Lingying Wu MD, Jing Wang MD, Qingshui Li BS, Danbo Wang PhD, Cuiying Zhang MM, Junying Tang MD, Guonan Zhang BS, Min Hao PhD, Desheng Yao MD, PhD, Qinglei Gao MD, Youzhong Zhang PhD, Ruifang An MD, Rutie Yin MD, Li Wang BS, Bairong Xia MD, Qi Zhou MS, Hongying Yang MM, Jianqing Zhu MD, Kui Jiang MM, Zhengzheng Chen MM, Qiang Wu MD, Wei Duan MM, Yi Huang MM, Hui Zhang PhD, Shuqing Wei MM, Guiling Li MD, Yuanguang Meng MD, Ke Wang MM, Xinfeng Yang BS, Xianghua Huang PhD, Lingya Pan MD, Jinjin Yu BS, Ge Lou PhD, Yu Zhang PhD, Huaijun Zhou MD, Xiaoqing Guo MD, PhD, Hong Yang PhD, Xiaodong Cheng MD, Xiumin Li MM, Wuliang Wang MD, Hongqin Zhao BS, Yunxia Li BS, Yingjie Yang PhD, An Lin BS, Wenjun Cheng MD, Lihong Chen MD, Xiaoying Xie BS, Wen Di MD, PhD, Yuanjing Hu MD, Mo Chen MD, Hongwu Wen MD, Liping Cai MM, Xiaohua Wu MD, PhD, Zhongqiu Lin MD, PhD, Quanren Wang PhD, Xinfeng Yang PhD, Ning Li MD
Although poly(adenosine diphosphate-ribose) polymerase inhibitors (PARPis) and bevacizumab were approved as first-line maintenance for advanced ovarian cancer (OC), evidence comparing this combination with PARPi monotherapy, especially in BRCA-mutated/homologous recombination-deficient (HRD) patients, is lacking. This study compared combined fuzuloparib (a PARPi) plus apatinib (a vascular endothelial growth factor receptor-2 inhibitor) with either fuzuloparib or placebo as first-line maintenance in patients with advanced OC. Patients who had newly diagnosed, advanced OC and responded to first-line, platinum-based chemotherapy were randomized 2:2:1 to receive combined fuzuloparib (100 mg twice daily) plus apatinib (375 mg daily), fuzuloparib (150 mg twice daily) plus placebo, or double-placebo treatment. The primary end point was blinded independent review committee (BIRC)-assessed progression-free survival (PFS). Six hundred seventy-four patients were randomized to receive fuzuloparib plus apatinib (n = 269), fuzuloparib (n = 269), or placebo (n = 136). At the final analysis (November 1, 2024; 385 BIRC-assessed PFS events; median follow-up, 40 months), the median BIRC-assessed PFS was 26.9 months with the combination versus placebo (hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.44–0.75; one-sided p < .0001) and 29.9 months with fuzuloparib monotherapy versus placebo (HR, 0.58; 95% CI, 0.44–0.75; one-sided p < .0001) compared with 11.1 months with placebo. A PFS benefit was observed regardless of germline BRCA1/2 mutation status. In homologous recombination-deficient patients (including those with BRCA1/2 mutations), combined fuzuloparib and apatinib produced a PFS similar to that of fuzuloparib (34.1 vs. 35.8 months, respectively); in homologous recombination-proficient patients, PFS had a trend favoring the combination (16.6 vs. 11.0 months; HR, 0.73; 95% CI, 0.45–1.19). Both treatments were well tolerated. Overall survival was immature. Both fuzuloparib and combination therapy improved PFS compared with placebo as maintenance therapy for patients who had newly diagnosed, advanced OC. Adding apatinib to fuzuloparib did not prolong PFS among homologous recombination-deficient patients. There was a PFS benefit trend among homologous recombination-proficient patients who received combination therapy compared with those who received monotherapy.
{"title":"Fuzuloparib with or without apatinib as maintenance therapy in newly diagnosed, advanced ovarian cancer (FZOCUS-1): A multicenter, randomized, double-blind, placebo-controlled phase 3 trial","authors":"Lingying Wu MD, Jing Wang MD, Qingshui Li BS, Danbo Wang PhD, Cuiying Zhang MM, Junying Tang MD, Guonan Zhang BS, Min Hao PhD, Desheng Yao MD, PhD, Qinglei Gao MD, Youzhong Zhang PhD, Ruifang An MD, Rutie Yin MD, Li Wang BS, Bairong Xia MD, Qi Zhou MS, Hongying Yang MM, Jianqing Zhu MD, Kui Jiang MM, Zhengzheng Chen MM, Qiang Wu MD, Wei Duan MM, Yi Huang MM, Hui Zhang PhD, Shuqing Wei MM, Guiling Li MD, Yuanguang Meng MD, Ke Wang MM, Xinfeng Yang BS, Xianghua Huang PhD, Lingya Pan MD, Jinjin Yu BS, Ge Lou PhD, Yu Zhang PhD, Huaijun Zhou MD, Xiaoqing Guo MD, PhD, Hong Yang PhD, Xiaodong Cheng MD, Xiumin Li MM, Wuliang Wang MD, Hongqin Zhao BS, Yunxia Li BS, Yingjie Yang PhD, An Lin BS, Wenjun Cheng MD, Lihong Chen MD, Xiaoying Xie BS, Wen Di MD, PhD, Yuanjing Hu MD, Mo Chen MD, Hongwu Wen MD, Liping Cai MM, Xiaohua Wu MD, PhD, Zhongqiu Lin MD, PhD, Quanren Wang PhD, Xinfeng Yang PhD, Ning Li MD","doi":"10.3322/caac.70042","DOIUrl":"https://doi.org/10.3322/caac.70042","url":null,"abstract":"<p>Although poly(adenosine diphosphate-ribose) polymerase inhibitors (PARPis) and bevacizumab were approved as first-line maintenance for advanced ovarian cancer (OC), evidence comparing this combination with PARPi monotherapy, especially in <i>BRCA</i>-mutated/homologous recombination-deficient (HRD) patients, is lacking. This study compared combined fuzuloparib (a PARPi) plus apatinib (a vascular endothelial growth factor receptor-2 inhibitor) with either fuzuloparib or placebo as first-line maintenance in patients with advanced OC. Patients who had newly diagnosed, advanced OC and responded to first-line, platinum-based chemotherapy were randomized 2:2:1 to receive combined fuzuloparib (100 mg twice daily) plus apatinib (375 mg daily), fuzuloparib (150 mg twice daily) plus placebo, or double-placebo treatment. The primary end point was blinded independent review committee (BIRC)-assessed progression-free survival (PFS). Six hundred seventy-four patients were randomized to receive fuzuloparib plus apatinib (<i>n</i> = 269), fuzuloparib (<i>n</i> = 269), or placebo (<i>n</i> = 136). At the final analysis (November 1, 2024; 385 BIRC-assessed PFS events; median follow-up, 40 months), the median BIRC-assessed PFS was 26.9 months with the combination versus placebo (hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.44–0.75; one-sided <i>p</i> < .0001) and 29.9 months with fuzuloparib monotherapy versus placebo (HR, 0.58; 95% CI, 0.44–0.75; one-sided <i>p</i> < .0001) compared with 11.1 months with placebo. A PFS benefit was observed regardless of germline <i>BRCA1/2</i> mutation status. In homologous recombination-deficient patients (including those with <i>BRCA1/2</i> mutations), combined fuzuloparib and apatinib produced a PFS similar to that of fuzuloparib (34.1 vs. 35.8 months, respectively); in homologous recombination-proficient patients, PFS had a trend favoring the combination (16.6 vs. 11.0 months; HR, 0.73; 95% CI, 0.45–1.19). Both treatments were well tolerated. Overall survival was immature. Both fuzuloparib and combination therapy improved PFS compared with placebo as maintenance therapy for patients who had newly diagnosed, advanced OC. Adding apatinib to fuzuloparib did not prolong PFS among homologous recombination-deficient patients. There was a PFS benefit trend among homologous recombination-proficient patients who received combination therapy compared with those who received monotherapy.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>In 2020, the multicenter, randomized, phase 3 FAST-Forward trial reported 5-year results showing that delivery of whole breast or chest wall adjuvant radiotherapy was a safe and effective alternative to the 3-week regimen. Current UK and European guidelines support 26 Gy in 5 daily fractions (Fr) as a standard of care for early breast cancer.</p><p>In a FAST-Forward substudy published in Radiotherapy & Oncology (doi:10.1016/j.radonc.2025.110915), researchers sought to assess normal tissue effects on the axilla after the same 1- and 3-week radiotherapy dose schedules. Findings showed no patient-reported differences between the two protocols after 5 years and thus indicated that 26-Gy/5-Fr/1-week hypofractionation radiotherapy is safe for patients with breast cancer who need it.</p><p>This substudy followed the same design as the randomized, noninferiority, nonblinded FAST-Forward trial. The ongoing trial compares two 5-Fr schedules of adjuvant radiotherapy to the whole breast or chest wall delivered in 1 week with the 15-Fr/3-week schedule. A total of 469 patients with invasive breast cancer from 50 UK centers were included in the substudy. Participants had surgery (either lumpectomy or mastectomy) and required axillary radiotherapy (any or all levels [1–4]). The analysis compared 40 Gy and 5 Fr (3 weeks, control) to 26 Gy and 5 Fr (1 week). The primary endpoint was 5-year patient-reported moderate or marked arm or hand swelling. The median age was 61 years.</p><p>In the group, 54% and 39% of the patients had grade 2 and 3 tumors, respectively, and 56% of the patients had axillary dissection. Patients were randomized to either the 3-week control group (<i>n</i> = 182) or the 1-week treatment group (<i>n</i> = 183). A third arm (27 Gy and 5 Fr) that enrolled 104 patients was stopped early because increased toxicity was detected.</p><p>Participants completed questionnaires at the baseline and 3, 6, 12, 24, and 60 months after randomization. These included the European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life tool, a breast cancer module, a body image scale, and fatigue questionnaires. In addition, patients were asked protocol-specific questions about the adverse effects of radiotherapy and were clinically assessed.</p><p>The primary endpoint was 5-year patient-reported moderate or marked arm or hand swelling reported via the EORTC Quality of Life questionnaire. Secondary endpoints included patient- and clinician-reported outcomes for late radiotherapy adverse effects. A composite endpoint consisted of the worst grade for problems and other adverse effects such as breast distortion, shrinkage, induration, and lymphedema.</p><p>The 5-year questionnaires were returned by 307 patients, with 300 including data on the primary endpoint. Clinicians provided 5-year assessments for 376 patients. At 5 years, moderate or marked hand or arm swelling was reported by 11 of 107 patients (10%) in the 3-week radiotherapy group
{"title":"Study assesses normal tissue effects after axillary radiotherapy for early breast cancer","authors":"Carrie Printz","doi":"10.3322/caac.70039","DOIUrl":"https://doi.org/10.3322/caac.70039","url":null,"abstract":"<p>In 2020, the multicenter, randomized, phase 3 FAST-Forward trial reported 5-year results showing that delivery of whole breast or chest wall adjuvant radiotherapy was a safe and effective alternative to the 3-week regimen. Current UK and European guidelines support 26 Gy in 5 daily fractions (Fr) as a standard of care for early breast cancer.</p><p>In a FAST-Forward substudy published in Radiotherapy & Oncology (doi:10.1016/j.radonc.2025.110915), researchers sought to assess normal tissue effects on the axilla after the same 1- and 3-week radiotherapy dose schedules. Findings showed no patient-reported differences between the two protocols after 5 years and thus indicated that 26-Gy/5-Fr/1-week hypofractionation radiotherapy is safe for patients with breast cancer who need it.</p><p>This substudy followed the same design as the randomized, noninferiority, nonblinded FAST-Forward trial. The ongoing trial compares two 5-Fr schedules of adjuvant radiotherapy to the whole breast or chest wall delivered in 1 week with the 15-Fr/3-week schedule. A total of 469 patients with invasive breast cancer from 50 UK centers were included in the substudy. Participants had surgery (either lumpectomy or mastectomy) and required axillary radiotherapy (any or all levels [1–4]). The analysis compared 40 Gy and 5 Fr (3 weeks, control) to 26 Gy and 5 Fr (1 week). The primary endpoint was 5-year patient-reported moderate or marked arm or hand swelling. The median age was 61 years.</p><p>In the group, 54% and 39% of the patients had grade 2 and 3 tumors, respectively, and 56% of the patients had axillary dissection. Patients were randomized to either the 3-week control group (<i>n</i> = 182) or the 1-week treatment group (<i>n</i> = 183). A third arm (27 Gy and 5 Fr) that enrolled 104 patients was stopped early because increased toxicity was detected.</p><p>Participants completed questionnaires at the baseline and 3, 6, 12, 24, and 60 months after randomization. These included the European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life tool, a breast cancer module, a body image scale, and fatigue questionnaires. In addition, patients were asked protocol-specific questions about the adverse effects of radiotherapy and were clinically assessed.</p><p>The primary endpoint was 5-year patient-reported moderate or marked arm or hand swelling reported via the EORTC Quality of Life questionnaire. Secondary endpoints included patient- and clinician-reported outcomes for late radiotherapy adverse effects. A composite endpoint consisted of the worst grade for problems and other adverse effects such as breast distortion, shrinkage, induration, and lymphedema.</p><p>The 5-year questionnaires were returned by 307 patients, with 300 including data on the primary endpoint. Clinicians provided 5-year assessments for 376 patients. At 5 years, moderate or marked hand or arm swelling was reported by 11 of 107 patients (10%) in the 3-week radiotherapy group ","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"75 6","pages":"466-468"},"PeriodicalIF":232.4,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145449814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Researchers have long known that frailty is associated with worse cancer outcomes. Half of older adults with cancer as well as some young patients with cancer have frailty, which is defined as a loss of biological reserves that makes people more vulnerable to physical stressors. Previous research has shown that frailty often is associated with increased risks of toxicity and death related to cancer treatment.
Clinicians need effective screening tools to determine which patients with cancer are at risk for frailty and poor outcomes. This information can help them to determine the best protocol for each patient.
Although several frailty screening tools exist, the Geriatric 8 (G8) geriatric screening tool is the only one that has been evaluated and undergone systematic reviews for its prognostic ability. The G8 assesses eight areas: age, food intake, mobility, weight loss, body mass index, number of prescription drug medications, neuropsychological condition, and self-reported health.
In a study published in the Journal of the National Cancer Institute (doi:10.1093/jnci/djaf017), researchers conducted a meta-analysis of 58 studies that synthesizes and summarizes current evidence on the association between frailty assessment tools and cancer treatment outcomes in adults with cancer.
“I think the findings synthesize a lot of what we already know,” says Mina Sedrak, MD, an associate professor and director of the Cancer and Aging Program at the David Geffen School of Medicine of the University of California, Los Angeles. “Ultimately, these tools are just as important as the biomarkers we use to test for tumor biology in determining treatment.”
Screening tools such as the G8 can identify some of the subtle changes that cannot be seen with eye tests to identify patients who require more in-depth frailty assessment, he adds.
Researchers searched five databases from inception to January 2023 to identify 58 prognostic-factor studies for this meta-analysis. These studies reported on the associations between validated pre-treatment frailty assessments and outcomes in adults with solid-organ cancers who were undergoing treatment. Outcomes included survival, toxicity, treatment tolerance, functional decline/quality of life, and hospitalization.
The research occurred for a range of tumor sites and mainly in older patients and in advanced and/or palliative disease settings. Nine frailty assessment tools were evaluated. The meta-analysis showed the prognostic value of two screening tools: the G8 and the Vulnerable Elders Survey 13 (VES-13). The latter helps to identify seniors who are at greater risk of functional decline or death during the next 2 years. Its score is based on age, self-reported health, and physical and functional ability limitations. Both tools are simple and quick to administer.
Pooled estimates show that frailty is associated with an increased risk of mortality (hazard ratio, 1.68; 95% co
{"title":"Frailty in patients undergoing cancer treatment linked to significantly more adverse outcomes","authors":"Carrie Printz","doi":"10.3322/caac.70038","DOIUrl":"https://doi.org/10.3322/caac.70038","url":null,"abstract":"<p>Researchers have long known that frailty is associated with worse cancer outcomes. Half of older adults with cancer as well as some young patients with cancer have frailty, which is defined as a loss of biological reserves that makes people more vulnerable to physical stressors. Previous research has shown that frailty often is associated with increased risks of toxicity and death related to cancer treatment.</p><p>Clinicians need effective screening tools to determine which patients with cancer are at risk for frailty and poor outcomes. This information can help them to determine the best protocol for each patient.</p><p>Although several frailty screening tools exist, the Geriatric 8 (G8) geriatric screening tool is the only one that has been evaluated and undergone systematic reviews for its prognostic ability. The G8 assesses eight areas: age, food intake, mobility, weight loss, body mass index, number of prescription drug medications, neuropsychological condition, and self-reported health.</p><p>In a study published in the <i>Journal of the National Cancer Institute</i> (doi:10.1093/jnci/djaf017), researchers conducted a meta-analysis of 58 studies that synthesizes and summarizes current evidence on the association between frailty assessment tools and cancer treatment outcomes in adults with cancer.</p><p>“I think the findings synthesize a lot of what we already know,” says Mina Sedrak, MD, an associate professor and director of the Cancer and Aging Program at the David Geffen School of Medicine of the University of California, Los Angeles. “Ultimately, these tools are just as important as the biomarkers we use to test for tumor biology in determining treatment.”</p><p>Screening tools such as the G8 can identify some of the subtle changes that cannot be seen with eye tests to identify patients who require more in-depth frailty assessment, he adds.</p><p>Researchers searched five databases from inception to January 2023 to identify 58 prognostic-factor studies for this meta-analysis. These studies reported on the associations between validated pre-treatment frailty assessments and outcomes in adults with solid-organ cancers who were undergoing treatment. Outcomes included survival, toxicity, treatment tolerance, functional decline/quality of life, and hospitalization.</p><p>The research occurred for a range of tumor sites and mainly in older patients and in advanced and/or palliative disease settings. Nine frailty assessment tools were evaluated. The meta-analysis showed the prognostic value of two screening tools: the G8 and the Vulnerable Elders Survey 13 (VES-13). The latter helps to identify seniors who are at greater risk of functional decline or death during the next 2 years. Its score is based on age, self-reported health, and physical and functional ability limitations. Both tools are simple and quick to administer.</p><p>Pooled estimates show that frailty is associated with an increased risk of mortality (hazard ratio, 1.68; 95% co","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"75 6","pages":"463-465"},"PeriodicalIF":232.4,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145449849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Don S. Dizon MD, Sumanta Kumar Pal MD, Banu E. Symington MD, MACP, Razelle Kurzrock MD, Arif H. Kamal MD, Christina M. Annunziata MD, PhD, Shanthi Sivendran MD, MSCR, MBA, Ahmedin Jemal DVM, MPH, William L. Dahut MD
<p><i>CA: A Cancer Journal for Clinicians</i> (<i>CA</i>) began in 1950 as <i>CA: A Bulletin of Cancer Progress</i> (Figure 1) and, in 2025, celebrates its 75th year in continuous publication. Today, it is the flagship journal of the American Cancer Society (ACS) and is associated with the highest impact factor of any medical or scientific journal, inside and outside of oncology—a testament to its value, not only to professionals in this space but to the wider public at large. The core reason for its domestic and global reach is <i>cancer statistics</i>, a continuous and evolving effort to describe the incidence and mortality of cancers and how changes in exposures, diagnosis, and treatment affect them. We would be remiss if not acknowledging the 14 years of significant contributions made to the intellectual rigor and refined analyses of these reports, assembled under the guidance of Dr Ahmedin Jemal, Senior Vice President of the Surveillance and Health Equity Science Department.</p><p>Beyond cancer statistics, <i>CA</i> fulfills a major role: the dissemination of information about cancer across its continuum. It has provided our peers and the public contemporary and updated, expert, open-access reviews, at no cost, actively demonstrating a core value of the ACS on the widespread dissemination of cancer practice, research, and education. Reflecting the collaboration of the editorial team and authors, these reviews serve as a resource for everyone and do not require specialization in oncology to comprehend them.</p><p>As <i>CA</i> celebrated its 60th year, the editorial team led by Dr Ted Gansler reflected on seminal publications during its first decade, from the Papanicolaou smear for the early detection of cervical cancer to prognostic disclosure in clinician–patient communication.<span><sup>1</sup></span> It seems fitting then that, as members of the editorial board, we offer our own perspective as we highlight significant publications since that first decade. Finally, we collectively reflect on our mission as we move into the future.</p><p>Colorectal cancer (CRC) is the fourth most common diagnosed cancer and the second leading cause of cancer death in the United States, effecting over 150,000 people and accounting for over 50,000 deaths.<span><sup>2</sup></span> In 2017, Siegel et al. reported increased CRC incidence rates in both men and women younger than 55 years, whereas rates continued to decline in aged 55 years or older.<span><sup>3</sup></span> Consequently, the proportion of CRC being diagnosed in people younger than 55 years rose from 11% of all cases in 1995 to 20% in 2019.<span><sup>2</sup></span> The increase in young-onset CRC is a global phenomenon, with rates rising in parts of Europe, South America, Oceania, and Asia as well as in Canada.<span><sup>4, 5</sup></span> Work is underway to understand the biologic and systemic factors that account for early onset CRC and ways to improve early detection and treatment.</p><p>A testa
{"title":"CA turns 75: Looking at the future but never forgetting the roots","authors":"Don S. Dizon MD, Sumanta Kumar Pal MD, Banu E. Symington MD, MACP, Razelle Kurzrock MD, Arif H. Kamal MD, Christina M. Annunziata MD, PhD, Shanthi Sivendran MD, MSCR, MBA, Ahmedin Jemal DVM, MPH, William L. Dahut MD","doi":"10.3322/caac.70040","DOIUrl":"10.3322/caac.70040","url":null,"abstract":"<p><i>CA: A Cancer Journal for Clinicians</i> (<i>CA</i>) began in 1950 as <i>CA: A Bulletin of Cancer Progress</i> (Figure 1) and, in 2025, celebrates its 75th year in continuous publication. Today, it is the flagship journal of the American Cancer Society (ACS) and is associated with the highest impact factor of any medical or scientific journal, inside and outside of oncology—a testament to its value, not only to professionals in this space but to the wider public at large. The core reason for its domestic and global reach is <i>cancer statistics</i>, a continuous and evolving effort to describe the incidence and mortality of cancers and how changes in exposures, diagnosis, and treatment affect them. We would be remiss if not acknowledging the 14 years of significant contributions made to the intellectual rigor and refined analyses of these reports, assembled under the guidance of Dr Ahmedin Jemal, Senior Vice President of the Surveillance and Health Equity Science Department.</p><p>Beyond cancer statistics, <i>CA</i> fulfills a major role: the dissemination of information about cancer across its continuum. It has provided our peers and the public contemporary and updated, expert, open-access reviews, at no cost, actively demonstrating a core value of the ACS on the widespread dissemination of cancer practice, research, and education. Reflecting the collaboration of the editorial team and authors, these reviews serve as a resource for everyone and do not require specialization in oncology to comprehend them.</p><p>As <i>CA</i> celebrated its 60th year, the editorial team led by Dr Ted Gansler reflected on seminal publications during its first decade, from the Papanicolaou smear for the early detection of cervical cancer to prognostic disclosure in clinician–patient communication.<span><sup>1</sup></span> It seems fitting then that, as members of the editorial board, we offer our own perspective as we highlight significant publications since that first decade. Finally, we collectively reflect on our mission as we move into the future.</p><p>Colorectal cancer (CRC) is the fourth most common diagnosed cancer and the second leading cause of cancer death in the United States, effecting over 150,000 people and accounting for over 50,000 deaths.<span><sup>2</sup></span> In 2017, Siegel et al. reported increased CRC incidence rates in both men and women younger than 55 years, whereas rates continued to decline in aged 55 years or older.<span><sup>3</sup></span> Consequently, the proportion of CRC being diagnosed in people younger than 55 years rose from 11% of all cases in 1995 to 20% in 2019.<span><sup>2</sup></span> The increase in young-onset CRC is a global phenomenon, with rates rising in parts of Europe, South America, Oceania, and Asia as well as in Canada.<span><sup>4, 5</sup></span> Work is underway to understand the biologic and systemic factors that account for early onset CRC and ways to improve early detection and treatment.</p><p>A testa","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"75 6","pages":"469-472"},"PeriodicalIF":232.4,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145428275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-01Epub Date: 2025-06-26DOI: 10.3322/caac.70020
Deep Chakrabarti, Peter Albertsen, Aidan Adkins, Amar Kishan, Vedang Murthy, Chris Parker, Angela Pathmanathan, Alison Reid, Oliver Sartor, Nicholas Van As, Jochen Walz, Alison Tree
Prostate cancer is the most common cancer in two thirds of the world, with an expected doubling in both incidence and mortality in the next two decades. No strong environmental associations exist for the development of prostate cancer; therefore, lifestyle measures are unlikely to mitigate this increasing burden. The last three decades have seen rapid developments in the diagnostic and therapeutic landscape of prostate cancer, including multiparametric magnetic resonance imaging, positron emission tomography, robotic surgery, image-guided hypofractionated and stereotactic radiotherapy, novel anti-androgens and radioligand therapies. Prostate cancer is unique in that not everyone with a diagnosis needs treatment, and active surveillance is the preferred option for some. This review discusses the contemporary management of all stages of prostate cancer in the light of these modern developments, enabling holistic individualization of treatment, and describes the promise of future research to further improve outcomes.
{"title":"The contemporary management of prostate cancer.","authors":"Deep Chakrabarti, Peter Albertsen, Aidan Adkins, Amar Kishan, Vedang Murthy, Chris Parker, Angela Pathmanathan, Alison Reid, Oliver Sartor, Nicholas Van As, Jochen Walz, Alison Tree","doi":"10.3322/caac.70020","DOIUrl":"10.3322/caac.70020","url":null,"abstract":"<p><p>Prostate cancer is the most common cancer in two thirds of the world, with an expected doubling in both incidence and mortality in the next two decades. No strong environmental associations exist for the development of prostate cancer; therefore, lifestyle measures are unlikely to mitigate this increasing burden. The last three decades have seen rapid developments in the diagnostic and therapeutic landscape of prostate cancer, including multiparametric magnetic resonance imaging, positron emission tomography, robotic surgery, image-guided hypofractionated and stereotactic radiotherapy, novel anti-androgens and radioligand therapies. Prostate cancer is unique in that not everyone with a diagnosis needs treatment, and active surveillance is the preferred option for some. This review discusses the contemporary management of all stages of prostate cancer in the light of these modern developments, enabling holistic individualization of treatment, and describes the promise of future research to further improve outcomes.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":" ","pages":"552-586"},"PeriodicalIF":232.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>The population represents the ultimate uncontrolled experiment, yet data on cancer statistics provide an opportunity to learn about real-world outcomes of cancer control activities and policies. In the case of prostate cancer, population data have been critically important in generating and confirming hypotheses about the impacts of screening and treatment advances on the population burden of the disease. Tracking prostate cancer statistics—incidence, mortality, and survival—and how they change over time is thus a prerequisite for understanding the success (or lack thereof) of efforts to control this most common cancer in American men. But population statistics are multifactorial; explaining them requires also considering their many potential drivers and the mechanisms by which disease control efforts play out in the population.</p><p>Consider the example of prostate cancer incidence, prominently reported in this issue’s update on prostate cancer statistics.<span><sup>1</sup></span> Prostate cancer incidence is influenced by prostate-specific antigen (PSA) screening rates in the population. Incidence increased dramatically during the early years of the PSA screening era, prompting concerns that screening was leading to overdiagnosis. Although overdiagnosis did indeed turn out to be a problematic outcome of screening, work by Feuer and Wun<span><sup>2</sup></span> in the early 1990s assured that increases in disease incidence were to be expected when a new screening test was adopted at the population level. The mechanism—initial depletion of the prevalent pool of cases by the screening test—leads to a predicted peak in incidence followed by declines because of the absence in the prevalent pool of those previously detected cases. Feuer and Wun demonstrated that the height and duration of the peak would be driven by the lead time, which is the time by which screening advances disease diagnosis. The lead time is critical not only in the timing of incidence swings after the adoption of screening but also in the delay until any effects of screening on disease mortality are observed. And the average lead time associated with prostate cancer screening is not short—estimates based on the first decade of PSA screening place the mean lead time between 5 and 7 years.<span><sup>3</sup></span></p><p>The update of prostate cancer statistics in this issue of <i>CA: A Cancer Journal for Clinicians</i> highlights more recent incidence trends, specifically the persistence of recent increases overall and in advanced-stage disease. These trends have generated concern because they are what one would expect in a population abandoning screening. Indeed, studies tracking both incidence and screening patterns have been on the alert for such trends, particularly after the issuance of the D recommendation against routine prostate cancer screening for all ages by the US Preventive Services Task Force in 2012.<span><sup>4</sup></span> Although some modest reductions in pro
人口代表了最终的不受控制的实验，但癌症统计数据提供了一个了解癌症控制活动和政策的现实结果的机会。就前列腺癌而言，人口数据在产生和确认关于筛查和治疗进展对该疾病人口负担影响的假设方面至关重要。跟踪前列腺癌的统计数据——发病率、死亡率和存活率——以及它们如何随时间变化，是了解成功（或失败）控制这种美国男性最常见癌症的先决条件。但人口统计是多因素的；解释它们还需要考虑它们的许多潜在驱动因素以及疾病控制工作在人群中发挥作用的机制。以前列腺癌发病率为例，在本期更新的前列腺癌统计数据中有显著的报道前列腺癌发病率受人群中前列腺特异性抗原（PSA）筛查率的影响。在PSA筛查时代的早期，发病率急剧上升，引发了人们对筛查导致过度诊断的担忧。虽然过度诊断确实被证明是筛查的一个有问题的结果，Feuer和Wun2在20世纪90年代初的工作确信，当在人群水平上采用新的筛查试验时，疾病发病率的增加是可以预期的。这种机制——筛查试验最初耗尽流行病例库——导致发病率达到预期峰值，随后下降，因为以前检测到的病例在流行库中缺失。Feuer和Wun证明，峰值的高度和持续时间将由提前期驱动，提前期是筛查提前疾病诊断的时间。提前期不仅对采用筛查后发病率波动的时机至关重要，而且对观察到筛查对疾病死亡率的任何影响之前的延迟也至关重要。前列腺癌筛查的平均提前期并不短根据PSA筛查的头十年估计平均提前期在5到7年之间。3本期《CA: A cancer Journal for clinical》中更新的前列腺癌统计数据强调了最近的发病率趋势，特别是近期总体和晚期疾病的持续增长。这些趋势引起了人们的关注，因为这是人们在放弃筛查的人群中所期望的。事实上，跟踪发病率和筛查模式的研究已经对这种趋势保持警惕，特别是在2012年美国预防服务工作组发布了反对所有年龄段常规前列腺癌筛查的D建议之后。2.4尽管在该建议之后发现前列腺癌筛查略有减少，但没有研究将这些模式与最近的发病率趋势联系起来。当然，这样做是非常具有挑战性的，但一个必要的条件是，发病率的模式符合在人口中进行筛查的机制效果和考虑到其他潜在影响因素的情况下所预期的结果。从机制的角度来看，减少筛查预计将导致筛查时代开始时观察到的模式的逆转，但逆转的时间和幅度将取决于减少的程度以及前置时间。一个预测大规模停止PSA筛查后发病率的机制模型表明，发病率最初会大幅下降，但随后很快开始上升预计晚期发病率不会下降，反而会增加。在2012年美国预防服务工作组提出建议后，发病率确实下降了，但这种下降只是加速了已经在进行的下降。此后，远期发病率呈上升趋势。因此，从机制的角度来看，最近的晚期和总体发病率趋势与PSA检测减少是一致的。然而，其他可能导致这些趋势的因素值得考虑，包括筛查方式和前列腺癌分期方法的变化所起的作用。自从在人群中采用PSA筛查以来，男性筛查和诊断的方式发生了许多变化。随着时间的推移，活检技术已经发生了显著的变化，这是导致筛查下发病率的一个关键因素。活检芯从4个或6个增加到10个或12个，随后努力减少临床无关紧要的癌症的诊断，主要是通过反射测试（例如使用磁共振成像）。在解释疾病发病率趋势时，这些变化在疾病诊断和检测到的癌症概况中的作用值得考虑。 此外，使用更先进的成像技术和病理技术的改进可能会抢走病例的风头，并导致晚期诊断的明显增加。最近的分析研究了对观察到的发病率趋势的相互矛盾的解释。Owens等人7研究了前列腺癌初诊时年龄和PSA的最新趋势，并得出结论，这些数量的变化更符合检测延迟（例如，因为停止筛查），而不是诊断时的优势。Nyame等人8使用了一个机制模型来预测减少筛查使用率对晚期发病率的影响，并得出结论，这些数据与减少筛查的影响是一致的。这些研究为以下评估提供了额外的支持：前列腺癌发病率和晚期发病率的当前趋势可能是由人口筛查的减少引起的。这一解释前列腺癌发病率趋势的讨论显示了人口癌症统计的多因素性质。诊断技术和实践的变化将影响观察到的发病率和生存率趋势，但其中一些变化可能是人为的。了解筛查实践变化的机制含义对于正确解释前列腺癌趋势是必要的。筛查的增加通常会导致同期发病率上升，但随后下降。减少年轻人群的筛查将对老年人群的晚期发病率产生影响。采用新的疾病分期技术，如前列腺特异性膜抗原-正电子发射断层扫描/计算机断层扫描，将不可避免地改变疾病的发病率，甚至改变晚期疾病的定义认识到机械驱动因素是如何随着时间的推移产生疾病模式的，并扩大对解释的考虑，而不是简单的，近端因素，这将是必要的，以避免在从前列腺癌统计数据中学习时过度简化或跳到预先的结论。利益冲突声明除了提交的工作，Etzioni还拥有Seno Medical的股票。两位作者都报告了国家癌症研究所的资助/合同。
{"title":"Learning from prostate cancer statistics","authors":"Ruth Etzioni PhD, Lukas Owens BA","doi":"10.3322/caac.70037","DOIUrl":"10.3322/caac.70037","url":null,"abstract":"<p>The population represents the ultimate uncontrolled experiment, yet data on cancer statistics provide an opportunity to learn about real-world outcomes of cancer control activities and policies. In the case of prostate cancer, population data have been critically important in generating and confirming hypotheses about the impacts of screening and treatment advances on the population burden of the disease. Tracking prostate cancer statistics—incidence, mortality, and survival—and how they change over time is thus a prerequisite for understanding the success (or lack thereof) of efforts to control this most common cancer in American men. But population statistics are multifactorial; explaining them requires also considering their many potential drivers and the mechanisms by which disease control efforts play out in the population.</p><p>Consider the example of prostate cancer incidence, prominently reported in this issue’s update on prostate cancer statistics.<span><sup>1</sup></span> Prostate cancer incidence is influenced by prostate-specific antigen (PSA) screening rates in the population. Incidence increased dramatically during the early years of the PSA screening era, prompting concerns that screening was leading to overdiagnosis. Although overdiagnosis did indeed turn out to be a problematic outcome of screening, work by Feuer and Wun<span><sup>2</sup></span> in the early 1990s assured that increases in disease incidence were to be expected when a new screening test was adopted at the population level. The mechanism—initial depletion of the prevalent pool of cases by the screening test—leads to a predicted peak in incidence followed by declines because of the absence in the prevalent pool of those previously detected cases. Feuer and Wun demonstrated that the height and duration of the peak would be driven by the lead time, which is the time by which screening advances disease diagnosis. The lead time is critical not only in the timing of incidence swings after the adoption of screening but also in the delay until any effects of screening on disease mortality are observed. And the average lead time associated with prostate cancer screening is not short—estimates based on the first decade of PSA screening place the mean lead time between 5 and 7 years.<span><sup>3</sup></span></p><p>The update of prostate cancer statistics in this issue of <i>CA: A Cancer Journal for Clinicians</i> highlights more recent incidence trends, specifically the persistence of recent increases overall and in advanced-stage disease. These trends have generated concern because they are what one would expect in a population abandoning screening. Indeed, studies tracking both incidence and screening patterns have been on the alert for such trends, particularly after the issuance of the D recommendation against routine prostate cancer screening for all ages by the US Preventive Services Task Force in 2012.<span><sup>4</sup></span> Although some modest reductions in pro","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"75 6","pages":"473-474"},"PeriodicalIF":232.4,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hetal D. Mistry MD, MacKenzie R. Adams MD, Charu Taneja MD, Lauren J. Massingham MD, Elizabeth H. Dibble MD, Kara L. Leonard MD, MS, Jesse Hart DO, Galina G. Lagos MD, Mary Anne Fenton MD
<p>A 36-year-old, nulligravid woman with a history of controlled eosinophilic esophagitis, asthma, and dense fibrocystic breasts was referred to the Breast Health Center after abnormal screening mammography. She reported recent fatigue and intermittent diarrhea but had a negative colonoscopy and food allergy testing this year.</p><p>Her family history was significant for a maternal grandmother with a question of uterine cancer, a maternal grandfather who died of renal cancer at age 62 years, a paternal grandmother who died of brain cancer at age 56 years, a paternal grandfather who died of brain cancer at age 80 years, and a history of premalignant changes in the esophagus in her father. She has never smoked tobacco and consumes zero to three drinks of alcohol weekly. She has been physically active in multiple sports, including biking and swimming, and played the cello.</p><p>Mammography demonstrated extremely dense breast tissue with new calcifications in both breasts. Diagnostic mammography demonstrated indeterminate grouped calcifications spanning 19 mm in the right breast at 5 o'clock and 7 mm in the left breast 12 o'clock. She subsequently underwent stereotactic needle biopsies of both areas, which revealed right breast ductal carcinoma in situ (DCIS), nuclear grade 3, with 90% estrogen receptor (ER) expression; and left ductal carcinoma, nuclear grade 3, with 95% ER expression, 40% progesterone receptor (PR) expression, negative human epidermal growth factor receptor 2 (HER-2) status, and a Ki-67 index of 40%. Within the left breast biopsy there was an absence of myoepithelial cells, raising concern that the findings reflected an unusual type of invasive carcinoma. She then underwent bilateral breast magnetic resonance imaging (MRI), which revealed the known areas of DCIS in the bilateral breasts and also revealed a 1.0-cm mass inferior to the left breast DCIS at 12 o'clock that was considered suspicious. On subsequent ultrasound, it corresponded to an 8-mm mass in the left breast at 10 o'clock. A biopsy of the mass demonstrated a spindle cell tumor, favoring malignant phyllodes tumor with pleomorphic liposarcomatous differentiation that was negative for ER, PR, and HER2 (triple-negative), with a Ki-67 index of 30%.</p><p>At her multidisciplinary consultation, she was referred for genetic evaluation having met National Comprehensive Cancer Network (NCCN) criteria based on her diagnosis of breast cancer when younger than 50 years.<span><sup>1</sup></span> Given the concern for invasive left breast cancer and possible need for chemotherapy, she was also referred for fertility preservation.</p><p>She completed a comprehensive 76-gene germline genetic test, which revealed tumor protein p53 (<i>TP53)</i> likely pathogenic variant (LPV; c.716A>G; p.N239S). Pathogenic variants (PVs) and LPVs are DNA sequence changes that are associated with increased risk of disease. There is well established evidence that PVs are disease-causing, and LPVs are
{"title":"A patient with newly diagnosed breast cancer found to have mosaic TP53 likely pathogenic variant","authors":"Hetal D. Mistry MD, MacKenzie R. Adams MD, Charu Taneja MD, Lauren J. Massingham MD, Elizabeth H. Dibble MD, Kara L. Leonard MD, MS, Jesse Hart DO, Galina G. Lagos MD, Mary Anne Fenton MD","doi":"10.3322/caac.70034","DOIUrl":"10.3322/caac.70034","url":null,"abstract":"<p>A 36-year-old, nulligravid woman with a history of controlled eosinophilic esophagitis, asthma, and dense fibrocystic breasts was referred to the Breast Health Center after abnormal screening mammography. She reported recent fatigue and intermittent diarrhea but had a negative colonoscopy and food allergy testing this year.</p><p>Her family history was significant for a maternal grandmother with a question of uterine cancer, a maternal grandfather who died of renal cancer at age 62 years, a paternal grandmother who died of brain cancer at age 56 years, a paternal grandfather who died of brain cancer at age 80 years, and a history of premalignant changes in the esophagus in her father. She has never smoked tobacco and consumes zero to three drinks of alcohol weekly. She has been physically active in multiple sports, including biking and swimming, and played the cello.</p><p>Mammography demonstrated extremely dense breast tissue with new calcifications in both breasts. Diagnostic mammography demonstrated indeterminate grouped calcifications spanning 19 mm in the right breast at 5 o'clock and 7 mm in the left breast 12 o'clock. She subsequently underwent stereotactic needle biopsies of both areas, which revealed right breast ductal carcinoma in situ (DCIS), nuclear grade 3, with 90% estrogen receptor (ER) expression; and left ductal carcinoma, nuclear grade 3, with 95% ER expression, 40% progesterone receptor (PR) expression, negative human epidermal growth factor receptor 2 (HER-2) status, and a Ki-67 index of 40%. Within the left breast biopsy there was an absence of myoepithelial cells, raising concern that the findings reflected an unusual type of invasive carcinoma. She then underwent bilateral breast magnetic resonance imaging (MRI), which revealed the known areas of DCIS in the bilateral breasts and also revealed a 1.0-cm mass inferior to the left breast DCIS at 12 o'clock that was considered suspicious. On subsequent ultrasound, it corresponded to an 8-mm mass in the left breast at 10 o'clock. A biopsy of the mass demonstrated a spindle cell tumor, favoring malignant phyllodes tumor with pleomorphic liposarcomatous differentiation that was negative for ER, PR, and HER2 (triple-negative), with a Ki-67 index of 30%.</p><p>At her multidisciplinary consultation, she was referred for genetic evaluation having met National Comprehensive Cancer Network (NCCN) criteria based on her diagnosis of breast cancer when younger than 50 years.<span><sup>1</sup></span> Given the concern for invasive left breast cancer and possible need for chemotherapy, she was also referred for fertility preservation.</p><p>She completed a comprehensive 76-gene germline genetic test, which revealed tumor protein p53 (<i>TP53)</i> likely pathogenic variant (LPV; c.716A>G; p.N239S). Pathogenic variants (PVs) and LPVs are DNA sequence changes that are associated with increased risk of disease. There is well established evidence that PVs are disease-causing, and LPVs are ","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a dismal prognosis, largely because of late-stage diagnosis and therapeutic resistance. PDAC incidence has been rising, with modifiable and non-modifiable risk factors contributing to disease development. Chronic pancreatitis, diabetes mellitus, smoking, obesity, and familial predisposition have been implicated in PDAC pathogenesis. Early clinical manifestations are vague and insidious; therefore, PDAC is often diagnosed at an advanced stage, limiting curative treatment options. Efforts to improve early detection have focused on serum biomarkers (e.g., carbohydrate antigen 19-9), imaging modalities, and liquid biopsies. Endoscopic ultrasound and magnetic resonance imaging have demonstrated potential in identifying early-stage disease in certain high-risk populations. Surgical resection remains the only potentially curative option, but only 15%–20% of patients have resectable disease at diagnosis. Neoadjuvant chemotherapy has emerged as a promising strategy to improve resectability and survival outcomes. For patients with locally advanced or metastatic PDAC, combination chemotherapy regimens such as FOLFIRINOX (folinic acid, 5-fluorouracil, irinotecan, and oxaliplatin), NALIRIFOX (5-fluorouracil, oxaliplatin, liposomal irinotecan, and leucovorin), and combined gemcitabine/nanoparticle albumen-bound paclitaxel offer survival benefits, although toxicity remains a concern, especially for platinum-based therapies. Several breakthroughs in molecular profiling have led to the development of targeted therapies, including sotorasib and olaparib. Immunotherapy has shown limited success in PDAC due to its immunosuppressive tumor microenvironment. However, novel combination approaches are under investigation, including quadruplet therapy, immune checkpoint inhibitors with oncolytic viruses, stromal-targeting agents, and personalized neoantigen vaccines. Key priorities for future research include identifying reliable biomarkers for early detection, refining patient selection for targeted therapies, and developing innovative strategies to overcome treatment resistance.
{"title":"Advances in pancreatic cancer early diagnosis, prevention, and treatment: The past, the present, and the future","authors":"Alessandro Mannucci MD, Ajay Goel PhD","doi":"10.3322/caac.70035","DOIUrl":"10.3322/caac.70035","url":null,"abstract":"<p>Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a dismal prognosis, largely because of late-stage diagnosis and therapeutic resistance. PDAC incidence has been rising, with modifiable and non-modifiable risk factors contributing to disease development. Chronic pancreatitis, diabetes mellitus, smoking, obesity, and familial predisposition have been implicated in PDAC pathogenesis. Early clinical manifestations are vague and insidious; therefore, PDAC is often diagnosed at an advanced stage, limiting curative treatment options. Efforts to improve early detection have focused on serum biomarkers (e.g., carbohydrate antigen 19-9), imaging modalities, and liquid biopsies. Endoscopic ultrasound and magnetic resonance imaging have demonstrated potential in identifying early-stage disease in certain high-risk populations. Surgical resection remains the only potentially curative option, but only 15%–20% of patients have resectable disease at diagnosis. Neoadjuvant chemotherapy has emerged as a promising strategy to improve resectability and survival outcomes. For patients with locally advanced or metastatic PDAC, combination chemotherapy regimens such as FOLFIRINOX (folinic acid, 5-fluorouracil, irinotecan, and oxaliplatin), NALIRIFOX (5-fluorouracil, oxaliplatin, liposomal irinotecan, and leucovorin), and combined gemcitabine/nanoparticle albumen-bound paclitaxel offer survival benefits, although toxicity remains a concern, especially for platinum-based therapies. Several breakthroughs in molecular profiling have led to the development of targeted therapies, including sotorasib and olaparib. Immunotherapy has shown limited success in PDAC due to its immunosuppressive tumor microenvironment. However, novel combination approaches are under investigation, including quadruplet therapy, immune checkpoint inhibitors with oncolytic viruses, stromal-targeting agents, and personalized neoantigen vaccines. Key priorities for future research include identifying reliable biomarkers for early detection, refining patient selection for targeted therapies, and developing innovative strategies to overcome treatment resistance.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145083925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In order to maintain the high standards of CA’s content, the Editors of CA rely on the knowledge and dedication of many experts in deciding which topics to pursue, which manuscripts to publish, and what modifications to make to ensure medical and scientific accuracy and suitability for our readers. We thank our Associate Editors and our Editorial Advisory Board, who continue to provide these services for us time and time again.
We are also greatly indebted to the effort and expertise of the following individuals for reviewing manuscripts for the journal from July 1, 2024, to June 30, 2025. These individuals go beyond expectations by consistently and expeditiously delivering comprehensive, discerning reviews.
{"title":"Reviewer acknowledgement 2025","authors":"","doi":"10.3322/caac.70033","DOIUrl":"10.3322/caac.70033","url":null,"abstract":"<p>In order to maintain the high standards of <i>CA</i>’s content, the Editors of <i>CA</i> rely on the knowledge and dedication of many experts in deciding which topics to pursue, which manuscripts to publish, and what modifications to make to ensure medical and scientific accuracy and suitability for our readers. We thank our Associate Editors and our Editorial Advisory Board, who continue to provide these services for us time and time again.</p><p>We are also greatly indebted to the effort and expertise of the following individuals for reviewing manuscripts for the journal from July 1, 2024, to June 30, 2025. These individuals go beyond expectations by consistently and expeditiously delivering comprehensive, discerning reviews.</p><p>Lauren Antrim</p><p>Pedro Barata</p><p>Nabila Bennani</p><p>Ari Birnbaum</p><p>Sue Bornstein</p><p>Donald Cannon</p><p>Michael Carney</p><p>Elizabeth Cathcart-Rake</p><p>Annie Chan</p><p>Huizi Chen</p><p>Carissa Chu</p><p>Sean David</p><p>Ruth Etzioni</p><p>Robert Ferris</p><p>Courtney Finlayson</p><p>Bryan Fuchs</p><p>Elizabeth Garrett-Mayer</p><p>William Hall</p><p>Michael Halpern</p><p>Ole-Petter Hamnvik</p><p>David Hui</p><p>Linda Jacobs</p><p>Salvador Jaime-Casas</p><p>Rebecca Johnson</p><p>Corinne Joshu</p><p>David Keefe</p><p>WonSeog Kim</p><p>Elise Kohn</p><p>Lindsay M. Kuroki</p><p>Rita Kuwahara</p><p>Richard Lee</p><p>Shing Lee</p><p>Phebe Lemert</p><p>Stanley Liauw</p><p>Stephen Liu</p><p>Shail Maingi</p><p>Sendurai Mani</p><p>Jonathan Marron</p><p>Brittany C. McGill</p><p>Jacob Miller</p><p>Paul Montgomery</p><p>Susan O'Brien</p><p>Krishnan Patel</p><p>Rodolfo Alberto Rey</p><p>Tina Rizack</p><p>Nabil Saba</p><p>Stephanie Smith</p><p>Umang Swami</p><p>Wade Swenson</p><p>Russell Taichman</p><p>Yungan Tao</p><p>Molly Taylor</p><p>Ayalew Tefferi</p><p>Sarah Temkin</p><p>William Tew</p><p>Premal Thaker</p><p>Jonathan Thompson</p><p>Michael Thun</p><p>Katherine Tossas</p><p>Zaza Tsitsishvili</p><p>Adam Wahida</p><p>Thomas Zilli</p><p>Miguel Zugman</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"75 6","pages":""},"PeriodicalIF":232.4,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145078376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wagle NS, Nogueira L, Devasia TP, et al. Cancer treatment and survivorship statistics, 2025. CA Cancer J Clin. 2025;75(4):308-340. doi:10.3322/caac.70011
In the “Cancers in children and adolescents” section, the first sentence currently reads: “As of January 1, 2025, it is estimated that 40,260 children (aged 14 years and older) and 44,290 adolescents (aged 15–19 years) are living in the United States with a previous cancer diagnosis.” The correct age category for children is “0–14 years” and should read: “As of January 1, 2025, it is estimated that 40,260 children (aged 0–14 years) and 44,290 adolescents (aged 15–19 years) are living in the United States with a previous cancer diagnosis.”
{"title":"Correction to “Cancer treatment and survivorship statistics, 2025”","authors":"","doi":"10.3322/caac.70036","DOIUrl":"10.3322/caac.70036","url":null,"abstract":"<p>Wagle NS, Nogueira L, Devasia TP, et al. Cancer treatment and survivorship statistics, 2025. <i>CA Cancer J Clin</i>. 2025;75(4):308-340. doi:10.3322/caac.70011</p><p>In the “Cancers in children and adolescents” section, the first sentence currently reads: “As of January 1, 2025, it is estimated that 40,260 children (<i>aged 14 years and older</i>) and 44,290 adolescents (aged 15–19 years) are living in the United States with a previous cancer diagnosis.” The correct age category for children is “0–14 years” and should read: “As of January 1, 2025, it is estimated that 40,260 children (<i>aged 0–14 years</i>) and 44,290 adolescents (aged 15–19 years) are living in the United States with a previous cancer diagnosis.”</p><p>The authors apologize for this oversight.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"75 6","pages":""},"PeriodicalIF":232.4,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145043807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号