Sayaka Ishizawa, Jiangong Niu, Martin C Tammemagi, Ehsan Irajizad, Yu Shen, Karen H Lu, Larissa A Meyer, Iakovos Toumazis
Background: Ovarian cancer is among the leading causes of gynecologic cancer-related death. Past ovarian cancer screening trials using combination of cancer antigen 125 testing and transvaginal ultrasound failed to yield statistically significant mortality reduction. Estimates of ovarian cancer sojourn time-that is, the period from when the cancer is first screen detectable until clinical detection-may inform future screening programs.
Methods: We modeled ovarian cancer progression as a continuous time Markov chain and estimated screening modality-specific sojourn time and sensitivity using a Bayesian approach. Model inputs were derived from the screening arms (multimodal and ultrasound) of the UK Collaborative Trial of Ovarian Cancer Screening and the Prostate, Lung, Colorectal and Ovarian cancer screening trials. We assessed the quality of our estimates by using the posterior predictive P value. We derived histology-specific sojourn times by adjusting the overall sojourn time based on the corresponding histology-specific survival from the Surveillance, Epidemiology, and End Results Program.
Results: The overall ovarian cancer sojourn time was 2.1 years (posterior predictive P value = .469) in the Prostate, Lung, Colorectal and Ovarian studies, with 65.7% screening sensitivity. The sojourn time was 2.0 years (posterior predictive P value = .532) in the United Kingdom Collaborative Trial of Ovarian Cancer Screening's multimodal screening arm and 2.4 years (posterior predictive P value = .640) in the ultrasound screening arm, with sensitivities of 93.2% and 64.5%, respectively. Stage-specific screening sensitivities in the Prostate, Lung, Colorectal and Ovarian studies were 39.1% and 82.9% for early-stage and advanced-stage disease, respectively. The histology-specific sojourn times ranged from 0.8 to 1.8 years for type II ovarian cancer and 2.9 to 6.6 years for type I ovarian cancer.
Conclusions: Annual screening is not effective for all ovarian cancer subtypes. Screening sensitivity for early-stage ovarian cancers is not sufficient for substantial mortality reduction.
背景:卵巢癌是妇科癌症相关死亡的主要原因之一。过去采用癌抗原 125 检测和经阴道超声相结合的卵巢癌筛查试验未能在统计学上显著降低死亡率。估计卵巢癌的存活时间,即从首次筛查出癌症到临床检测出癌症的这段时间,可以为未来的筛查计划提供参考:方法:我们将卵巢癌的进展过程模拟为连续时间马尔可夫链,并采用贝叶斯方法估算了筛查模式的特定停留时间和敏感性。模型输入来自英国卵巢癌筛查合作试验和前列腺癌、肺癌、结直肠癌和卵巢癌筛查试验的筛查臂(多模态和超声)。我们使用后验预测 P 值评估了估计值的质量。我们根据 "监测、流行病学和最终结果计划 "中相应的组织学特异性存活率调整了总体存活时间,从而得出了组织学特异性存活时间:在前列腺癌、肺癌、结直肠癌和卵巢癌研究中,卵巢癌的总体存活时间为 2.1 年(后位预测 P 值 = .469),筛查灵敏度为 65.7%。英国卵巢癌筛查合作试验的多模式筛查组的停留时间为 2.0 年(后验预测 P 值 = 0.532),超声筛查组的停留时间为 2.4 年(后验预测 P 值 = 0.640),筛查灵敏度分别为 93.2% 和 64.5%。在前列腺癌、肺癌、结直肠癌和卵巢癌研究中,早期和晚期疾病的特异性筛查敏感性分别为 39.1%和 82.9%。II型卵巢癌的组织学特异性停留时间为0.8至1.8年,I型卵巢癌的组织学特异性停留时间为2.9至6.6年:结论:年度筛查并非对所有卵巢癌亚型都有效。对早期卵巢癌的筛查敏感性不足以大幅降低死亡率。
{"title":"Estimating sojourn time and sensitivity of screening for ovarian cancer using a Bayesian framework.","authors":"Sayaka Ishizawa, Jiangong Niu, Martin C Tammemagi, Ehsan Irajizad, Yu Shen, Karen H Lu, Larissa A Meyer, Iakovos Toumazis","doi":"10.1093/jnci/djae145","DOIUrl":"10.1093/jnci/djae145","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer is among the leading causes of gynecologic cancer-related death. Past ovarian cancer screening trials using combination of cancer antigen 125 testing and transvaginal ultrasound failed to yield statistically significant mortality reduction. Estimates of ovarian cancer sojourn time-that is, the period from when the cancer is first screen detectable until clinical detection-may inform future screening programs.</p><p><strong>Methods: </strong>We modeled ovarian cancer progression as a continuous time Markov chain and estimated screening modality-specific sojourn time and sensitivity using a Bayesian approach. Model inputs were derived from the screening arms (multimodal and ultrasound) of the UK Collaborative Trial of Ovarian Cancer Screening and the Prostate, Lung, Colorectal and Ovarian cancer screening trials. We assessed the quality of our estimates by using the posterior predictive P value. We derived histology-specific sojourn times by adjusting the overall sojourn time based on the corresponding histology-specific survival from the Surveillance, Epidemiology, and End Results Program.</p><p><strong>Results: </strong>The overall ovarian cancer sojourn time was 2.1 years (posterior predictive P value = .469) in the Prostate, Lung, Colorectal and Ovarian studies, with 65.7% screening sensitivity. The sojourn time was 2.0 years (posterior predictive P value = .532) in the United Kingdom Collaborative Trial of Ovarian Cancer Screening's multimodal screening arm and 2.4 years (posterior predictive P value = .640) in the ultrasound screening arm, with sensitivities of 93.2% and 64.5%, respectively. Stage-specific screening sensitivities in the Prostate, Lung, Colorectal and Ovarian studies were 39.1% and 82.9% for early-stage and advanced-stage disease, respectively. The histology-specific sojourn times ranged from 0.8 to 1.8 years for type II ovarian cancer and 2.9 to 6.6 years for type I ovarian cancer.</p><p><strong>Conclusions: </strong>Annual screening is not effective for all ovarian cancer subtypes. Screening sensitivity for early-stage ovarian cancers is not sufficient for substantial mortality reduction.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141748255","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}
Joseph R Habib, Ingmar F Rompen, Brady A Campbell, Paul C M Andel, Benedict Kinny-Köster, Ryte Damaseviciute, D Brock Hewitt, Greg D Sacks, Ammar A Javed, Marc G Besselink, Hjalmar C van Santvoort, Lois A Daamen, Martin Loos, Jin He, I Quintus Molenaar, Markus W Büchler, Christopher L Wolfgang
Background: Intraductal papillary mucinous neoplasm (IPMN)-derived pancreatic ductal adenocarcinoma (PDAC) is resected at smaller sizes compared to its biologically distinct counterpart, pancreatic intraepithelial neoplasia (PanIN)-derived PDAC. Thus, experts proposed T1 sub-staging for IPMN-derived PDAC. However, this has never been validated.
Methods: Consecutive upfront surgery patients with IPMN-derived PDAC from five international high-volume centers were classified by the proposed T1 sub-staging classification (T1a ≤ 0.5, T1b > 0.5 and ≤1.0, and T1c >1.0 and ≤2.0 cm) using the invasive component size. Kaplan-Meier and log-rank tests were utilized to compare overall survival (OS). A multivariable Cox-regression was used to determine hazard ratios (HR) with confidence intervals (95%CI).
Results: Among 747 patients, 69 (9.2%), 50 (6.7%), 99 (13.0%), and 531 patients (71.1%), comprised the T1a, T1b, T1c, and T2-4 subgroups, respectively. Increasing T-stage was associated with elevated CA19-9, poorer grade, nodal positivity, R1-margin, and tubular subtype. Median OS for T1a, T1b, T1c, and T2-4 were 159.0 (95%CI:126.0-NR), 128.8 (98.3-NR), 77.6 (48.3-108.2), and 31.4 (27.5-37.7) months, respectively (p < .001). OS decreased with increasing T-stage for all pairwise comparisons (all p < .05). After risk-adjustment, age > 65, elevated CA19-9, T1b [HR : 2.55 (1.22-5.32)], T1c [HR : 3.04 (1.60-5.76)], and T2-4 [HR : 3.41 (1.89-6.17)] compared to T1a, nodal positivity, R1-margin, and no adjuvant chemotherapy were associated with worse OS. Disease recurrence was more common in T2-4 tumors (56.4%) compared to T1a (18.2%), T1b (23.9%), and T1c (36.1%, p < .001).
Conclusion: T1 sub-staging of IPMN-derived PDAC is valid and has significant prognostic value. Advancing T1 sub-stage is associated with worse histopathology, survival, and recurrence. T1 sub-staging is recommended for future guidelines.
背景:导管内乳头状粘液瘤(IPMN)衍生的胰腺导管腺癌(PDAC)与其生物学上不同的对应物--胰腺上皮内瘤变(PanIN)衍生的PDAC相比,切除面积较小。因此,专家建议对 IPMN 衍生型 PDAC 进行 T1 亚分期。然而,这一观点从未得到验证:方法:根据提出的 T1 亚分期分类法(T1a ≤ 0.5、T1b > 0.5 且 ≤ 1.0、T1c > 1.0 且 ≤ 2.0 cm),使用侵袭性成分大小对来自五个国际高容量中心的连续 IPMN 衍生 PDAC 前期手术患者进行分类。采用卡普兰-梅耶(Kaplan-Meier)检验和对数秩检验比较总生存率(OS)。采用多变量考克斯回归法确定危险比(HR)及置信区间(95%CI):在747名患者中,T1a、T1b、T1c和T2-4亚组分别有69人(9.2%)、50人(6.7%)、99人(13.0%)和531人(71.1%)。T分期的增加与CA19-9升高、分级较差、结节阳性、R1-边缘和管状亚型有关。T1a、T1b、T1c和T2-4的中位OS分别为159.0(95%CI:126.0-NR)、128.8(98.3-NR)、77.6(48.3-108.2)和31.4(27.5-37.7)个月(P 65,CA19-9升高,T1b [HR : 2.55 (1.22-5.32)], T1c [HR : 3.04 (1.60-5.76)], and T2-4 [HR : 3.41 (1.89-6.17)] compared to T1a, nodal positivity, R1-margin, and no adjuvant chemotherapy were associated with worse OS.与T1a(18.2%)、T1b(23.9%)和T1c(36.1%)相比,疾病复发在T2-4肿瘤(56.4%)中更为常见:IPMN衍生型PDAC的T1亚分期是有效的,具有重要的预后价值。T1亚分期越前,组织病理学、生存率和复发率越差。建议将 T1 亚分期纳入未来指南。
{"title":"An international Multi-Institutional validation of T1 Sub-staging of intraductal papillary mucinous neoplasm-derived pancreatic cancer.","authors":"Joseph R Habib, Ingmar F Rompen, Brady A Campbell, Paul C M Andel, Benedict Kinny-Köster, Ryte Damaseviciute, D Brock Hewitt, Greg D Sacks, Ammar A Javed, Marc G Besselink, Hjalmar C van Santvoort, Lois A Daamen, Martin Loos, Jin He, I Quintus Molenaar, Markus W Büchler, Christopher L Wolfgang","doi":"10.1093/jnci/djae166","DOIUrl":"https://doi.org/10.1093/jnci/djae166","url":null,"abstract":"<p><strong>Background: </strong>Intraductal papillary mucinous neoplasm (IPMN)-derived pancreatic ductal adenocarcinoma (PDAC) is resected at smaller sizes compared to its biologically distinct counterpart, pancreatic intraepithelial neoplasia (PanIN)-derived PDAC. Thus, experts proposed T1 sub-staging for IPMN-derived PDAC. However, this has never been validated.</p><p><strong>Methods: </strong>Consecutive upfront surgery patients with IPMN-derived PDAC from five international high-volume centers were classified by the proposed T1 sub-staging classification (T1a ≤ 0.5, T1b > 0.5 and ≤1.0, and T1c >1.0 and ≤2.0 cm) using the invasive component size. Kaplan-Meier and log-rank tests were utilized to compare overall survival (OS). A multivariable Cox-regression was used to determine hazard ratios (HR) with confidence intervals (95%CI).</p><p><strong>Results: </strong>Among 747 patients, 69 (9.2%), 50 (6.7%), 99 (13.0%), and 531 patients (71.1%), comprised the T1a, T1b, T1c, and T2-4 subgroups, respectively. Increasing T-stage was associated with elevated CA19-9, poorer grade, nodal positivity, R1-margin, and tubular subtype. Median OS for T1a, T1b, T1c, and T2-4 were 159.0 (95%CI:126.0-NR), 128.8 (98.3-NR), 77.6 (48.3-108.2), and 31.4 (27.5-37.7) months, respectively (p < .001). OS decreased with increasing T-stage for all pairwise comparisons (all p < .05). After risk-adjustment, age > 65, elevated CA19-9, T1b [HR : 2.55 (1.22-5.32)], T1c [HR : 3.04 (1.60-5.76)], and T2-4 [HR : 3.41 (1.89-6.17)] compared to T1a, nodal positivity, R1-margin, and no adjuvant chemotherapy were associated with worse OS. Disease recurrence was more common in T2-4 tumors (56.4%) compared to T1a (18.2%), T1b (23.9%), and T1c (36.1%, p < .001).</p><p><strong>Conclusion: </strong>T1 sub-staging of IPMN-derived PDAC is valid and has significant prognostic value. Advancing T1 sub-stage is associated with worse histopathology, survival, and recurrence. T1 sub-staging is recommended for future guidelines.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141727126","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}
{"title":"Continued prioritization of biomedical research over sociomedical research may widen disparities in cancer outcomes.","authors":"Rebecca D Kehm","doi":"10.1093/jnci/djae150","DOIUrl":"https://doi.org/10.1093/jnci/djae150","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141723687","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}
Amber N Hurson, Thomas U Ahearn, Hela Koka, Brittany D Jenkins, Alexandra R Harris, Sylvia Roberts, Sharon Fan, Jamirra Franklin, Gisela Butera, Renske Keeman, Audrey Y Jung, Pooja Middha, Gretchen L Gierach, Xiaohong R Yang, Jenny Chang-Claude, Rulla M Tamimi, Melissa A Troester, Elisa V Bandera, Mustapha Abubakar, Marjanka K Schmidt, Montserrat Garcia-Closas
Background: Breast cancer is comprised of distinct molecular subtypes. Studies have reported differences in risk factor associations with breast cancer subtypes, especially by tumor estrogen receptor (ER) status, but their consistency across racial and ethnic populations has not been comprehensively evaluated.
Methods: We conducted a qualitative, scoping literature review using the Preferred Reporting Items for Systematic Reviews and Meta-analysis, extension for Scoping Reviews to investigate consistencies in associations between 18 breast cancer risk factors (reproductive, anthropometric, lifestyle, and medical history) and risk of ER-defined subtypes in women who self-identify as Asian, Black or African American, Hispanic or Latina, or White. We reviewed publications between January 1, 1990 and July 1, 2022. Etiologic heterogeneity evidence (convincing, suggestive, none, or inconclusive) was determined by expert consensus.
Results: Publications per risk factor ranged from 14 (benign breast disease history) to 66 (parity). Publications were most abundant for White women, followed by Asian, Black or African American, and Hispanic or Latina women. Etiologic heterogeneity evidence was strongest for parity, followed by age at first birth, post-menopausal BMI, oral contraceptive use, and estrogen-only and combined menopausal hormone therapy. Evidence was limited for other risk factors. Findings were consistent across racial and ethnic groups, although the strength of evidence varied.
Conclusion: The literature supports etiologic heterogeneity by ER for some established risk factors that are consistent across race and ethnicity groups. However, in non-White populations evidence is limited. Larger, more comparable data in diverse populations is needed to better characterize breast cancer etiologic heterogeneity.
背景:乳腺癌由不同的分子亚型组成。有研究报告称,风险因素与乳腺癌亚型的相关性存在差异,尤其是按肿瘤雌激素受体(ER)状态划分,但尚未对不同种族和族裔人群的相关性进行全面评估:我们采用《系统综述和荟萃分析首选报告项目》(Preferred Reporting Items for Systematic Reviews and Meta-analysis)进行了一项定性、范围性文献综述,以调查自我认同为亚裔、黑人或非裔美国人、西班牙裔或拉丁裔美国人或白人女性的 18 种乳腺癌风险因素(生殖、人体测量、生活方式和病史)与 ER 定义亚型风险之间的一致性。我们查阅了 1990 年 1 月 1 日至 2022 年 7 月 1 日期间的出版物。病因异质性证据(令人信服、提示性、无或不确定)由专家共识决定:每个风险因素的文献从 14 篇(良性乳腺疾病史)到 66 篇(奇偶性)不等。白种女性的文献最多,其次是亚裔、黑人或非裔美国人以及西班牙裔或拉丁裔女性。病因异质性证据中,以奇偶性最强,其次是初产年龄、绝经后体重指数、口服避孕药、纯雌激素和联合绝经激素治疗。其他风险因素的证据有限。不同种族和族裔群体的研究结果是一致的,尽管证据的强度有所不同:文献支持一些已确定的风险因素在 ER 方面的病因异质性,这些因素在不同种族和族裔群体中是一致的。然而,非白人群体的证据有限。为了更好地描述乳腺癌病因异质性,需要在不同人群中获得更多更具可比性的数据。
{"title":"Risk factors for breast cancer subtypes by race and ethnicity: A scoping review.","authors":"Amber N Hurson, Thomas U Ahearn, Hela Koka, Brittany D Jenkins, Alexandra R Harris, Sylvia Roberts, Sharon Fan, Jamirra Franklin, Gisela Butera, Renske Keeman, Audrey Y Jung, Pooja Middha, Gretchen L Gierach, Xiaohong R Yang, Jenny Chang-Claude, Rulla M Tamimi, Melissa A Troester, Elisa V Bandera, Mustapha Abubakar, Marjanka K Schmidt, Montserrat Garcia-Closas","doi":"10.1093/jnci/djae172","DOIUrl":"10.1093/jnci/djae172","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is comprised of distinct molecular subtypes. Studies have reported differences in risk factor associations with breast cancer subtypes, especially by tumor estrogen receptor (ER) status, but their consistency across racial and ethnic populations has not been comprehensively evaluated.</p><p><strong>Methods: </strong>We conducted a qualitative, scoping literature review using the Preferred Reporting Items for Systematic Reviews and Meta-analysis, extension for Scoping Reviews to investigate consistencies in associations between 18 breast cancer risk factors (reproductive, anthropometric, lifestyle, and medical history) and risk of ER-defined subtypes in women who self-identify as Asian, Black or African American, Hispanic or Latina, or White. We reviewed publications between January 1, 1990 and July 1, 2022. Etiologic heterogeneity evidence (convincing, suggestive, none, or inconclusive) was determined by expert consensus.</p><p><strong>Results: </strong>Publications per risk factor ranged from 14 (benign breast disease history) to 66 (parity). Publications were most abundant for White women, followed by Asian, Black or African American, and Hispanic or Latina women. Etiologic heterogeneity evidence was strongest for parity, followed by age at first birth, post-menopausal BMI, oral contraceptive use, and estrogen-only and combined menopausal hormone therapy. Evidence was limited for other risk factors. Findings were consistent across racial and ethnic groups, although the strength of evidence varied.</p><p><strong>Conclusion: </strong>The literature supports etiologic heterogeneity by ER for some established risk factors that are consistent across race and ethnicity groups. However, in non-White populations evidence is limited. Larger, more comparable data in diverse populations is needed to better characterize breast cancer etiologic heterogeneity.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141633558","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}
Emily Tonorezos, Theresa Devasia, Angela B Mariotto, Michelle A Mollica, Lisa Gallicchio, Paige Green, Michelle Doose, Rachelle Brick, Brennan Streck, Crystal Reed, Janet S de Moor
Background: With aging of the population and improvements in diagnosis, treatment, and supportive care, the number of cancer survivors in the United States (US) has increased; updated prevalence estimates are needed.
Methods: Cancer prevalence on January 1, 2022 was estimated using the Prevalence Incidence Approach Model, utilizing incidence, survival, and mortality. Prevalence by age decade, sex, and time from diagnosis were calculated. The percentage of cancer survivors in the projected US population by age and sex was calculated as the ratio of the sex-specific projected prevalence to the sex-specific projected US population.
Results: There were an estimated 18.1 million US cancer survivors as of January 1, 2022. From 2022 to 2030, the number of US cancer survivors is projected to increase to 21.6 million; by 2040, the number is projected to be 26 million. Long-term survivors are highly prevalent; in 2022, 70% of cancer survivors survived 5 years or more after diagnosis, and 11% of cancer survivors survived 25 years or more after diagnosis. Among all US females aged 40-54, 3.6% were cancer survivors; among females aged 65-74, 14.5% were cancer survivors; among females aged 85 and older, 36.4% were cancer survivors. Among all US males aged 40-54, 2.1% were cancer survivors; among males aged 65-74, 16% were cancer survivors; among those aged 85 and older, 48.3% were cancer survivors.
Conclusions: Cancer survivors are growing in number. In the US, most cancer survivors are long-term and very long-term survivors, representing a significant proportion of the US population.
{"title":"Prevalence of cancer survivors in the United States.","authors":"Emily Tonorezos, Theresa Devasia, Angela B Mariotto, Michelle A Mollica, Lisa Gallicchio, Paige Green, Michelle Doose, Rachelle Brick, Brennan Streck, Crystal Reed, Janet S de Moor","doi":"10.1093/jnci/djae135","DOIUrl":"https://doi.org/10.1093/jnci/djae135","url":null,"abstract":"<p><strong>Background: </strong>With aging of the population and improvements in diagnosis, treatment, and supportive care, the number of cancer survivors in the United States (US) has increased; updated prevalence estimates are needed.</p><p><strong>Methods: </strong>Cancer prevalence on January 1, 2022 was estimated using the Prevalence Incidence Approach Model, utilizing incidence, survival, and mortality. Prevalence by age decade, sex, and time from diagnosis were calculated. The percentage of cancer survivors in the projected US population by age and sex was calculated as the ratio of the sex-specific projected prevalence to the sex-specific projected US population.</p><p><strong>Results: </strong>There were an estimated 18.1 million US cancer survivors as of January 1, 2022. From 2022 to 2030, the number of US cancer survivors is projected to increase to 21.6 million; by 2040, the number is projected to be 26 million. Long-term survivors are highly prevalent; in 2022, 70% of cancer survivors survived 5 years or more after diagnosis, and 11% of cancer survivors survived 25 years or more after diagnosis. Among all US females aged 40-54, 3.6% were cancer survivors; among females aged 65-74, 14.5% were cancer survivors; among females aged 85 and older, 36.4% were cancer survivors. Among all US males aged 40-54, 2.1% were cancer survivors; among males aged 65-74, 16% were cancer survivors; among those aged 85 and older, 48.3% were cancer survivors.</p><p><strong>Conclusions: </strong>Cancer survivors are growing in number. In the US, most cancer survivors are long-term and very long-term survivors, representing a significant proportion of the US population.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141603666","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}
Weiwei Chen, Rachel D Altshuler, Phil Daschner, Carolina Salvador Morales, Diane C St Germain, Jennifer Guida, Pataje G S Prasanna, Jeffrey C Buchsbaum
The older American population is rapidly increasing, and millions of older adults will be cancer survivors with comorbidities. This population faces specific challenges regarding treatment and has unique clinical needs. Recognizing this need, the National Cancer Institute (NCI), in collaboration with the National Institute on Aging (NIA), hosted a webinar series, entitled "Cancer, Aging, and Comorbidities." This commentary provides a reflection of five thematic areas covered by the webinar series, which was focused on improving cancer treatment for older adults with cancer and comorbidities: i) the impact of comorbidities on treatment tolerability and patient outcomes; ii) the impact of comorbidities on cancer clinical trial design; iii) the development of wearable devices in measuring comorbidities in cancer treatment; iv) the effects of nutrition and the microbiome on cancer therapy and; v) the role of senescence and senotherapy in age-related diseases. While advances have been made in these areas, many gaps and challenges exist and are discussed in this commentary. To improve cancer survivorship in older populations with comorbidities, aging and comorbidities must be jointly considered and incorporated across the spectrum of cancer research. This includes more basic research of the mechanisms linking comorbidities and cancer development and treatment response, building critical resources and infrastructure (eg, preclinical models and patient samples), conducting clinical trials focused on the older population, integrating geriatric assessment into cancer treatment, and incorporating novel technologies, such as wearable devices into clinical trials and cancer care.
{"title":"Older Adults with Cancer and Common Comorbidities-Challenges and Opportunities in Improving Their Cancer Treatment Outcomes.","authors":"Weiwei Chen, Rachel D Altshuler, Phil Daschner, Carolina Salvador Morales, Diane C St Germain, Jennifer Guida, Pataje G S Prasanna, Jeffrey C Buchsbaum","doi":"10.1093/jnci/djae163","DOIUrl":"https://doi.org/10.1093/jnci/djae163","url":null,"abstract":"<p><p>The older American population is rapidly increasing, and millions of older adults will be cancer survivors with comorbidities. This population faces specific challenges regarding treatment and has unique clinical needs. Recognizing this need, the National Cancer Institute (NCI), in collaboration with the National Institute on Aging (NIA), hosted a webinar series, entitled \"Cancer, Aging, and Comorbidities.\" This commentary provides a reflection of five thematic areas covered by the webinar series, which was focused on improving cancer treatment for older adults with cancer and comorbidities: i) the impact of comorbidities on treatment tolerability and patient outcomes; ii) the impact of comorbidities on cancer clinical trial design; iii) the development of wearable devices in measuring comorbidities in cancer treatment; iv) the effects of nutrition and the microbiome on cancer therapy and; v) the role of senescence and senotherapy in age-related diseases. While advances have been made in these areas, many gaps and challenges exist and are discussed in this commentary. To improve cancer survivorship in older populations with comorbidities, aging and comorbidities must be jointly considered and incorporated across the spectrum of cancer research. This includes more basic research of the mechanisms linking comorbidities and cancer development and treatment response, building critical resources and infrastructure (eg, preclinical models and patient samples), conducting clinical trials focused on the older population, integrating geriatric assessment into cancer treatment, and incorporating novel technologies, such as wearable devices into clinical trials and cancer care.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141599829","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}
Muhammad Bilal Mirza, Jungyoon Choi, Paula Marincola Smith, Jordan J Baechle, Chandrasekhar Padmanabhan, Andreana N Holowatyj, Shailja C Shah, Xingyi Guo, Kamran Idrees
Overall, gastric adenocarcinoma (GC) incidence rates have declined in recent years, but racial/ethnic disparities persist. Individuals who identify as Hispanic/Spanish/Latino are diagnosed with GC at younger ages and have poorer outcomes than non-Hispanic individuals. However, our understanding of GC biology across racial/ethnic groups remains limited. We assessed tumor genomic patterns by race/ethnicity among 1019 patients with primary GC in the AACR Project GENIE Consortium. Hispanic individuals presented with significantly higher rates of ERBB2/HER2 amplification vs other racial/ethnic groups (Hispanic: 13.9% vs 9.8% non-Hispanic White, 8.1% non-Hispanic Asian, and 11.0% non-Hispanic Black; p < .001, FDR adjusted q < 0.001). Hispanic patients also had higher odds of an ERBB2 amplification vs non-Hispanic whites in adjusted models (OR = 2.52, 95%CI = 1.20-5.33, p = .015). These findings underscore the important role of genomic factors in GC disparities. Ensuring equitable access to genomic profiling and targeted therapies, such as trastuzumab for HER2-overexpressing GC, is a promising avenue to mitigate GC disparities and improve outcomes.
{"title":"ERBB2 amplification in gastric cancer: a genomic insight into ethnic disparities.","authors":"Muhammad Bilal Mirza, Jungyoon Choi, Paula Marincola Smith, Jordan J Baechle, Chandrasekhar Padmanabhan, Andreana N Holowatyj, Shailja C Shah, Xingyi Guo, Kamran Idrees","doi":"10.1093/jnci/djae147","DOIUrl":"https://doi.org/10.1093/jnci/djae147","url":null,"abstract":"<p><p>Overall, gastric adenocarcinoma (GC) incidence rates have declined in recent years, but racial/ethnic disparities persist. Individuals who identify as Hispanic/Spanish/Latino are diagnosed with GC at younger ages and have poorer outcomes than non-Hispanic individuals. However, our understanding of GC biology across racial/ethnic groups remains limited. We assessed tumor genomic patterns by race/ethnicity among 1019 patients with primary GC in the AACR Project GENIE Consortium. Hispanic individuals presented with significantly higher rates of ERBB2/HER2 amplification vs other racial/ethnic groups (Hispanic: 13.9% vs 9.8% non-Hispanic White, 8.1% non-Hispanic Asian, and 11.0% non-Hispanic Black; p < .001, FDR adjusted q < 0.001). Hispanic patients also had higher odds of an ERBB2 amplification vs non-Hispanic whites in adjusted models (OR = 2.52, 95%CI = 1.20-5.33, p = .015). These findings underscore the important role of genomic factors in GC disparities. Ensuring equitable access to genomic profiling and targeted therapies, such as trastuzumab for HER2-overexpressing GC, is a promising avenue to mitigate GC disparities and improve outcomes.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590352","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}
Siyi He, Zhiyi Zhang, Guohui Song, Zhenhai Wang, He Li, Maomao Cao, Fan Yang, Dianqin Sun, Xinxin Yan, Shaoli Zhang, Yi Teng, Qianru Li, Changfa Xia, Wanqing Chen
Background: The current recommended starting age for gastric cancer (GC) lacks unified guideline and individualized criteria. We aimed to determine risk-stratified starting age for GC screening in China based on individuals' risk profiles, and develop an online calculator for clinical application.
Methods: In this multi-center population-based prospective study, we divided participants enrolled during 2015-2017 (n = 59,771, aged 40-69) into screened and unscreened groups and observed them for primary endpoints-GC occurrence, all-cause and GC-specific deaths. The median follow-up was 6.07 years. To determine the reference starting age, the effectiveness of GC screening was assessed by age-groups after propensity-score-matching. Further, we categorized the calculated individual risk scores (using well-established risk factors) by quantiles. Subsequently, we used age-specific 10-year cumulative risk curves to estimate the risk-stratified starting age-when the individual's risk level matches reference starting age risk threshold.
Results: During follow-up, 475 GC cases, 182 GC deaths and 1,860 all-cause deaths occurred. All-cause and GC-specific mortality decreased among screened individuals aged ≥45 and 50-59 years, respectively. Thus, the average population (reference) starting age was set as 50 years. The 10-year cumulative risk of GC in average population aged 50 was 1.147%. We stratified the starting age using eight risk factors, and categorized participants as low-, medium-, and high-risk individuals, whose risk-stratified starting age was 58, 50, and 46, respectively.
Conclusion: While high-risk individuals warrant 3-5 years earlier GC screening than average population (age 50), low-risk individuals can tolerate delayed screening. Our online, personalized starting-age calculator will help risk-adapted GC screening (https://web.consultech.com.cn/gastric/#/).
{"title":"Personalized starting age of gastric cancer screening based on individuals' risk profiles: a population-based prospective study.","authors":"Siyi He, Zhiyi Zhang, Guohui Song, Zhenhai Wang, He Li, Maomao Cao, Fan Yang, Dianqin Sun, Xinxin Yan, Shaoli Zhang, Yi Teng, Qianru Li, Changfa Xia, Wanqing Chen","doi":"10.1093/jnci/djae162","DOIUrl":"https://doi.org/10.1093/jnci/djae162","url":null,"abstract":"<p><strong>Background: </strong>The current recommended starting age for gastric cancer (GC) lacks unified guideline and individualized criteria. We aimed to determine risk-stratified starting age for GC screening in China based on individuals' risk profiles, and develop an online calculator for clinical application.</p><p><strong>Methods: </strong>In this multi-center population-based prospective study, we divided participants enrolled during 2015-2017 (n = 59,771, aged 40-69) into screened and unscreened groups and observed them for primary endpoints-GC occurrence, all-cause and GC-specific deaths. The median follow-up was 6.07 years. To determine the reference starting age, the effectiveness of GC screening was assessed by age-groups after propensity-score-matching. Further, we categorized the calculated individual risk scores (using well-established risk factors) by quantiles. Subsequently, we used age-specific 10-year cumulative risk curves to estimate the risk-stratified starting age-when the individual's risk level matches reference starting age risk threshold.</p><p><strong>Results: </strong>During follow-up, 475 GC cases, 182 GC deaths and 1,860 all-cause deaths occurred. All-cause and GC-specific mortality decreased among screened individuals aged ≥45 and 50-59 years, respectively. Thus, the average population (reference) starting age was set as 50 years. The 10-year cumulative risk of GC in average population aged 50 was 1.147%. We stratified the starting age using eight risk factors, and categorized participants as low-, medium-, and high-risk individuals, whose risk-stratified starting age was 58, 50, and 46, respectively.</p><p><strong>Conclusion: </strong>While high-risk individuals warrant 3-5 years earlier GC screening than average population (age 50), low-risk individuals can tolerate delayed screening. Our online, personalized starting-age calculator will help risk-adapted GC screening (https://web.consultech.com.cn/gastric/#/).</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141558799","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}
Guoqiao Zheng, Louise Baandrup, Jiangrong Wang, Rasmus Hertzum-Larsen, Charlotte Gerd Hannibal, Mette Tuxen Faber, Karin Sundström, Susanne K Kjær
Background: Women with a family history of breast and/or ovarian cancer have an increased ovarian cancer risk. Yet it remains uncertain if common ovarian cancer risk factors-especially those which are modifiable-affect this high-risk population similarly to the general population.
Methods: Using the Danish and Swedish nationwide registers, we established two nested case-control study populations in women with a family history of breast and/or ovarian cancer (2,138 ovarian cancers, 85,240 controls) and women without (10,730 ovarian cancers, 429,200 controls). The overall and histology-specific associations were assessed with conditional logistic regression. The country-specific estimates were combined based on a fixed-effect assumption.
Results: Multiparity, hysterectomy, tubal ligation, salpingectomy, and oral contraceptive (OC) use were associated with a reduced risk of ovarian cancer in both women with and without a family history, while endometriosis and menopausal hormone treatment (MHT) were associated with increased risk. Multiparity and OC use presented protective effects across all histologic subtypes except mucinous ovarian cancer which was not associated with OC use. MHT increased the risk of serous ovarian cancer but decreased the risk of the mucinous and clear cell cancers. Endometriosis was especially related to an increased risk of endometrioid and clear cell ovarian cancer.
Conclusion: Factors associated with a decreased ovarian cancer risk were similar between women with and without a family history of breast and/or ovarian cancer. Given the higher baseline risk for women with a family history, special attention should be paid to risk factors like endometriosis and nulliparity in this high-risk population.
{"title":"Ovarian cancer risk factors in relation to family history.","authors":"Guoqiao Zheng, Louise Baandrup, Jiangrong Wang, Rasmus Hertzum-Larsen, Charlotte Gerd Hannibal, Mette Tuxen Faber, Karin Sundström, Susanne K Kjær","doi":"10.1093/jnci/djae164","DOIUrl":"https://doi.org/10.1093/jnci/djae164","url":null,"abstract":"<p><strong>Background: </strong>Women with a family history of breast and/or ovarian cancer have an increased ovarian cancer risk. Yet it remains uncertain if common ovarian cancer risk factors-especially those which are modifiable-affect this high-risk population similarly to the general population.</p><p><strong>Methods: </strong>Using the Danish and Swedish nationwide registers, we established two nested case-control study populations in women with a family history of breast and/or ovarian cancer (2,138 ovarian cancers, 85,240 controls) and women without (10,730 ovarian cancers, 429,200 controls). The overall and histology-specific associations were assessed with conditional logistic regression. The country-specific estimates were combined based on a fixed-effect assumption.</p><p><strong>Results: </strong>Multiparity, hysterectomy, tubal ligation, salpingectomy, and oral contraceptive (OC) use were associated with a reduced risk of ovarian cancer in both women with and without a family history, while endometriosis and menopausal hormone treatment (MHT) were associated with increased risk. Multiparity and OC use presented protective effects across all histologic subtypes except mucinous ovarian cancer which was not associated with OC use. MHT increased the risk of serous ovarian cancer but decreased the risk of the mucinous and clear cell cancers. Endometriosis was especially related to an increased risk of endometrioid and clear cell ovarian cancer.</p><p><strong>Conclusion: </strong>Factors associated with a decreased ovarian cancer risk were similar between women with and without a family history of breast and/or ovarian cancer. Given the higher baseline risk for women with a family history, special attention should be paid to risk factors like endometriosis and nulliparity in this high-risk population.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141534473","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}
Eric S Schafer, Teresa Rushing, Kristine R Crews, Colleen Annesley, Susan I Colace, Nicole Kaiser, Lauren Pommert, Laura B Ramsey, Himalee S Sabnis, Kenneth Wong, Bill H Chang, Todd M Cooper, Nirali N Shah, Susan R Rheingold, Andrew E Place, Yueh-Yun Chi, Deepa Bhojwani, Alan S Wayne, M Brooke Bernhardt
Purpose: The National Cancer Institute (NCI) issued a 2021 memorandum adopting the American Society of Clinical Oncology (ASCO) and Friends of Cancer Research (Friends) task force recommendations to broaden clinical study eligibility criteria. They recommended that washout periods be eliminated for most prior cancer therapy and when required, to utilize evidence/rationale-based criteria. The Therapeutic Advances in Childhood Leukemia and Lymphoma (TACL) consortium responded to this guidance.
Process: A TACL task force reviewed the consortium's research portfolio, the relevant literature and guidance documents from ASCO-Friends, NCI, and US Food and Drug Administration (FDA) to make expert consensus and evidence-based recommendations for modernizing, broadening and codifying TACL-study washout periods while ensuring consistency with pediatric ethics and federal regulations. TACL's screening log was reviewed to estimate the impact that updated washout periods would have on patient inclusivity and recruitment.
Results: Over a 19-year period, 42 patients (14.6% of all screened ineligible (n = 287) patients), were identified as excluded from TACL early-phase studies exclusively due to not meeting washout criteria. An additional six (2.1%) did not meet washout and at least one other exclusion criterion. A new TACL washout guidance document was developed/adopted for use. Where washout criteria were not eliminated, rationale/evidenced-based criteria were established with citation.
Conclusion: In an effort to reduce unnecessary exclusion from clinical trials, TACL created rationale/evidenced-based washout period standards largely following guidance from the NCI/ASCO-Friends recommendations. These new, expanded eligibility criteria are expected to increase access to TACL clinical trials while maintaining safety and scientific excellence.
{"title":"Optimizing early phase clinical trial washout periods: a report from the therapeutic advances in childhood leukemia and lymphoma (TACL) consortium.","authors":"Eric S Schafer, Teresa Rushing, Kristine R Crews, Colleen Annesley, Susan I Colace, Nicole Kaiser, Lauren Pommert, Laura B Ramsey, Himalee S Sabnis, Kenneth Wong, Bill H Chang, Todd M Cooper, Nirali N Shah, Susan R Rheingold, Andrew E Place, Yueh-Yun Chi, Deepa Bhojwani, Alan S Wayne, M Brooke Bernhardt","doi":"10.1093/jnci/djae165","DOIUrl":"https://doi.org/10.1093/jnci/djae165","url":null,"abstract":"<p><strong>Purpose: </strong>The National Cancer Institute (NCI) issued a 2021 memorandum adopting the American Society of Clinical Oncology (ASCO) and Friends of Cancer Research (Friends) task force recommendations to broaden clinical study eligibility criteria. They recommended that washout periods be eliminated for most prior cancer therapy and when required, to utilize evidence/rationale-based criteria. The Therapeutic Advances in Childhood Leukemia and Lymphoma (TACL) consortium responded to this guidance.</p><p><strong>Process: </strong>A TACL task force reviewed the consortium's research portfolio, the relevant literature and guidance documents from ASCO-Friends, NCI, and US Food and Drug Administration (FDA) to make expert consensus and evidence-based recommendations for modernizing, broadening and codifying TACL-study washout periods while ensuring consistency with pediatric ethics and federal regulations. TACL's screening log was reviewed to estimate the impact that updated washout periods would have on patient inclusivity and recruitment.</p><p><strong>Results: </strong>Over a 19-year period, 42 patients (14.6% of all screened ineligible (n = 287) patients), were identified as excluded from TACL early-phase studies exclusively due to not meeting washout criteria. An additional six (2.1%) did not meet washout and at least one other exclusion criterion. A new TACL washout guidance document was developed/adopted for use. Where washout criteria were not eliminated, rationale/evidenced-based criteria were established with citation.</p><p><strong>Conclusion: </strong>In an effort to reduce unnecessary exclusion from clinical trials, TACL created rationale/evidenced-based washout period standards largely following guidance from the NCI/ASCO-Friends recommendations. These new, expanded eligibility criteria are expected to increase access to TACL clinical trials while maintaining safety and scientific excellence.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":null,"pages":null},"PeriodicalIF":9.9,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141534472","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}