The Contributions of Improved Therapy and Earlier Detection to Cancer Survival Gains, 1988-2000

2010 ◽  
Vol 13 (2) ◽  
Author(s):  
Eric Sun ◽  
Anupam B Jena ◽  
Darius Lakdawalla ◽  
Carolina Reyes ◽  
Tomas J Philipson ◽  
...  

Prior literature has documented improvements in cancer survival over time. However, ambiguity remains over the relative contributions of improved treatment and earlier detection to survival gains. Using registry data, we developed a novel framework to estimate the relative contributions of advances in treatment and detection. Our approach compares changes in the probability of early detection, which we interpret as the effects of advances in detection, to improvements in stage-conditional survival, which we interpret as the effects of treatment. We applied this methodology using SEER data to estimate probabilities of early detection and stage-conditional survival curves for several cancers, by race, between 1988 and 2000. Survival increased for all of the cancers we examined, with blacks experiencing larger survival gains than whites for all cancers combined. Our baseline analysis found that treatment advances account for the vast majority of survival gains for all the cancers examined: breast cancer (83%), lung cancer (85%), colorectal cancer (76%), pancreatic cancer (100%), and non-Hodgkin’s lymphoma (96%). Compared to whites, treatments appear to explain a lower percentage of survival gains for blacks for all cancers combined; breast cancer, NHL, and pancreatic cancer show a higher percentage of survival gains than lung cancer; and roughly the same percentage for the colorectal cancer. These results are robust to sensitivity analyses examining potential length and lead time bias. Overall, our results suggest that while improved treatment and early detection both contributed to the recent gains in survival, the majority of gains from 1988 to 2000 appear to have been driven by better treatment, manifested by improved stage-conditional survival. These results have important policy implications regarding investment in research and development and the evaluation of efforts to improve cancer screening.

2019 ◽  
Vol 65 (6) ◽  
pp. 457-467 ◽  
Author(s):  
N.A. Shushkova ◽  
S.E. Novikova ◽  
V.G. Zgoda

The main problems in the diagnostics and treatment of malignant tumors are early detection of the disease, prediction of the course of the disease and response to therapy. The solution may be associated with identification of biomarkers secreted by tumor cells within extracellular vesicles, known as exosomes. The study of exosome proteins attracts special attention, because their molecular composition can have information about tumor identity, and also represent a set of signaling molecules that regulate the processes of tumor progression and growth. In addition, the analysis of exosomes secreted into the extracellular space corresponds to the promising concept of a liquid biopsy. In this review, we have summarized the current experience in the molecular study of exosomes in various types of malignant tumors, including colorectal cancer, lung cancer, ovaries, prostate and breast cancer, with special emphasis on omics methods and outlined the prospects for their use in diagnosis.


2021 ◽  
Vol 9 (Suppl 3) ◽  
pp. A24-A24
Author(s):  
Christina Jensen ◽  
Jeppe Thorlacius-Ussing ◽  
Patryk Drobinski ◽  
Morten Karsdal ◽  
Anne-Christine Bay-Jensen ◽  
...  

BackgroundAutoantibodies are classically associated with autoimmune diseases but have recently emerged as attractive cancer biomarkers as they can be easily assessed in serum. Certain autoantibodies have been shown to promote cancer while others contribute to the body’s defense against it. Cancer progression is associated with excessive remodeling of the extracellular matrix (ECM) and collagen, but little is known about the role of autoantibodies against collagen in cancer. To investigate autoreactivity against collagen in cancer, we developed a novel biomarker assay to quantify autoantibodies against type III collagen products in serum from patients with various solid tumor types and compared levels with those find in healthy controls.MethodsThe presence and levels of autoantibodies against denatured type III collagen were measured in pretreatment serum from 223 patients with bladder cancer (n=20), breast cancer (n=20), colorectal cancer (n=20), head and neck cancer (n=20), kidney cancer (n=20), liver cancer (n=3), lung cancer (n=20), melanoma (n=20), ovarian cancer (n=20), pancreatic cancer (n=20), prostate cancer (n=20), and stomach cancer (n=20), and compared to age-matched healthy controls (n=33). Statistical differences were analyzed using the Kruskal-Wallis test adjusted for Dunn’s multiple comparisons test.ResultsSerum levels of autoantibodies against type III collagen were significantly lower in patients with bladder cancer (p=0.0007), breast cancer (p=0.0002), colorectal cancer (p<0.0001), head and neck cancer (p=0.0005), kidney cancer (p=0.005), liver cancer (p=0.030), lung cancer (p=0.0004), melanoma (p<0.0001), ovarian cancer (p<0.0001), pancreatic cancer (p<0.0001), prostate cancer (p<0.0001), and stomach cancer (p<0.0001) compared to healthy controls. This autoimmunity biomarker could discriminate between cancer and healthy controls with an AUROC value of 0.88 (p<0.0001).ConclusionsIn this study, we observed that cancer patients with different solid tumor types have downregulated levels of circulating autoantibodies directed against type III collagen compared to healthy controls suggesting that autoantibodies against type III collagen and tumor fibrosis may be important for tumor control and eradication. This autoimmunity biomarker may have the potential for studying and monitoring the close relationship between autoimmunity and cancer such as the risk of developing cancer on rheumatoid arthritis immunosuppressant or the risk of developing immune-related adverse events on cancer immunotherapy.Ethics ApprovalThe serum samples in this study were obtained from the commercial vendor Proteogenex and BioIVT, and according to the vendors, sample collection was approved by an Institutional Review Board or Independent Ethical Committee and patients gave their informed consent (Protocol numbers PG-ONC 2003/1 and WIRB® Protocol #20161665). All investigations were carried out according to the Helsinki Declaration.


2021 ◽  
Vol 27 ◽  
Author(s):  
Qi Zhang ◽  
Yinxin Wu ◽  
Jinlan Chen ◽  
Yuxuan Cai ◽  
Bei Wang ◽  
...  

Background: MBNL1, a protein encoded by q25 gene on chromosome 3, belongs to the tissue-specific RNA metabolic regulation family, which controls RNA splicing.[1]MBNL1 formed in the process of development drive large transcriptomic changes in cell differentiation,[2] it serves as a kind of tumor differentiation inhibitory factor.MBNL1 has a close relationship with cancer, comprehensive analysis, [3]found that breast cancer, leukemia, stomach cancer, esophageal adenocarcinoma, glial cell carcinoma and another common tumor in the cut, and cut in Huntington's disease. But MBNL1 plays a promoting role in cervical cancer, is contradictory in colorectal cancer, It promotes colorectal cancer cell proliferation, On the other hand, it inhibits its metastasis, so it is an important physiological marker in many cancers. When we integrated the role of MBNL1 protein in various tumors, we found that its antisense RNA, MBNL1-AS1, had a good inhibitory effect in several colorectal cancer, non-small cell lung cancer, and gastric cancer. Objective: To elucidate the expression of MBNL1 and MBNL1-AS1 in various tumors, and to search for their physiological markers. Methods: It was searched by the PUMUB system and summarized its expression in various cancers. Results: MBNL1 was down-regulated, leukemia, breast cancer, glioblastoma, gastric cancer, overall survival rate, recurrence, metastasis increased. While the metastasis of colon cancer decreased, proliferation was promoted, and the effect of both was promoted for cervical cancer.MBNL1-AS1 was down-regulated, and the overall survival rate, recurrence, and metastasis of lung cancer, colorectal cancer, and bladder cancer increased. Conclusion: MBNL1 may be an important regulator of cancer, and MBNL1-AS1 is a better tumor suppressor.


BMJ Open ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. e036176
Author(s):  
Nina Grundmann ◽  
Christa Meisinger ◽  
Martin Trepel ◽  
Jacqueline Müller-Nordhorn ◽  
Gerhard Schenkirsch ◽  
...  

ObjectivesKnowledge about time trends of cancer incidence and cancer survival in a defined region is an essential prerequisite for the planning of regional healthcare infrastructure. The aim of the study was to provide population-based analyses of all common tumour sites to assess the cancer burden in the Augsburg study region.SettingTotal population of the study region of Augsburg (668 522 residents), Southern Germany.ParticipantsThe data obtained from the Cancer Registry Augsburg comprised 37 487 incident cases of malignant tumours (19 313 men and 18 174 women) diagnosed between 2005 and 2016 in the Augsburg region’s resident population.Primary and secondary outcome measuresWe calculated sex-specific, age-standardised incidence rates and annual percent change to assess time trends. In men and in women, 3-year and 5-year relative survival was calculated and results were compared with the latest German estimates. Survival trends were presented for the most common cancers only.ResultsDecreasing age-standardised incidence rates were observed for prostate cancer and for colorectal cancer in men. For oropharyngeal cancer, rates declined in men, but significantly increased in women. Incidence for female breast cancer remained stable. Five-year relative survival ranged between 6.4% (95% CI: 4.1% to 10.1%) for pancreatic cancer and 97.7% (95% CI: 96.0% to 99.4%) for prostate cancer in men and between 10.2% (95% CI: 7.1% to 14.6%) for pancreatic cancer and 96.6% (95% CI: 93.6% to 99.6%) for malignant melanoma in women. Trends in 3-year survival of the five most common tumour sites in men showed a significant increase for lung and oropharyngeal cancer. In women, continuously rising survival trends were observed for breast cancer.ConclusionsSurvival of cancer patients in the Augsburg study region was largely concordant with the situation in Germany as a whole, while incidence showed slight deviations in some cancer sites. Regional evaluations on cancer survival are a valuable instrument for identifying deficits and determining advances in oncological health management.


2001 ◽  
Vol 3 (14) ◽  
pp. 1-10 ◽  
Author(s):  
Meghan A. Arnold ◽  
Michael Goggins

Pancreatic adenocarcinoma is a major cause of cancer deaths in the industrialised world. Recent work has focused on the genetics of pancreatic cancer with a goal of finding an early detection marker that might allow for greater rates of survival than are currently possible. The breast cancer 2 gene (BRCA2) is one of numerous genes implicated in familial pancreatic cancer. Carriers of germline mutations of the BRCA2 gene have an increased risk of several cancers, among them pancreatic adenocarcinoma. During pancreatic carcinogenesis, bi-allelic inactivation of BRCA2 occurs as a late event, suggesting that other genetic events must occur before neoplastic cells can tolerate loss of BRCA2.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4696-4696
Author(s):  
Scott Davi d Ramsey ◽  
Jeannine S McCune ◽  
David K Blough ◽  
Lauren C Clarke ◽  
Cara L McDermott ◽  
...  

Abstract Chemotherapy regimens, patient factors, and the use of colony stimulating factor (CSF) influence cancer patients’ risk for febrile neutropenia (FN) when they receive myelosuppressive chemotherapy. The incidence of FN and patient factors influencing that risk are relatively unknown in community settings. Using claims from Medicare, Medicaid and two private health insurance plan enrollees linked to the Puget Sound SEER registry, we examined the incidence of FN among breast, lung and colorectal cancer patients diagnosed 2002–05 who received adjuvant chemotherapy. We used logistic regression models to determine factors influencing the risk for FN within the first chemotherapy cycle, controlling for cancer stage, age, sex, race, comorbidities, chemotherapy-regimen related FN risk (as designated by the National Comprehensive Cancer Network), CSF use, health insurance type, and surgery or radiation ≤30 days from administration of first chemotherapy. Over the time horizon, 1096 breast, 1142 lung, and 755 colorectal cancer patients received chemotherapy. The incidence of any FN in the first chemotherapy cycle was (counts per 100 recipients by high, intermediate, and low-risk myelosuppressive chemotherapy according to NCCN categories respectively) 7.36, 10.0, 4.70 for breast cancer, 17.12, 14.15, 12.22 for lung cancer, and 25.0, 8.96, 6.37 for colorectal cancer. Significant predictors (p&lt;0.05) of any FN were: breast cancer—radiation ≤ 30 days from first chemotherapy administration (OR 2.90, 95% CI 1.21–6.94), other non-black race vs. white race (OR 2.82, 95% CI 1.29–6.17), or Medicaid insurance (OR 2.31, 95% CI 1.10–4.89); lung cancer—radiation ≤ 30 days from first chemotherapy administration (OR 1.63, 95% CI 1.01–2.61), surgery ≤ 30 days from first chemotherapy administration (OR 2.08, 95% CI 1.02–4.25), Medicaid insurance (OR 2.29, 95% CI 1.08–4.84), or a Charlson comorbidity score ≥ 2 (OR 2.56, 95% CI 1.11–5.91); colorectal cancer—female gender (OR 1.86, 95% CI 1.02–3.41) or high myelosuppressive risk chemotherapy regimen (OR 7.66, 95% CI 2.95–19.89). In this analysis, predictors of FN varied between cancers. Limitations of this analysis include lack of information about chemotherapy and CSF doses, as this is not captured in the SEER registry or claims data. These results indicate that several factors may interact to influence a patient’s likelihood of developing FN in the first cycle of adjuvant chemotherapy.


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 2992-2992
Author(s):  
Smita Bhatia ◽  
Cor van den Bos ◽  
Can-Lan Sun ◽  
Jillian Birch ◽  
Lisa Diller ◽  
...  

Abstract Background We describe the pattern and incidence of SMNs with 10 additional years of follow-up of an international cohort (Bhatia, N Engl J Med, 1996; Bhatia, J Clin Oncol, 2003) of children with HL diagnosed between 1955 and 1986 at age 16 y or younger. Methods Medical record review was used to identify SMNs, define vital status and describe therapeutic exposures. Pathology reports served to validate SMNs. Cumulative incidence (CI) utilized competing risk methods. Standardized incidence ratio (SIR) and absolute excess risk (AER/10,000 p-y) utilized age-, gender- and year-matched rates in the general population. Cox regression techniques (using calendar time as time scale) identified predictors of SMN risk. Results The cohort included 1023 patients diagnosed with HL at a median age of 11 y, and followed for a median of 26.8 y (IQR, 16.4-33.7). Eighty-nine percent had received radiation, either alone (22%), or in combination with chemotherapy (67%). Alkylating agent (AA) score was defined as follows: 1 AA for 6 m = AA score of 1; 2 AA for 6 m or 1 AA for 12 m = AA score of 2, etc. The AA score was 1-2 for 54% and 3+ for 16%; 30% did not receive AA. A total of 188 solid SMNs developed in 139 patients (breast [54], thyroid [24], lung [11], colorectal [11], bone [8], other malignancies [80]. Table summarizes SIR (95%CI), CI, and AER by attained age. The cohort was at an 11.1-fold increased risk of developing solid SMNs (excluding non-melanoma skin cancers) compared with the general population (95% CI, 9.4-13.0). CI of solid SMNs was 25.2% at 40 y from HL diagnosis (Fig 1). Among patients aged ≥40 y, 79% of total AER was attributable to breast, thyroid, colorectal and lung SMNs (Table). Thirty-seven patients developed >1 solid SMN; the cumulative incidence of the 2nd SMN was 19.6% at 10 years from diagnosis of the 1st SMN. Breast Cancer: Females (n=41) had a 20.9-fold increased risk, and males (n=3) a 45.8-fold increased risk c/w general population. Age at HL of 10-16 y vs. <10 y (RR=9.7, 95%CI, 2.3-40.6, p=0.002), and exposure to chest radiation (RR=5.9, 95%CI, 1.4-25.9) were associated with increased risk. Among females aged 10-16 y at chest radiation, cumulative incidence was 24.3% by age 45 y, as opposed to 2.6% for those <10 y, p=0.001 (Fig 2). Exposure to AA was associated with a lower risk (RR=0.4, p=0.002). Diagnosis of HL after 1975 was associated with decreased risk (RR=0.25, 95%CI 0.12-0.53), explained, in part by the increasing use of AA after 1975 (78%) vs. before 1975 (61%). By age 40 y, the risk of breast cancer among females exposed to chest radiation at age 10-16 y (18.2%) was comparable to the risk for BRCA1 mutation carriers (15%-20% by age 40 y; Chen, J Clin Oncol, 2007). Lung cancer: Ten of 11 lung cancer cases were diagnosed in males (males: SIR=24.7; females: SIR=3.2, p=0.05); all had received neck/chest radiation. The CI of lung cancer among males was 3.8% by age 50 y, comparable to the risk among male smokers (2% by age 50 y, Bilello, Clinics Chest Med, 2002). Colorectal cancer: There was a 11.5-fold increased risk c/w general population. The CI among those with abdominal/pelvic radiation was 4.1% by age 50 y ; this risk is higher than that observed in individuals with ≥2 first degree relatives affected with colorectal cancer (1.2% by age 50 y, Butterworth, Eur J Cancer, 2006). Thyroid cancer: Survivors had a 22.2-fold increased risk; all developed within radiation field. Females (RR=4.3, 95%CI 1.8-10.4) were at increased risk. Conclusion In this cohort of HL survivors with 20,344 p-y of follow-up, the greatest excess risk of SMNs among those > 40 y was attributable to breast, thyroid, colorectal and lung SMNs. Observed risks for the most common SMNs were comparable to or greater than known high-risk groups within the general population. Disclosures: No relevant conflicts of interest to declare.


2013 ◽  
Vol 31 (31_suppl) ◽  
pp. 94-94
Author(s):  
Fumiaki Nakamura ◽  
Masato Masuda ◽  
Norihiro Teramoto ◽  
Kazuhiro Mizumoto ◽  
Eiji Mekata ◽  
...  

94 Background: To establish systematic monitoring of cancer care quality, we measured the quality of cancer care in several facilities through chart reviews by tumor registrars. However, this method required both extensive effort of and skills in registrars. To explore less-labor–intensive methods of measuring care quality, we assessed quality measurement using health insurance claims data linked to the Hospital Based Cancer Registry (HBCR). Methods: We previously developed 206 quality indicators (QIs) to assess cancer care processes in collaboration with clinical experts. Ten of these (stomach cancer, 1; colorectal cancer, 1; lung cancer, 2; breast cancer, 3; liver cancer, 1; and supportive care, 2) could be used for analyzing HBCR health insurance claims data. Patients treated at 7 designated cancer hospitals in Japan in 2010 were included. Their characteristics and tumor stages were obtained from HBCR, and processes of care administered to the patients in 2010–2011 were obtained from health insurance claims data. We calculated a score for each QI based on the proportion of patients receiving care among those eligible for QI. Results: Data of 4,785 patients were analyzed (stomach cancer, 1,181; patients with colorectal cancer, 1,077; lung cancer, 1,091; breast cancer, 1,184; and liver cancer, 252). Quality scores of essential laboratory tests were high; 91% patients underwent the HER2 test for invasive breast cancer and 95% underwent the liver function test using indocyanine green clearance before liver cancer surgery. However, indicator scores for adjuvant chemotherapy were relatively lower at only 59% for stomach cancer patients, 57% for colorectal cancer patients, and 56% for lung cancer patients receiving adjuvant chemotherapy. The supportive care scores had even more scope for improvement as only 43% patients received antiemetics for highly emetic chemotherapy and 66% patients received laxatives along with narcotics. Conclusions: These QIs can be implemented for health insurance claims data linked to HBCR and used to identify the potential target area for improvement. In future, such electronic systems will enable rapid cycles of quality measurement and feedback.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. 1566-1566 ◽  
Author(s):  
Lola Rahib ◽  
Mackenzie Wehner ◽  
Lynn McCormick Matrisian ◽  
Kevin Thomas Nead

1566 Background: Coping with the current and future burden of cancer requires an in-depth understanding of cancer incidence and death trends. As of 2020, breast, lung, prostate, and colorectal cancer are the most incident cancers, while lung, colorectal, pancreas, and breast cancer result in the most deaths. Here we integrate observed cancer statistics and trends with observed and estimated US demographic data to project cancer incidences and deaths to the year 2040. Methods: Demographic cancer-specific delay-adjusted incidence and death rates from the Surveillance, Epidemiology, and End Results Program (2014-2016) were combined with US Census Bureau population growth projections (2016) and average annual percentage changes in incidence (2011-2015) and death (2012-2016) rates to project cancer incidences and deaths through the year 2040. We examined the 10 most incident and deadly cancers as of 2020. We utilized Joinpoint analysis to examine changes in incidence and death rates over time relative to changes in screening guidelines. Results: We predict the most incident cancers in 2040 in the US will be breast (322,000 diagnoses in 2040) and lung (182,000 diagnoses in 2040) cancer. Continuing decades long observed incident rate trends we predict that melanoma (173,000 diagnoses in 2040) will become the 3rd most common cancer while prostate cancer (63,000 diagnoses in 2040) will become the 5th most common cancer after colorectal cancer (139,000 diagnoses in 2040). Lung cancer (61,000 deaths in 2040) is predicted to continue to be the leading cause of cancer related death, with pancreas (45,000 deaths in 2040) and liver & intrahepatic bile duct (38,000 deaths in 2040) cancer surpassing colorectal cancer (34,000 deaths in 2040) to become the second and third most common causes of cancer related death, respectively. Breast cancer deaths (29,000 in 2040) are predicted to continue to decrease and become the fifth most common cause of cancer death. Joinpoint analysis of incidence and death rates supports a significant past, present, and future impact of cancer screening programs on the number of cancer diagnoses and deaths, particularly for prostate, thyroid, melanoma incidences, and lung cancer deaths. Conclusions: We demonstrate marked changes in the predicted landscape of cancer incidence and deaths by 2040. Our analysis reveals an influence of cancer screening programs on the number of cancer diagnoses and deaths in future years. These projections are important to guide future research funding allocations, healthcare planning, and health policy efforts.


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