Joshua Burshtein MD, Alexander Witkowski MD, PhD, Danny Zakria MD, MBA, Milaan Shah MD, Angela Rosenberg DO, Lauren DeBusk MD, Joanna Ludzik MD, PhD, Giovanni Pellacani MD, Darrell Rigel MD, MS
The early detection of cutaneous melanoma is critical to survival outcomes. Because less than one half of melanomas in the United States are diagnosed by dermatologists, the ABCD (asymmetry, border irregularity, color variation, diameter >6 mm) acronym, created 40 years ago with the later addition of “E” for evolution (ABCDE), was developed for nondermatologist health care professionals and the public to simplify and enhance the diagnosis of early melanoma. It continues to be the global, naked-eye, nondevice-assisted standard for initial triage of pigmented lesions. This clinical review discusses the changing clinical diagnostic landscape and examines the currently available first-line and second-line detection modalities for melanoma. It also provides updates to the first-line triage approach and discusses the challenges of regulatory agency oversight for the safe and effective use of current and emerging skin cancer detection technologies. It is critical that health care professionals globally have knowledge of these technologies to enhance their diagnosis of melanoma.
{"title":"Advances in the noninvasive diagnosis of melanoma—40 years beyond the ABCDs","authors":"Joshua Burshtein MD, Alexander Witkowski MD, PhD, Danny Zakria MD, MBA, Milaan Shah MD, Angela Rosenberg DO, Lauren DeBusk MD, Joanna Ludzik MD, PhD, Giovanni Pellacani MD, Darrell Rigel MD, MS","doi":"10.3322/caac.70065","DOIUrl":"10.3322/caac.70065","url":null,"abstract":"<p>The early detection of cutaneous melanoma is critical to survival outcomes. Because less than one half of melanomas in the United States are diagnosed by dermatologists, the ABCD (asymmetry, border irregularity, color variation, diameter >6 mm) acronym, created 40 years ago with the later addition of “E” for evolution (ABCDE), was developed for nondermatologist health care professionals and the public to simplify and enhance the diagnosis of early melanoma. It continues to be the global, naked-eye, nondevice-assisted standard for initial triage of pigmented lesions. This clinical review discusses the changing clinical diagnostic landscape and examines the currently available first-line and second-line detection modalities for melanoma. It also provides updates to the first-line triage approach and discusses the challenges of regulatory agency oversight for the safe and effective use of current and emerging skin cancer detection technologies. It is critical that health care professionals globally have knowledge of these technologies to enhance their diagnosis of melanoma.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12856975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146083776","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}
McKay RR, Pal S, Xie W, et al. Advanced Urologic Cancer Consensus Conference (AUC3) 2025: expert consensus on the management of renal cell and urinary tract cancers. CA Cancer J Clin. 2026;e70052. doi:10.3322/caac.70052
Please note that Oleksandr N. Kryvenko’s middle initial was omitted in the originally published version of this article.
We apologize for this error.
{"title":"Correction to “Advanced Urologic Cancer Consensus Conference (AUC3) 2025: Expert consensus on the management of renal cell and urinary tract cancers”","authors":"","doi":"10.3322/caac.70070","DOIUrl":"10.3322/caac.70070","url":null,"abstract":"<p>McKay RR, Pal S, Xie W, et al. Advanced Urologic Cancer Consensus Conference (AUC3) 2025: expert consensus on the management of renal cell and urinary tract cancers. <i>CA Cancer J Clin</i>. 2026;e70052. doi:10.3322/caac.70052</p><p>Please note that Oleksandr N. Kryvenko’s middle initial was omitted in the originally published version of this article.</p><p>We apologize for this error.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12857780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146083773","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}
Perkins RB, Wolf AMD, Church TR, et al. Self-collected vaginal specimens for human papillomavirus testing and guidance on screening exit: An update to the American Cancer Society cervical cancer screening guideline. CA Cancer J Clin. 2026;e70041. doi:10.3322/caac.70041
In this article by Perkins, et al., there is an incorrect statement in Table 2 at column 3, row 4.
The original text read:
“Does not qualify for screening exit; very limited data.”
The statement should read:
“May qualify for screening exit; very limited data.”
In Table 2, the footnote was incorrectly stated. The correct footnote should read:
“Abbreviations: ACOG, American College of Obstetricians and Gynecologists; AIS, adenocarcinoma in situ; ASCCP, American Society of Colposcopy and Cervical Pathology; CIN, cervical intraepithelial neoplasia; CIN2, cervical intraepithelial neoplasia grade 2; CIN3, cervical intraepithelial neoplasia grade 3; HIV, human immunodeficiency virus; HPV, human papillomavirus; HSIL, high-grade squamous intraepithelial lesion; LSIL, low-grade squamous intraepithelial lesion.”
In Table 3, the footnote was incorrectly stated. The correct footnote should read:
“Abbreviations: CIN3+, cervical intraepithelial neoplasia grade 3 or worse; FDA, US Food and Drug Administration; HPV, human papillomavirus.”
On page 3 first column, “or the Abbott Alinity m with the Evalyn Brush or Qvintip swab (part of simpli-COLLECT kit)” should not be italicized.
We apologize for these errors.
{"title":"Correction to “Self-collected vaginal specimens for human papillomavirus testing and guidance on screening exit: An update to the American Cancer Society cervical cancer screening guideline”","authors":"","doi":"10.3322/caac.70066","DOIUrl":"10.3322/caac.70066","url":null,"abstract":"<p>Perkins RB, Wolf AMD, Church TR, et al. Self-collected vaginal specimens for human papillomavirus testing and guidance on screening exit: An update to the American Cancer Society cervical cancer screening guideline. <i>CA Cancer J Clin</i>. 2026;e70041. doi:10.3322/caac.70041</p><p>In this article by Perkins, et al., there is an incorrect statement in Table 2 at column 3, row 4.</p><p>The original text read:</p><p>“Does not qualify for screening exit; very limited data.”</p><p>The statement should read:</p><p>“May qualify for screening exit; very limited data.”</p><p>In Table 2, the footnote was incorrectly stated. The correct footnote should read:</p><p>“Abbreviations: ACOG, American College of Obstetricians and Gynecologists; AIS, adenocarcinoma in situ; ASCCP, American Society of Colposcopy and Cervical Pathology; CIN, cervical intraepithelial neoplasia; CIN2, cervical intraepithelial neoplasia grade 2; CIN3, cervical intraepithelial neoplasia grade 3; HIV, human immunodeficiency virus; HPV, human papillomavirus; HSIL, high-grade squamous intraepithelial lesion; LSIL, low-grade squamous intraepithelial lesion.”</p><p>In Table 3, the footnote was incorrectly stated. The correct footnote should read:</p><p>“Abbreviations: CIN3+, cervical intraepithelial neoplasia grade 3 or worse; FDA, US Food and Drug Administration; HPV, human papillomavirus.”</p><p>On page 3 first column, “or the Abbott Alinity m with the Evalyn Brush or Qvintip swab (part of simpli-COLLECT kit)” should not be italicized.</p><p>We apologize for these errors.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12851406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146058355","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}
Laura V. M. Baum MD, Kimberly L. Johung MD, PhD, Joanna Gibson MD, Gabriel Cartagena PhD, Daniel J. Boffa MD, Jill Lacy MD
<p>This patient is a man aged 55 years with a past medical history significant for hypertension, hyperlipidemia, post-traumatic stress (PTS) disorder, opioid use disorder on maintenance therapy, and tobacco dependence. He presented to the emergency department in 2023 with progressive dysphagia to solid food over 3 months. He did not report hematemesis, respiratory difficulties, or weight loss. His Eastern Cooperative Oncology Group performance status was 0. A complete metabolic profile and blood count were normal.</p><p>He underwent urgent esophagogastroduodenoscopy, which revealed a near complete obstructing esophageal mass at the gastroesophageal junction (GEJ), extending proximally 5 cm into the distal esophagus; biopsy confirmed a moderately differentiated adenocarcinoma (Figure 1). The tumor was negative for human epidermal growth factor receptor 2 (HER2/neu), mismatch-repair (MMR) proteins were intact (not shown), and programmed cell death ligand-1 (PD-L1) was detectable with a combined positive score (CPS) of 5–9 (Figure 1).</p><p>Staging computed tomography (CT) scan of the neck, chest, abdomen, and pelvis revealed nodular thickening of the GEJ and upper abdominal lymphadenopathy, with gastrohepatic nodes measuring up to 1 cm, prominent nodes adjacent to the gastric cardia, and a nonspecific, prominent, subcentimeter left periaortic node; there was no definitive evidence of distant metastases. On subsequent endoscopic ultrasound (EUS), the tumor was staged as clinical stage T3 and N2 (cT3N2) by sonographic criteria. Subsequent fluorodeoxyglucose–positron emission tomography (PET)/CT revealed a hypermetabolic distal esophageal GEJ (E/GEJ) mass as well as hypermetabolic upper abdominal and left axillary lymph nodes (Figure 2A,B). Biopsy of the left axillary node showed reactive lymphoid tissue in the setting of recent coronavirus disease vaccination.</p><p>He underwent staging laparoscopy, which showed no evidence of occult peritoneal carcinomatosis. Thus the final clinical stage was cT3N2M0 stage III adenocarcinoma of the GEJ according the American Joint Committee on Cancer (AJCC) 8th Edition clinical staging system for esophageal and GEJ adenocarcinoma.</p><p>After consultation with thoracic surgery and a multidisciplinary gastrointestinal tumor board discussion, the consensus was to proceed with curative-intent trimodality treatment with neoadjuvant chemoradiotherapy (CRT) followed by esophagectomy.</p><p>Because of severe dysphagia, the patient was treated initially with three cycles of induction chemotherapy with folinic acid (leucovorin), fluorouracil and oxaliplatin (FOLFOX; according to the Cancer and Leukemia Group B [CALGB] 80803 trial<span><sup>1</sup></span>) with marked improvement in symptoms, followed by neoadjuvant CRT (radiotherapy [RT] with concurrent FOLFOX for three cycles). Postneoadjuvant therapy PET imaging revealed marked interval decrease in size and metabolic activity of the distal E/GEJ mass and resolution of fluo
{"title":"Adenocarcinoma of the esophagus and gastroesophageal junction: The evolving treatment landscape for locally advanced and metastatic disease in the era of immune checkpoint inhibitors and biomarker-driven therapeutics","authors":"Laura V. M. Baum MD, Kimberly L. Johung MD, PhD, Joanna Gibson MD, Gabriel Cartagena PhD, Daniel J. Boffa MD, Jill Lacy MD","doi":"10.3322/caac.70050","DOIUrl":"10.3322/caac.70050","url":null,"abstract":"<p>This patient is a man aged 55 years with a past medical history significant for hypertension, hyperlipidemia, post-traumatic stress (PTS) disorder, opioid use disorder on maintenance therapy, and tobacco dependence. He presented to the emergency department in 2023 with progressive dysphagia to solid food over 3 months. He did not report hematemesis, respiratory difficulties, or weight loss. His Eastern Cooperative Oncology Group performance status was 0. A complete metabolic profile and blood count were normal.</p><p>He underwent urgent esophagogastroduodenoscopy, which revealed a near complete obstructing esophageal mass at the gastroesophageal junction (GEJ), extending proximally 5 cm into the distal esophagus; biopsy confirmed a moderately differentiated adenocarcinoma (Figure 1). The tumor was negative for human epidermal growth factor receptor 2 (HER2/neu), mismatch-repair (MMR) proteins were intact (not shown), and programmed cell death ligand-1 (PD-L1) was detectable with a combined positive score (CPS) of 5–9 (Figure 1).</p><p>Staging computed tomography (CT) scan of the neck, chest, abdomen, and pelvis revealed nodular thickening of the GEJ and upper abdominal lymphadenopathy, with gastrohepatic nodes measuring up to 1 cm, prominent nodes adjacent to the gastric cardia, and a nonspecific, prominent, subcentimeter left periaortic node; there was no definitive evidence of distant metastases. On subsequent endoscopic ultrasound (EUS), the tumor was staged as clinical stage T3 and N2 (cT3N2) by sonographic criteria. Subsequent fluorodeoxyglucose–positron emission tomography (PET)/CT revealed a hypermetabolic distal esophageal GEJ (E/GEJ) mass as well as hypermetabolic upper abdominal and left axillary lymph nodes (Figure 2A,B). Biopsy of the left axillary node showed reactive lymphoid tissue in the setting of recent coronavirus disease vaccination.</p><p>He underwent staging laparoscopy, which showed no evidence of occult peritoneal carcinomatosis. Thus the final clinical stage was cT3N2M0 stage III adenocarcinoma of the GEJ according the American Joint Committee on Cancer (AJCC) 8th Edition clinical staging system for esophageal and GEJ adenocarcinoma.</p><p>After consultation with thoracic surgery and a multidisciplinary gastrointestinal tumor board discussion, the consensus was to proceed with curative-intent trimodality treatment with neoadjuvant chemoradiotherapy (CRT) followed by esophagectomy.</p><p>Because of severe dysphagia, the patient was treated initially with three cycles of induction chemotherapy with folinic acid (leucovorin), fluorouracil and oxaliplatin (FOLFOX; according to the Cancer and Leukemia Group B [CALGB] 80803 trial<span><sup>1</sup></span>) with marked improvement in symptoms, followed by neoadjuvant CRT (radiotherapy [RT] with concurrent FOLFOX for three cycles). Postneoadjuvant therapy PET imaging revealed marked interval decrease in size and metabolic activity of the distal E/GEJ mass and resolution of fluo","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2026-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12812016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994123","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}
Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths in the United States and compiles the most recent data on population-based cancer occurrence and outcomes using data collected by central cancer registries (incidence, through 2022) and the National Center for Health Statistics (mortality, through 2023). In 2026, approximately 2,114,850 new cancer cases and 626,140 cancer deaths are projected to occur in the United States. The cancer mortality rate continued to decline through 2023, averting 4.8 million deaths since 1991, largely because of smoking reductions, earlier detection, and improved treatment. These interventions are also evident in rising 5-year relative survival, which reached a milestone 70% for diagnoses during 2015–2021 overall, 69% for regional-stage disease, and 35% for distant-stage (metastatic) disease, up from 63%, 54%, and 17%, respectively, in the mid-1990s. People with high-mortality cancers and advanced diagnoses had the largest gains, including increases from 32% to 62% for myeloma, 7% to 22% for liver cancer, 16% to 35% for metastatic melanoma, 8% to 18% for metastatic rectal cancer, 20% to 37% for regional lung cancer, and 2% to 10% for metastatic lung cancer. Nevertheless, lung cancer will cause more deaths in 2026 than second-ranking colorectal cancer and third-ranking pancreatic cancer combined. In summary, decades of scientific investment have translated to longer lives for people with even the most fatal cancers. However, continued progress is threatened by proposed federal cuts to cancer research and health insurance, which provides access to life-saving cancer treatment.
{"title":"Cancer statistics, 2026","authors":"Rebecca L. Siegel MPH, Tyler B. Kratzer MPH, Nikita Sandeep Wagle PhD, MBBS, MHA, Hyuna Sung PhD, Ahmedin Jemal DVM, PhD","doi":"10.3322/caac.70043","DOIUrl":"10.3322/caac.70043","url":null,"abstract":"<p>Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths in the United States and compiles the most recent data on population-based cancer occurrence and outcomes using data collected by central cancer registries (incidence, through 2022) and the National Center for Health Statistics (mortality, through 2023). In 2026, approximately 2,114,850 new cancer cases and 626,140 cancer deaths are projected to occur in the United States. The cancer mortality rate continued to decline through 2023, averting 4.8 million deaths since 1991, largely because of smoking reductions, earlier detection, and improved treatment. These interventions are also evident in rising 5-year relative survival, which reached a milestone 70% for diagnoses during 2015–2021 overall, 69% for regional-stage disease, and 35% for distant-stage (metastatic) disease, up from 63%, 54%, and 17%, respectively, in the mid-1990s. People with high-mortality cancers and advanced diagnoses had the largest gains, including increases from 32% to 62% for myeloma, 7% to 22% for liver cancer, 16% to 35% for metastatic melanoma, 8% to 18% for metastatic rectal cancer, 20% to 37% for regional lung cancer, and 2% to 10% for metastatic lung cancer. Nevertheless, lung cancer will cause more deaths in 2026 than second-ranking colorectal cancer and third-ranking pancreatic cancer combined. In summary, decades of scientific investment have translated to longer lives for people with even the most fatal cancers. However, continued progress is threatened by proposed federal cuts to cancer research and health insurance, which provides access to life-saving cancer treatment.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70043","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145956226","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 this issue of <i>CA: A Cancer Journal for Clinicians</i>, the American Cancer Society (ACS) delivers its highly anticipated annual portrait of the nation's cancer burden.<span><sup>1</sup></span> As in previous years, this authoritative and widely cited report draws on data from every state and the District of Columbia, aggregating data from cancer registries and the National Center for Health Statistics to provide the most comprehensive and detailed view of cancer incidence, mortality, demographics, and disparities.</p><p>In 2026, the ACS estimates that there will be more than 2.1 million new cancer diagnoses (or about 5800 cases daily) in the United States. In men, the most common malignancies continue to be prostate, lung, and colorectal cancers; in women, breast, lung, and colorectal cancers are most common. Yet this year's projections also bring some troubling trends: more men with prostate cancer will be diagnosed at advanced stages, in which a cure is less attainable; breast cancer incidence continues to rise, especially among women younger than 50 years; and colorectal cancer is also increasing in adults younger than 50 years.</p><p>Counterbalancing these concerns is a profoundly encouraging trend: cancer mortality in the United States continues its long, steady decline. Since 1991, cancer death rates have fallen by 34%, translating to 4.8 million lives saved. This extraordinary progress reflects decades of iterative and transformative advances in cancer research and the implementation of those findings into prevention, screening, and clinical care. In short, research saves lives!</p><p>In the case of publicly funded clinical trials conducted through the National Cancer Institute's (NCI's) National Clinical Trials Network (NCTN), this progress has also been remarkably cost effective. In a study of NCTN trials since 1980, approximately 14.2 million additional life-years were gained by patients with cancer, with projected gains of 24.1 million life-years by 2030. Incredibly, the federal investment cost per life-year gained was estimated to be just $326.<span><sup>2</sup></span></p><p>These ACS projections have provided a rigorous, empirical foundation for shaping, prioritizing, and implementing research strategies across both laboratory and clinical settings. They also clarify where our knowledge falls short and expose where cancer health disparities persist. In spotlighting malignancies with rising incidence, stubbornly high mortality, or persistent inequities, these data direct researchers to focus efforts on the most urgent unmet needs in cancer research, ensuring that progress will have a profound impact on patients and communities.</p><p>Within the United States research ecosystem of federally funded clinical trials, the NCI's NCTN, Experimental Therapeutics Clinical Trials Network (ETCTN), and Cancer Centers Program all play pivotal roles in translating the ACS's cancer statistics into actionable research. Within the NCTN cooper
{"title":"Cancer statistics, 2026: Charting a course for a national cancer research agenda","authors":"Primo N. Lara Jr MD, Dawn L. Hershman MD, MS","doi":"10.3322/caac.70061","DOIUrl":"10.3322/caac.70061","url":null,"abstract":"<p>In this issue of <i>CA: A Cancer Journal for Clinicians</i>, the American Cancer Society (ACS) delivers its highly anticipated annual portrait of the nation's cancer burden.<span><sup>1</sup></span> As in previous years, this authoritative and widely cited report draws on data from every state and the District of Columbia, aggregating data from cancer registries and the National Center for Health Statistics to provide the most comprehensive and detailed view of cancer incidence, mortality, demographics, and disparities.</p><p>In 2026, the ACS estimates that there will be more than 2.1 million new cancer diagnoses (or about 5800 cases daily) in the United States. In men, the most common malignancies continue to be prostate, lung, and colorectal cancers; in women, breast, lung, and colorectal cancers are most common. Yet this year's projections also bring some troubling trends: more men with prostate cancer will be diagnosed at advanced stages, in which a cure is less attainable; breast cancer incidence continues to rise, especially among women younger than 50 years; and colorectal cancer is also increasing in adults younger than 50 years.</p><p>Counterbalancing these concerns is a profoundly encouraging trend: cancer mortality in the United States continues its long, steady decline. Since 1991, cancer death rates have fallen by 34%, translating to 4.8 million lives saved. This extraordinary progress reflects decades of iterative and transformative advances in cancer research and the implementation of those findings into prevention, screening, and clinical care. In short, research saves lives!</p><p>In the case of publicly funded clinical trials conducted through the National Cancer Institute's (NCI's) National Clinical Trials Network (NCTN), this progress has also been remarkably cost effective. In a study of NCTN trials since 1980, approximately 14.2 million additional life-years were gained by patients with cancer, with projected gains of 24.1 million life-years by 2030. Incredibly, the federal investment cost per life-year gained was estimated to be just $326.<span><sup>2</sup></span></p><p>These ACS projections have provided a rigorous, empirical foundation for shaping, prioritizing, and implementing research strategies across both laboratory and clinical settings. They also clarify where our knowledge falls short and expose where cancer health disparities persist. In spotlighting malignancies with rising incidence, stubbornly high mortality, or persistent inequities, these data direct researchers to focus efforts on the most urgent unmet needs in cancer research, ensuring that progress will have a profound impact on patients and communities.</p><p>Within the United States research ecosystem of federally funded clinical trials, the NCI's NCTN, Experimental Therapeutics Clinical Trials Network (ETCTN), and Cancer Centers Program all play pivotal roles in translating the ACS's cancer statistics into actionable research. Within the NCTN cooper","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70061","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145956224","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}
Akshara Singareeka Raghavendra MD, MS, Senthil Damodaran MD, PhD, Carlos H. Barcenas MD, MSc, Suzanne A. Fuqua PhD, Rachel M. Layman MD, Debu Tripathy MD
The hormone receptor (HR)-positive/human epidermal growth factor receptor 2 (HER2)-negative breast cancer subtype accounts for most early and metastatic breast cancer (MBC) cases. HR-positive/HER2-negative MBC is characterized by a relatively prolonged, although variable, disease course and substantial intertumoral and intratumoral heterogeneity. Although endocrine-based therapies remain the cornerstone of treatment, nearly all patients eventually develop resistance, which is increasingly addressed with biologically targeted agents and newer-generation cytotoxic drugs. This review summarizes the current understanding of HR-positive/HER2-negative MBC biology, highlighting mechanisms of intrinsic and acquired resistance, including driver genomic alterations that, along with clinical factors, help guide therapeutic choices and sequencing. The authors specify and discuss how genomic and transcriptomic profiling inform treatment selection and how side effects and overall patient experience are considered in decision making. Advances in targeted therapies, such as CDK4/6 (cyclin-dependent kinase 4/6), PI3K (phosphatidylinositol 3-kinase), and AKT (protein kinase B) inhibitors, and next-generation estrogen receptor degraders are reviewed along with the expanding role of antibody–drug conjugates and biomarker-guided tumor-agnostic biologic therapies. The authors also explore evolving biologic concepts, including the impact of the tumor microenvironment on resistance and disease progression, and consider the distinct clinical behavior of invasive lobular carcinoma and current approaches. Emerging data from contemporary clinical trials promise to refine clinical and biomarker-driven algorithms and improve outcomes for patients with HR-positive/HER2-negative MBC. Ongoing multi-omic research and adaptive clinical strategies will be essential to further the application of precision oncology in this most common subtype of MBC. Importantly, patient-reported outcomes, shared decision making, and real-world evidence are increasingly useful in formulating comprehensive care plans, guidelines, and policy. The modern treatment landscape features a personalized approach that integrates clinical features, biomarkers, and patient preferences across the disease continuum.
{"title":"Personalizing therapies over the course of hormone receptor-positive/HER2-negative metastatic breast cancer","authors":"Akshara Singareeka Raghavendra MD, MS, Senthil Damodaran MD, PhD, Carlos H. Barcenas MD, MSc, Suzanne A. Fuqua PhD, Rachel M. Layman MD, Debu Tripathy MD","doi":"10.3322/caac.70055","DOIUrl":"10.3322/caac.70055","url":null,"abstract":"<p>The hormone receptor (HR)-positive/human epidermal growth factor receptor 2 (HER2)-negative breast cancer subtype accounts for most early and metastatic breast cancer (MBC) cases. HR-positive/HER2-negative MBC is characterized by a relatively prolonged, although variable, disease course and substantial intertumoral and intratumoral heterogeneity. Although endocrine-based therapies remain the cornerstone of treatment, nearly all patients eventually develop resistance, which is increasingly addressed with biologically targeted agents and newer-generation cytotoxic drugs. This review summarizes the current understanding of HR-positive/HER2-negative MBC biology, highlighting mechanisms of intrinsic and acquired resistance, including driver genomic alterations that, along with clinical factors, help guide therapeutic choices and sequencing. The authors specify and discuss how genomic and transcriptomic profiling inform treatment selection and how side effects and overall patient experience are considered in decision making. Advances in targeted therapies, such as CDK4/6 (cyclin-dependent kinase 4/6), PI3K (phosphatidylinositol 3-kinase), and AKT (protein kinase B) inhibitors, and next-generation estrogen receptor degraders are reviewed along with the expanding role of antibody–drug conjugates and biomarker-guided tumor-agnostic biologic therapies. The authors also explore evolving biologic concepts, including the impact of the tumor microenvironment on resistance and disease progression, and consider the distinct clinical behavior of invasive lobular carcinoma and current approaches. Emerging data from contemporary clinical trials promise to refine clinical and biomarker-driven algorithms and improve outcomes for patients with HR-positive/HER2-negative MBC. Ongoing multi-omic research and adaptive clinical strategies will be essential to further the application of precision oncology in this most common subtype of MBC. Importantly, patient-reported outcomes, shared decision making, and real-world evidence are increasingly useful in formulating comprehensive care plans, guidelines, and policy. The modern treatment landscape features a personalized approach that integrates clinical features, biomarkers, and patient preferences across the disease continuum.</p>","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949885","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>Breast cancer is the most common cancer among females in the United States, and metastatic breast cancer is estimated to cause more than 42,000 deaths in 2025.<span><sup>1</sup></span> Hormone receptor (HR)–positive, human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer is the most common subtype of metastatic breast cancer.<span><sup>1</sup></span> Although advances in endocrine and targeted therapies have improved patient outcomes, resistance and disease progression remain common, and the optimal sequencing of available treatments is unknown. In their review, Raghavendra and colleagues present a framework for managing patients with HR-positive, HER2-negative metastatic breast cancer, describing knowledge gaps and the growing role of precision oncology tools, such as genomic profiling of tumor tissue or circulating tumor DNA (ctDNA), in treatment selection.<span><sup>2</sup></span> The review describes advances in endocrine and targeted therapies that have improved patient outcomes.</p><p>As highlighted in the article, there have been two major advances in the treatment of HR-positive metastatic breast cancer over the last decade: first, the approval of cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors and, second, the increased use of genomic profiling of tumor tissue and ctDNA for treatment selection, driven primarily by the approval of novel, molecularly targeted therapies that were previously unavailable. An improved understanding of the estrogen receptor pathway and its downstream promotion of the cell cycle has led to the development and approval of CDK4/6 inhibitors in combination with endocrine therapy.<span><sup>3-6</sup></span> The introduction of these novel drugs is associated with significant improvements in progression-free survival and, in many patients, overall survival as well, making it one of the biggest advancements in the treatment of metastatic HR-positive breast cancer.<span><sup>4</sup></span> However, some patients do progress early on these therapies, and, as Raghavendra and colleagues have described, it is unclear whether CDK4/6 inhibitors need to be introduced in the first-line setting for all patients.<span><sup>7</sup></span> To improve precision, we need to develop biomarkers that help identify those patients who have intrinsic resistance to CDK4/6 inhibitors and those who can safely forego the addition of CDK4/6 inhibitors in the first-line setting.</p><p>A major shift in recent years has been the routine integration of genomic and molecular characterization using next-generation sequencing (NGS), including analyses of tumor tissue and ctDNA. These tools provide insight into acquired resistance mechanisms, guide targeted therapy selection, and recent data suggest that adaptive treatment changes based on the emergence of genomic alterations, before clinical or radiographic progression, could improve patient outcomes.<span><sup>8, 9</sup></span></p><p>NGS has become the standard for
{"title":"Pursuit of precision oncology in the treatment of metastatic hormone receptor–positive breast cancer: Making strides or barely moving?","authors":"Ilana Schlam MD, MPH, Ajay Dhakal MBBS","doi":"10.3322/caac.70060","DOIUrl":"10.3322/caac.70060","url":null,"abstract":"<p>Breast cancer is the most common cancer among females in the United States, and metastatic breast cancer is estimated to cause more than 42,000 deaths in 2025.<span><sup>1</sup></span> Hormone receptor (HR)–positive, human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer is the most common subtype of metastatic breast cancer.<span><sup>1</sup></span> Although advances in endocrine and targeted therapies have improved patient outcomes, resistance and disease progression remain common, and the optimal sequencing of available treatments is unknown. In their review, Raghavendra and colleagues present a framework for managing patients with HR-positive, HER2-negative metastatic breast cancer, describing knowledge gaps and the growing role of precision oncology tools, such as genomic profiling of tumor tissue or circulating tumor DNA (ctDNA), in treatment selection.<span><sup>2</sup></span> The review describes advances in endocrine and targeted therapies that have improved patient outcomes.</p><p>As highlighted in the article, there have been two major advances in the treatment of HR-positive metastatic breast cancer over the last decade: first, the approval of cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors and, second, the increased use of genomic profiling of tumor tissue and ctDNA for treatment selection, driven primarily by the approval of novel, molecularly targeted therapies that were previously unavailable. An improved understanding of the estrogen receptor pathway and its downstream promotion of the cell cycle has led to the development and approval of CDK4/6 inhibitors in combination with endocrine therapy.<span><sup>3-6</sup></span> The introduction of these novel drugs is associated with significant improvements in progression-free survival and, in many patients, overall survival as well, making it one of the biggest advancements in the treatment of metastatic HR-positive breast cancer.<span><sup>4</sup></span> However, some patients do progress early on these therapies, and, as Raghavendra and colleagues have described, it is unclear whether CDK4/6 inhibitors need to be introduced in the first-line setting for all patients.<span><sup>7</sup></span> To improve precision, we need to develop biomarkers that help identify those patients who have intrinsic resistance to CDK4/6 inhibitors and those who can safely forego the addition of CDK4/6 inhibitors in the first-line setting.</p><p>A major shift in recent years has been the routine integration of genomic and molecular characterization using next-generation sequencing (NGS), including analyses of tumor tissue and ctDNA. These tools provide insight into acquired resistance mechanisms, guide targeted therapy selection, and recent data suggest that adaptive treatment changes based on the emergence of genomic alterations, before clinical or radiographic progression, could improve patient outcomes.<span><sup>8, 9</sup></span></p><p>NGS has become the standard for ","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949868","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>Studying cancer incidence by country presents a unique global health opportunity to investigate lip, oral, and pharyngeal cancers (LOPCs), aiming to identify international disparities and understand disease burden across various levels of socioeconomic development. This cross-national approach highlights the central role that social determinants play in shaping LOPC burden inequalities worldwide.<span><sup>1</sup></span> LOPCs constitute a heterogeneous group of diseases with distinct etiologic profiles and anatomic subsites. Oral cavity cancers are primarily linked to tobacco use in its various forms and alcohol consumption, whereas oropharyngeal cancers share these traditional risk factors but are increasingly associated with high-risk human papillomavirus (HPV) infection, particularly HPV types 16 and 18.<span><sup>2</sup></span></p><p>The findings reported by Rumgay and colleagues<span><sup>3</sup></span> in this issue of <i>CA: A Cancer Journal for Clinicians</i> provide a comprehensive overview of LOPC incidence across 185 countries, using estimates from the International Agency for Research on Cancer. The authors estimated 758,000 new cases of LOPC globally in 2022 with a predominance of men (7:1 ratio), with cancers of the oral cavity, followed by the oropharynx and nasopharynx, representing the most incident cases. Their results reveal that oral cavity cancer incidence remains alarmingly high in South-Central Asia, Melanesia, Micronesia, and Polynesia; whereas oropharyngeal cancer rates are elevated in Europe, and represent the most common LOPC subsite among men in North and South America.<span><sup>3</sup></span></p><p>Given the distinct etiologies of oral and oropharyngeal cancers, these findings call for equitable health promotion and prevention strategies tailored to specific risk exposures within each country. Rumgay and colleagues<span><sup>3</sup></span> appropriately emphasize the World Health Organization (WHO) Framework Convention on Tobacco Control and its MPOWER measures (Monitoring tobacco use; Protecting people from tobacco smoke; Offering help to quit tobacco use; Warning about the dangers of tobacco; Enforcing bans on tobacco advertising, promotion, and sponsorship; and Raising tobacco taxes) as central tools to reduce exposure. Emerging evidence links comprehensive implementation of MPOWER policies with significant reductions in global smoking prevalence and consequent declines in incidence, mortality, and disability-adjusted life-years related to LOPCs.<span><sup>4, 5</sup></span></p><p>Efforts to curb alcohol consumption and increase adoption of gender-neutral HPV vaccination are both feasible and essential but have shown uneven progress compared with efforts to reduce consumption of tobacco products. In this regard, the WHO Global Alcohol Action Plan 2022–2030 and the SAFER initiative provide evidence-based, cost-effective strategies. However, evaluations indicate challenges, such as commercial interference, limite
{"title":"Global incidence of lip, oral cavity, and pharyngeal cancers: Disparities, determinants, and opportunities for prevention, early detection, and treatment","authors":"Fernando Neves Hugo DDS, MSc, PhD","doi":"10.3322/caac.70059","DOIUrl":"10.3322/caac.70059","url":null,"abstract":"<p>Studying cancer incidence by country presents a unique global health opportunity to investigate lip, oral, and pharyngeal cancers (LOPCs), aiming to identify international disparities and understand disease burden across various levels of socioeconomic development. This cross-national approach highlights the central role that social determinants play in shaping LOPC burden inequalities worldwide.<span><sup>1</sup></span> LOPCs constitute a heterogeneous group of diseases with distinct etiologic profiles and anatomic subsites. Oral cavity cancers are primarily linked to tobacco use in its various forms and alcohol consumption, whereas oropharyngeal cancers share these traditional risk factors but are increasingly associated with high-risk human papillomavirus (HPV) infection, particularly HPV types 16 and 18.<span><sup>2</sup></span></p><p>The findings reported by Rumgay and colleagues<span><sup>3</sup></span> in this issue of <i>CA: A Cancer Journal for Clinicians</i> provide a comprehensive overview of LOPC incidence across 185 countries, using estimates from the International Agency for Research on Cancer. The authors estimated 758,000 new cases of LOPC globally in 2022 with a predominance of men (7:1 ratio), with cancers of the oral cavity, followed by the oropharynx and nasopharynx, representing the most incident cases. Their results reveal that oral cavity cancer incidence remains alarmingly high in South-Central Asia, Melanesia, Micronesia, and Polynesia; whereas oropharyngeal cancer rates are elevated in Europe, and represent the most common LOPC subsite among men in North and South America.<span><sup>3</sup></span></p><p>Given the distinct etiologies of oral and oropharyngeal cancers, these findings call for equitable health promotion and prevention strategies tailored to specific risk exposures within each country. Rumgay and colleagues<span><sup>3</sup></span> appropriately emphasize the World Health Organization (WHO) Framework Convention on Tobacco Control and its MPOWER measures (Monitoring tobacco use; Protecting people from tobacco smoke; Offering help to quit tobacco use; Warning about the dangers of tobacco; Enforcing bans on tobacco advertising, promotion, and sponsorship; and Raising tobacco taxes) as central tools to reduce exposure. Emerging evidence links comprehensive implementation of MPOWER policies with significant reductions in global smoking prevalence and consequent declines in incidence, mortality, and disability-adjusted life-years related to LOPCs.<span><sup>4, 5</sup></span></p><p>Efforts to curb alcohol consumption and increase adoption of gender-neutral HPV vaccination are both feasible and essential but have shown uneven progress compared with efforts to reduce consumption of tobacco products. In this regard, the WHO Global Alcohol Action Plan 2022–2030 and the SAFER initiative provide evidence-based, cost-effective strategies. However, evaluations indicate challenges, such as commercial interference, limite","PeriodicalId":137,"journal":{"name":"CA: A Cancer Journal for Clinicians","volume":"76 1","pages":""},"PeriodicalIF":232.4,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acsjournals.onlinelibrary.wiley.com/doi/epdf/10.3322/caac.70059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807920","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}
Mariana Chavez-MacGregor MD, MSc, Inimfon Jackson MD, MPH, PhD
<p>Over the last few decades, there has been significant progress in the fight against cancer. In the United States between 1991 and 2022, cancer-related mortality decreased, with an estimated 4.5 million fewer deaths.<span><sup>2</sup></span> This is because of numerous factors, including reductions in smoking, early detection for cancers with available screening, and improved therapies in the management of both localized and metastatic cancer.<span><sup>2</sup></span> Despite such improvements, the American Cancer Society's (ACS) Report on the Status of Cancer Disparities by Islami and colleagues that accompanies this editorial, sheds light on the persistent and substantial disparities across the cancer care continuum, including risk factors, incidence, stage at diagnosis, receipt of care, survival, and mortality for many cancers.<span><sup>3</sup></span> The report evaluates not only the effect of race and ethnicity but also educational status, geographic location, sex, and social determinants of health. In a nation where some of the world’s most advanced treatments and medical technologies are available, it is tragic that not all individuals benefit equally from these innovations. These persistent cancer disparities reflect complex interactions between race and ethnicity, socioeconomic status, and geography.<span><sup>4</sup></span> Systemic inequities and policies that have not satisfactorily addressed the most vulnerable have widened the gap between the rich and the poor, disproportionately affecting racial and ethnically minoritized individuals.<span><sup>5</sup></span></p><p>According to the 2025 ACS report, the incidence of cancer is higher among Black and American Indian/Alaska Native men and women compared with White individuals across multiple cancers and, notably, these populations also have the highest cancer-related mortality rates.<span><sup>3</sup></span> Strategies to improve cancer outcomes have led to a modest narrowing of these gaps over time; however, Black–White mortality disparities persist.<span><sup>6</sup></span> Although cancer disparities are frequently described according to race and ethnicity, to better understand the implications of this report, it is crucial to detangle the concept of race, which nonetheless remains a strong predictor of higher cancer incidence and worse survival.<span><sup>7</sup></span> The statistics presented in the ACS report highlight that, beyond race and ethnicity, factors like inequitable access to care, poverty, social determinants of health, and other structural factors are key drivers of disparities and associated poor outcomes, rather than biologic differences alone.</p><p>Social determinants of health unequally affect racial and ethnically minoritized individuals, compromising their opportunities to have health care outcomes comparable to those of White populations. Black, American Indian/Alaska Native, and Hispanic individuals are more likely to be poor, less educated, lack health i
在过去的几十年里，与癌症的斗争取得了重大进展。在美国，1991年至2022年期间，癌症相关死亡率下降，估计死亡人数减少了450万这是由于许多因素，包括吸烟的减少，通过可用的筛查早期发现癌症，以及改善局部和转移性癌症的治疗方法尽管取得了这些进步，但美国癌症协会（ACS）的《癌症差异现状报告》（由Islami及其同事撰写，随本社论发表）揭示了癌症治疗连续体中持续存在的实质性差异，包括许多癌症的风险因素、发病率、诊断阶段、接受治疗、生存率和死亡率该报告不仅评估了种族和族裔的影响，还评估了教育状况、地理位置、性别和健康的社会决定因素。在一个拥有一些世界上最先进的治疗方法和医疗技术的国家，并非所有人都能从这些创新中平等受益，这是可悲的。这些持续存在的癌症差异反映了种族和民族、社会经济地位和地理之间复杂的相互作用系统性的不平等和政策未能令人满意地解决最弱势群体的问题，拉大了贫富差距，不成比例地影响到种族和少数民族的个人。5根据2025年美国癌症学会的报告，在多种癌症中，黑人和美洲印第安人/阿拉斯加土著男性和女性的癌症发病率高于白人，值得注意的是，这些人群的癌症相关死亡率也最高随着时间的推移，改善癌症预后的战略导致这些差距适度缩小；然而，黑人和白人的死亡率差距仍然存在虽然癌症差异经常根据种族和民族来描述，但为了更好地理解本报告的含义，理清种族的概念是至关重要的，尽管如此，种族仍然是高癌症发病率和低存活率的有力预测因素ACS报告中提供的统计数据强调，除了种族和族裔之外，诸如获得护理机会不公平、贫困、健康的社会决定因素和其他结构性因素等因素是造成差异和相关不良结果的关键因素，而不仅仅是生物差异。健康的社会决定因素不平等地影响到种族和少数民族的个人，损害了他们获得与白人相当的保健结果的机会。与白人相比，黑人、美洲印第安人/阿拉斯加原住民和西班牙裔人更有可能贫穷、受教育程度低、缺乏医疗保险、食物和住房不安全。例如，在2024年，大约21.4%的美国印第安人/阿拉斯加原住民、16%的黑人和15.7%的西班牙裔18-64岁的人的收入低于贫困线，而亚洲人和白人的这一比例分别为8.7%和7.7%这些不公平现象与获得癌症预防服务的机会减少、癌症晚期诊断、治疗延误和生存结果恶化有关。3,4此外，种族居住隔离、经济排斥、歧视性政策和有限的医疗保健基础设施等结构性因素加剧了这些差异，为优质医疗保健创造了障碍。所有这些因素加在一起，使弱势群体的健康状况不佳和不平等现象长期持续下去，形成一个不利的循环。鉴于这些结构性不平等和障碍，必须呼吁采取行动。例如，改善获得负担得起的高质量健康保险的机会是实现卫生公平的一种方式。2025年美国癌症学会的报告指出，没有保险的18-64岁的成年人更有可能因为费用问题而延迟或不接受必要的医疗护理，从而导致错过或延迟对结直肠癌和女性乳腺癌等癌症的筛查这些调查结果突出表明，迫切需要保护和扩大弱势群体获得负担得起的医疗保险的机会。尽管医疗保险通过提供医疗保险来保护大多数65岁以上的成年人，但年轻人，特别是那些收入和教育水平较低以及居住在非大都市地区的人，仍然处于危险之中研究表明，扩大医疗补助扩大了保险覆盖面，改善了癌症筛查，降低了低收入成年人的死亡率，10-12强烈表明，政策变化可以直接改善癌症治疗结果，有利于改善健康公平。 值得注意的是，正如ACS报告中所强调的那样，总体癌症死亡率最高的国会选区包括中西部的南部和东部中北部地区，3在很大程度上与那些根据2010年《平价医疗法案》（Affordable Care Act）没有扩大医疗补助计划的州的地区相对应。鉴于这些证据，有人可能会说，我们必须维持并寻求扩大医疗补助和市场补贴，并激励那些没有扩大补贴的州也这样做，以确保所有人都能获得癌症预防服务和及时的癌症治疗。当按城市化程度进行分析时，ACS的报告显示，与大都市地区相比，非大都市地区的癌症死亡率更高，从2019年到2023.3，男性死亡率增加23%，女性死亡率增加18%。差异最大的是肺癌（男性高47%，女性高40%）、宫颈癌（高36%）和结直肠癌（高28%）这些癌症要么与可改变的风险因素有关，要么可以通过筛查在早期阶段诊断出来。远程保健方案、邮寄上门的筛查测试包以及使用移动筛查设备成功地增加了癌症筛查和后续护理的机会。13-15 .通过赞助多方面的筛查项目，降低农村社区晚期可预防癌症的诊断比例，可以进一步提高早期癌症的检测水平。此外，远程保健应该便于医生和病人进行癌症预防访问和检查，特别是在交通不便的地方。癌症差异也会影响癌症定向治疗的接受。收入较低、没有保险或居住在农村地区的个人不太可能得到与指导方针一致的护理针对多种癌症类型的报告支持这样的观点，即这类人群更有可能经历经济上的毒性、医疗服务的碎片化以及获得专业医疗服务的机会有限，特别是在农村地区。16,17他们也更有可能经历治疗延误，从而导致更糟糕的结果。社会经济地位低的患者或在主要是社会经济地位低的人居住的设施中接受治疗的患者接受标准治疗的可能性较小。此外，那些生活在农村地区的人面临着额外的障碍，例如需要长途跋涉才能接受治疗，从而产生大量的交通费用。因此，他们面临更大的风险，经历财务毒性和不遵守规定，所有这些都可能导致更高的死亡率需要政策和机构战略来解决患者层面和机构层面的障碍，以确保所有人公平获得及时、高质量和符合指南的癌症治疗。除了治疗提供方面的差异外，临床试验中少数族裔患者的代表性不足仍然是公平癌症治疗的主要挑战。旨在了解临床试验参与障碍的研究表明，这些障碍存在于多个层面，19包括结构、机构、提供者层面、患者层面和研究层面的障碍。分散的临床试验已经证明可以显著改善社区环境中患者获得临床试验的机会，我们认为应该优先考虑这一点。联邦政府资助的研究，特别是国家临床试验网络和国家癌症研究所社区肿瘤研究项目，是美国国家癌症研究所的两个基石项目，它们共同使癌症临床试验在全国范围内更容易获得、公平和具有代表性。这些项目将学术中心、社区医院和私人诊所连接成一个进行临床试验的大网络。此外，国家癌症研究所社区肿瘤研究项目支持癌症预防、症状管理和生存研究，以及癌症护理研究。事实证明，这两个项目都是将临床试验引入全国社区实践的有力工具。它们的存在是确保所有人获得临床试验的关键，但对少数群体和生活在农村地区的人尤其重要，否则他们参与可能挽救生命的研究的机会有限。Islami等人的ACS报告强调了重要的差异，这些差异不仅影响到弱势群体和边缘人群，还影响到整个社区、整个社会和国家。为了改善保健公平，需要进行重大的结构性改革，以解决贫困和获得保健的问题。
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