TP53</i>m HR-MDS or AML, although without substantial improvement in OS when compared to historical benchmarks for AZA or AZA/VEN, respectively.</p>\u0000 </section>\u0000 </div>","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 19","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13634416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101610","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}
<p>The US Food and Drug Administration has approved an oral combination of the decitabine–cedazuridine hypomethylating agent (HMA) in tablet form with venetoclax for adults aged 75 years or older with newly diagnosed acute myeloid leukemia (AML) who are ineligible for intensive induction chemotherapy.<span><sup>1</sup></span></p><p>“HMAs together with venetoclax is the current standard for older, unfit patients with AML, but now we are trying to make that treatment simpler,” says Hagop M. Kantarjian, MD, a professor in the Department of Leukemia at The University of Texas MD Anderson Cancer Center in Houston. “Currently, when we use an HMA, it is either azacitidine given subcutaneously or intravenously daily for 7 days or decitabine given intravenously daily for 5 days. This becomes cumbersome to patients, particularly after they are in remission.”</p><p>The new all-oral combination was approved based on the results of the phase 1/2 ASCERTAIN-V trial.<span><sup>2</sup></span> All patients received 35 mg of decitabine and 100 mg of cedazuridine on Days 1–5 and 400 mg of venetoclax daily in 28-day cycles after the initial ramp-up in Cycle 1 to reduce tumor lysis syndrome. During phase 2b of the trial, decreased duration of decitabine and cedazuridine was allowed based on documented bone marrow blast clearance.</p><p>During phase 2b, 47% of patients achieved a complete response (CR), and 63% achieved a CR or CR with incomplete hematologic recovery. Among those patients who achieved a CR, 80% were still responding at 6 months, and 75% were still responding at 12 months. The median overall survival was 15.5 months.</p><p>There were no drug-drug interactions observed. During phase 2b, the most common adverse events of grade 3 or higher were anemia (30%), neutropenia (26%), and febrile neutropenia (25%).</p><p>“Traditionally, during induction, we end up admitting patients for inpatient therapy so that if there are complications, we can manage them appropriately and quickly to reduce mortality,” says Dr Kantarjian. With this regimen, the mortality rate was 3% at 30 days and 10% at 60 days. “This combination of oral decitabine with venetoclax allows us to do all the treatment as an outpatient, possibly even during induction if patients are monitored closely.”</p><p>Additionally, instead of patients coming to the clinic 7 days every month, this new regimen means that patients can come only 1 day a month, Dr Kantarjian says. However, there may be some concern about the potential cost of the oral medications.</p><p>“However, if you factor in the cost of the IV medications, cost of hospitalization, cost of clinic visits, that may even out,” Dr Kantarjian says. “Someone needs to do an analysis of the price of the drugs versus the potential benefits of all-oral therapy.”</p><p>The next steps will be to look at bringing this all-oral approach to targeted therapies, such as FLT3, IDH1, or menin inhibitors, in the form of “triplet regimens” for older patients and
{"title":"All-oral regimen approved for older patients with AML who are ineligible for intensive chemotherapy","authors":"Leah Lawrence","doi":"10.1002/cncr.70573","DOIUrl":"10.1002/cncr.70573","url":null,"abstract":"<p>The US Food and Drug Administration has approved an oral combination of the decitabine–cedazuridine hypomethylating agent (HMA) in tablet form with venetoclax for adults aged 75 years or older with newly diagnosed acute myeloid leukemia (AML) who are ineligible for intensive induction chemotherapy.<span><sup>1</sup></span></p><p>“HMAs together with venetoclax is the current standard for older, unfit patients with AML, but now we are trying to make that treatment simpler,” says Hagop M. Kantarjian, MD, a professor in the Department of Leukemia at The University of Texas MD Anderson Cancer Center in Houston. “Currently, when we use an HMA, it is either azacitidine given subcutaneously or intravenously daily for 7 days or decitabine given intravenously daily for 5 days. This becomes cumbersome to patients, particularly after they are in remission.”</p><p>The new all-oral combination was approved based on the results of the phase 1/2 ASCERTAIN-V trial.<span><sup>2</sup></span> All patients received 35 mg of decitabine and 100 mg of cedazuridine on Days 1–5 and 400 mg of venetoclax daily in 28-day cycles after the initial ramp-up in Cycle 1 to reduce tumor lysis syndrome. During phase 2b of the trial, decreased duration of decitabine and cedazuridine was allowed based on documented bone marrow blast clearance.</p><p>During phase 2b, 47% of patients achieved a complete response (CR), and 63% achieved a CR or CR with incomplete hematologic recovery. Among those patients who achieved a CR, 80% were still responding at 6 months, and 75% were still responding at 12 months. The median overall survival was 15.5 months.</p><p>There were no drug-drug interactions observed. During phase 2b, the most common adverse events of grade 3 or higher were anemia (30%), neutropenia (26%), and febrile neutropenia (25%).</p><p>“Traditionally, during induction, we end up admitting patients for inpatient therapy so that if there are complications, we can manage them appropriately and quickly to reduce mortality,” says Dr Kantarjian. With this regimen, the mortality rate was 3% at 30 days and 10% at 60 days. “This combination of oral decitabine with venetoclax allows us to do all the treatment as an outpatient, possibly even during induction if patients are monitored closely.”</p><p>Additionally, instead of patients coming to the clinic 7 days every month, this new regimen means that patients can come only 1 day a month, Dr Kantarjian says. However, there may be some concern about the potential cost of the oral medications.</p><p>“However, if you factor in the cost of the IV medications, cost of hospitalization, cost of clinic visits, that may even out,” Dr Kantarjian says. “Someone needs to do an analysis of the price of the drugs versus the potential benefits of all-oral therapy.”</p><p>The next steps will be to look at bringing this all-oral approach to targeted therapies, such as FLT3, IDH1, or menin inhibitors, in the form of “triplet regimens” for older patients and ","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 19","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cncr.70573","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149072949","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}
<p>Patients with newly diagnosed surgical brain metastases had significantly improved surgical bed control and overall survival (OS) when they were treated with cesium-131 tile-based radiation therapy (TBRT) during resection versus postoperative stereotactic radiation (SRT) according to results of the phase 3 ROADS trial presented at the 2026 American Society of Clinical Oncology Annual Meeting.<span><sup>1</sup></span></p><p>The current standard of care for patients undergoing resection for brain metastases is based on phase 3 data showing that resection followed by SRT improved freedom from local recurrence at a rate of 72% versus 43% with resection alone according to study presenter Jeffrey S. Weinberg, MD, FAANS, FACS, professor of neurosurgery and deputy chair and vice-chair of clinical operations in the Department of Neurosurgery at The University of Texas MD Anderson Cancer Center in Houston.<span><sup>2</sup></span> However, there are challenges associated with postoperative radiation.</p><p>In an attempt to improve on these outcomes, Dr Weinberg and his colleagues designed the ROADS trial to test the use of cesium-131 seeds placed at surgery and evaluated whether this method offered logistical and biological advantages. The tiles deliver a high focal dose of radiation but with limited penetration.</p><p>In the trial, 230 patients with one newly diagnosed brain metastasis requiring resection were enrolled at 32 US centers. Patients were randomly assigned to surgery plus SRT or surgery plus TBRT. The coprimary endpoints of the study were time to surgical bed recurrence (SBR) and surgical bed recurrence-free survival (SB-RFS).</p><p>TBRT demonstrated a superior time to SBR with the median not reached versus 17.4 months with resection plus SRT. The 12-month cumulative incidence of SBR was 1.3% with TBRT and 15.4% with SRT (<i>p</i> = .012).</p><p>TBRT also demonstrated superior SB-RFS in comparison with SRT. The median SB-RFS was not reached with TBRT but was 10.9 months with SRT (hazard ratio [HR], 0.48; 95% CI, 0.30–0.76; <i>p</i> = .0021).</p><p>The researchers performed a sensitivity analysis to remove patients assigned to the SRT arm who did not receive postoperative SRT as assigned. For both coprimary endpoints, the results held, with improvement in local control remaining statistically significant.</p><p>Finally, patients assigned to TBRT had significantly improved OS with a median of 42.5 months versus 17.6 months with SRT (HR, 0.59; 95% CI, 0.37–0.96; <i>p</i> = .032). The estimated 24-month OS was 61.7% with TBRT and 35.7% with SRT.</p><p>“The cesium-131 TBRT is a much more user friendly and convenient option for the patients,” says Gabriella Wernicke, MD, MS, a radiation oncologist with Northwell Health in New York. “It obviates the need for the 2 to 4 weeks’ delay needed prior to postoperative radiation therapy for postoperative healing. Immediate intra-operative TBRT prevents repopulation of tumor cells and hence provides a plat
根据2026年美国临床肿瘤学会年会上公布的3期ROADS试验结果，新诊断的外科脑转移患者在手术期间接受基于铯-131瓦的放射治疗（TBRT）与术后立体定向放射（SRT）相比，手术床控制和总生存率（OS）明显改善。目前，脑转移患者接受手术切除的护理标准是基于3期研究报告的主讲人Jeffrey S. Weinberg，医学博士，FAANS， FACS，神经外科教授，位于休斯顿的德克萨斯大学MD安德森癌症中心神经外科临床手术副主席和副主席，神经外科副主席和副主席指出，数据显示，切除后进行SRT可提高局部复发率72%，而单纯切除可提高局部复发率43%。为了改善这些结果，温伯格博士和他的同事们设计了ROADS试验，以测试在手术中放置铯-131种子的使用，并评估这种方法是否提供了后勤和生物学上的优势。这种瓷砖能提供高剂量的辐射，但穿透能力有限。在该试验中，美国32个中心招募了230名新诊断为需要切除的脑转移患者。患者被随机分配到手术加SRT或手术加TBRT。研究的主要终点是手术床复发时间（SBR）和手术床无复发生存期（SB-RFS）。与切除加SRT的17.4个月相比，TBRT的中位值未达到SBR的时间更长。TBRT组12个月SBR累积发生率为1.3%，SRT组为15.4% （p = 0.012）。与SRT相比，TBRT也显示出更好的SB-RFS。TBRT未达到中位SB-RFS，而SRT为10.9个月（风险比[HR]， 0.48; 95% CI, 0.30-0.76; p = 0.0021）。研究人员进行了敏感性分析，将未接受术后SRT的患者分配到SRT组。对于两个主要终点，结果保持不变，局部控制的改善仍然具有统计学意义。最后，分配到TBRT的患者的OS显著改善，中位时间为42.5个月，而SRT为17.6个月（HR, 0.59; 95% CI, 0.37-0.96; p = 0.032）。TBRT组24个月的OS为61.7%，SRT组为35.7%。“对病人来说，铯-131 TBRT是一种更友好和方便的选择，”纽约诺斯韦尔健康中心的放射肿瘤学家、医学博士、医学硕士加布里埃拉·韦尼克说。“它避免了术后放射治疗前2到4周的延迟。术中立即进行TBRT可防止肿瘤细胞再生，因此提供了比延迟SRS更好的肿瘤控制平台。”Wernicke博士指出，TBRT也不会延迟全身治疗的使用。这一点很重要，因为许多患者在等待术后放疗时存在全身进展的风险。此外，TBRT的优越疗效并没有以增加毒性为代价。两个治疗组患者的所有不良事件（ae）、严重ae和3级或以上治疗相关ae的发生率相似（TBRT组为18.1%，SRT组为19.3%）。Wernicke博士说：“我很高兴ROADS试验已经完成并取得了成熟的结果。“如果以口头摘要形式呈现的研究数据最终将以发表的手稿结束，则可能会改变护理标准。结果非常有希望和鼓舞人心。”
{"title":"Tile-based radiation therapy may be new standard of care for patients with surgical brain metastases","authors":"Leah Lawrence","doi":"10.1002/cncr.70575","DOIUrl":"10.1002/cncr.70575","url":null,"abstract":"<p>Patients with newly diagnosed surgical brain metastases had significantly improved surgical bed control and overall survival (OS) when they were treated with cesium-131 tile-based radiation therapy (TBRT) during resection versus postoperative stereotactic radiation (SRT) according to results of the phase 3 ROADS trial presented at the 2026 American Society of Clinical Oncology Annual Meeting.<span><sup>1</sup></span></p><p>The current standard of care for patients undergoing resection for brain metastases is based on phase 3 data showing that resection followed by SRT improved freedom from local recurrence at a rate of 72% versus 43% with resection alone according to study presenter Jeffrey S. Weinberg, MD, FAANS, FACS, professor of neurosurgery and deputy chair and vice-chair of clinical operations in the Department of Neurosurgery at The University of Texas MD Anderson Cancer Center in Houston.<span><sup>2</sup></span> However, there are challenges associated with postoperative radiation.</p><p>In an attempt to improve on these outcomes, Dr Weinberg and his colleagues designed the ROADS trial to test the use of cesium-131 seeds placed at surgery and evaluated whether this method offered logistical and biological advantages. The tiles deliver a high focal dose of radiation but with limited penetration.</p><p>In the trial, 230 patients with one newly diagnosed brain metastasis requiring resection were enrolled at 32 US centers. Patients were randomly assigned to surgery plus SRT or surgery plus TBRT. The coprimary endpoints of the study were time to surgical bed recurrence (SBR) and surgical bed recurrence-free survival (SB-RFS).</p><p>TBRT demonstrated a superior time to SBR with the median not reached versus 17.4 months with resection plus SRT. The 12-month cumulative incidence of SBR was 1.3% with TBRT and 15.4% with SRT (<i>p</i> = .012).</p><p>TBRT also demonstrated superior SB-RFS in comparison with SRT. The median SB-RFS was not reached with TBRT but was 10.9 months with SRT (hazard ratio [HR], 0.48; 95% CI, 0.30–0.76; <i>p</i> = .0021).</p><p>The researchers performed a sensitivity analysis to remove patients assigned to the SRT arm who did not receive postoperative SRT as assigned. For both coprimary endpoints, the results held, with improvement in local control remaining statistically significant.</p><p>Finally, patients assigned to TBRT had significantly improved OS with a median of 42.5 months versus 17.6 months with SRT (HR, 0.59; 95% CI, 0.37–0.96; <i>p</i> = .032). The estimated 24-month OS was 61.7% with TBRT and 35.7% with SRT.</p><p>“The cesium-131 TBRT is a much more user friendly and convenient option for the patients,” says Gabriella Wernicke, MD, MS, a radiation oncologist with Northwell Health in New York. “It obviates the need for the 2 to 4 weeks’ delay needed prior to postoperative radiation therapy for postoperative healing. Immediate intra-operative TBRT prevents repopulation of tumor cells and hence provides a plat","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 19","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cncr.70575","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149072755","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}
<p>England’s National Health Service (NHS)–Galleri trial was designed to evaluate whether a multicancer early detection (MCED) test, when used alongside existing cancer screening, could help the NHS to find cancer earlier. Unfortunately, results presented at the 2026 American Society of Clinical Oncology Annual Meeting showed that MCED testing did not significantly reduce the number of people diagnosed with late-stage cancer in comparison with a control group.<span><sup>1</sup></span></p><p>“Early trials [of MCED] established clinical validity—meaning these tests could identify cancers—but not clinical utility, that the identification of these cancers improved outcomes for patients,” says Ernest T. Hawk, MD, MPH, vice president and head of the Division of Cancer Prevention and Population Sciences at The University of Texas MD Anderson Cancer in Houston. “This was a very large, well-designed trial and it is the best available evidence around the use of a MCED test, but it has not yet proven that the test can identify cancers early enough to benefit individuals being tested by reducing late-stage diagnoses or improving survival. That is critical.”</p><p>The NHS-Galleri trial included 142,924 participants aged 50–79 years. Participants had blood samples taken at up to three annual visits. After the first blood draw, participants were randomly assigned to a control arm, where the blood was not tested, or to the MCED test, which detects a cancer signal from cell-free DNA in the blood and predicts the cancer signal origin to guide diagnostic evaluation.</p><p>Any participant assigned to MCED who had a cancer signal was referred to the NHS for a diagnostic workup. The clinical utility of the test was assessed by a reduction in late-stage cancers (stage III or IV); a reduction in stage IV cancer incidence was a key secondary objective.</p><p>The primary endpoint of a reduction in stage III/IV cancer was not met. No significant reduction in stage III/IV cancer was observed with MCED testing within the follow-up period, with only a 3% difference between the study arms.</p><p>Providing a more nuanced evaluation of the results, study presenter Charles Swanton, MBPhD, a clinician–scientist at the Francis Crick Institute in London, United Kingdom, looked at the evolution of the trial results. If screening had worked, there would have been an initial increase in the detection of advanced-stage cancers that were present but undiagnosed in the intervention arm, which then should have been followed by a reduction in advanced cancers over time.</p><p>During the first year of the trial, there was a 19% increase in the incidence of stage III/IV cancer detected in the intervention arm versus the control arm, and this was followed by 5% and 12% decreases in the second and third screening rounds, respectively. These decreases, however, were not enough to offset the initial increase in stage III/IV cancer, Dr Swanton said during his presentation.</p><p>However, Dr Hawk n
{"title":"Study raises important questions about the clinical utility of multicancer early detection testing","authors":"Leah Lawrence","doi":"10.1002/cncr.70574","DOIUrl":"10.1002/cncr.70574","url":null,"abstract":"<p>England’s National Health Service (NHS)–Galleri trial was designed to evaluate whether a multicancer early detection (MCED) test, when used alongside existing cancer screening, could help the NHS to find cancer earlier. Unfortunately, results presented at the 2026 American Society of Clinical Oncology Annual Meeting showed that MCED testing did not significantly reduce the number of people diagnosed with late-stage cancer in comparison with a control group.<span><sup>1</sup></span></p><p>“Early trials [of MCED] established clinical validity—meaning these tests could identify cancers—but not clinical utility, that the identification of these cancers improved outcomes for patients,” says Ernest T. Hawk, MD, MPH, vice president and head of the Division of Cancer Prevention and Population Sciences at The University of Texas MD Anderson Cancer in Houston. “This was a very large, well-designed trial and it is the best available evidence around the use of a MCED test, but it has not yet proven that the test can identify cancers early enough to benefit individuals being tested by reducing late-stage diagnoses or improving survival. That is critical.”</p><p>The NHS-Galleri trial included 142,924 participants aged 50–79 years. Participants had blood samples taken at up to three annual visits. After the first blood draw, participants were randomly assigned to a control arm, where the blood was not tested, or to the MCED test, which detects a cancer signal from cell-free DNA in the blood and predicts the cancer signal origin to guide diagnostic evaluation.</p><p>Any participant assigned to MCED who had a cancer signal was referred to the NHS for a diagnostic workup. The clinical utility of the test was assessed by a reduction in late-stage cancers (stage III or IV); a reduction in stage IV cancer incidence was a key secondary objective.</p><p>The primary endpoint of a reduction in stage III/IV cancer was not met. No significant reduction in stage III/IV cancer was observed with MCED testing within the follow-up period, with only a 3% difference between the study arms.</p><p>Providing a more nuanced evaluation of the results, study presenter Charles Swanton, MBPhD, a clinician–scientist at the Francis Crick Institute in London, United Kingdom, looked at the evolution of the trial results. If screening had worked, there would have been an initial increase in the detection of advanced-stage cancers that were present but undiagnosed in the intervention arm, which then should have been followed by a reduction in advanced cancers over time.</p><p>During the first year of the trial, there was a 19% increase in the incidence of stage III/IV cancer detected in the intervention arm versus the control arm, and this was followed by 5% and 12% decreases in the second and third screening rounds, respectively. These decreases, however, were not enough to offset the initial increase in stage III/IV cancer, Dr Swanton said during his presentation.</p><p>However, Dr Hawk n","PeriodicalId":138,"journal":{"name":"Cancer","volume":"132 19","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cncr.70574","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149072768","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}
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