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Article ; Online: Corrigendum to "Evaluating sex as a predictive marker for response to bevacizumab in metastatic colorectal carcinoma: Pooled analysis of 3369 patients in the ARCAD database" Eur J Cancer. 2023 Jan;178:162-170.

European journal of cancer (Oxford, England : 1990)

2023 Volume 194, Page(s) 113339

Language	English
Publishing date	2023-09-28
Publishing country	England
Document type	Published Erratum
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2023.113339
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Article ; Online: Comparison of longitudinal variance components and regression-based approaches for linkage detection on chromosome 17 for systolic blood pressure

Olswold Curtis / Andrade Mariza de

BMC Genetics, Vol 4, Iss Suppl 1, p S

2003 Volume 17

Abstract: Abstract We compare two methods to detect genetic linkage by using serial observations of systolic blood pressure in pedigree data from the Framingham Heart Study focusing on chromosome 17. The first method is a variance components (VC) approach that ... ...

Abstract	Abstract We compare two methods to detect genetic linkage by using serial observations of systolic blood pressure in pedigree data from the Framingham Heart Study focusing on chromosome 17. The first method is a variance components (VC) approach that incorporates longitudinal pedigree data, and the second method is a regression-based approach that summarizes all longitudinal measures in one single measure. No evidence of linkage was found either using the VC longitudinal approach or the regression-based approach, except when all time points were used from Cohorts 1 and 2 and only subjects aged 25 and 75 years were included.
Keywords	Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Language	English
Publishing date	2003-12-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Localization of genes involved in the metabolic syndrome using multivariate linkage analysis

Andrade Mariza de / Olswold Curtis

BMC Genetics, Vol 4, Iss Suppl 1, p S

2003 Volume 57

Abstract: Abstract There are no well accepted criteria for the diagnosis of the metabolic syndrome. However, the metabolic syndrome is identified clinically by the presence of three or more of these five variables: larger waist circumference, higher triglyceride ... ...

Abstract	Abstract There are no well accepted criteria for the diagnosis of the metabolic syndrome. However, the metabolic syndrome is identified clinically by the presence of three or more of these five variables: larger waist circumference, higher triglyceride levels, lower HDL-cholesterol concentrations, hypertension, and impaired fasting glucose. We use sets of two or three variables, which are available in the Framingham Heart Study data set, to localize genes responsible for this syndrome using multivariate quantitative linkage analysis. This analysis demonstrates the applicability of using multivariate linkage analysis and how its use increases the power to detect linkage when genes are involved in the same disease mechanism.
Keywords	Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Language	English
Publishing date	2003-12-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
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Article ; Online: Adverse event load, onset, and maximum grade: A novel method of reporting adverse events in cancer clinical trials.

Lopes, Guilherme S / Tournigand, Christophe / Olswold, Curtis L / Cohen, Romain / Kempf, Emmanuelle / Saltz, Leonard / Goldberg, Richard M / Hurwitz, Herbert / Fuchs, Charles / de Gramont, Aimery / Shi, Qian

Clinical trials (London, England)

2020 Volume 18, Issue 1, Page(s) 51–60

Abstract: Background: Current adverse event reporting practices do not document longitudinal characteristics of adverse effects, and alternative methods are not easily interpretable and have not been employed by clinical trials. Introducing time parameters in the ...

Abstract	Background: Current adverse event reporting practices do not document longitudinal characteristics of adverse effects, and alternative methods are not easily interpretable and have not been employed by clinical trials. Introducing time parameters in the evaluation of safety that are comprehensive yet easily interpretable could allow for a better understanding of treatment quality. In this study, we developed and applied a novel adverse event reporting method based on longitudinal adverse event changes to aid describing, summarizing, and presenting adverse event profile. We termed it the "Adverse Event Load, Onset, and Maximum Grade" method. Methods: We developed two adverse event summary metrics to complement the traditional maximum grade report. Onset time indicates the time period in which the maximum grade for a specific adverse event occurred and was defined as "early" (i.e. maximum grade happened for the first time before 6 weeks) or "late" (i.e. after the 6 Results: Our method provided additional information compared to traditional adverse event reports. For example, for nausea/vomiting, while patients in Irinotecan had a higher risk of experiencing maximum grade 3-4 (15.6% vs 7.6%, respectively; p < 0.001), patients in both groups experienced similar severity over time (adverse effect load = 0.102 and 0.096, respectively; p = 0.26), suggesting that patients in Oxaliplatin experienced a lower-grade but more persistent nausea/vomiting. For neutropenia/leukopenia, more patients in Irinotecan experienced their maximum grade for the first time early in the treatment compared to patients in Oxaliplatin (67.9% vs 41.7%; p < 0.001), regardless of maximum grade. Longitudinal information can help compare treatments or guide clinicians on choosing appropriate interventions for low-grade but persistent adverse event or early adverse event onset. Conclusion: We developed an adverse event reporting method that provides clinically relevant information about treatment toxicity by incorporating two longitudinal adverse event metrics to the traditional maximum grade approach. Future research should establish clinical benchmarks for metrics included in this adverse event reporting method.
MeSH term(s)	Adverse Drug Reaction Reporting Systems ; Antineoplastic Agents/adverse effects ; Clinical Trials as Topic ; Female ; Humans ; Irinotecan/adverse effects ; Male ; Neoplasms/drug therapy ; Oxaliplatin/adverse effects
Chemical Substances	Antineoplastic Agents ; Oxaliplatin (04ZR38536J) ; Irinotecan (7673326042)
Language	English
Publishing date	2020-10-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2138796-5
ISSN	1740-7753 ; 1740-7745
ISSN (online)	1740-7753
ISSN	1740-7745
DOI	10.1177/1740774520959313
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Article ; Online: Evaluating sex as a predictive marker for response to bevacizumab in metastatic colorectal carcinoma: Pooled analysis of 3,369 patients in the ARCAD database.

European journal of cancer (Oxford, England : 1990)

2022 Volume 178, Page(s) 162–170

Abstract: Background: Previous studies suggest a possible sex-specific response to bevacizumab in metastatic colorectal carcinoma (mCRC), showing a benefit in males, while the effect in females is less significant.: Methods: Data from 3369 patients with mCRC ... ...

Abstract	Background: Previous studies suggest a possible sex-specific response to bevacizumab in metastatic colorectal carcinoma (mCRC), showing a benefit in males, while the effect in females is less significant. Methods: Data from 3369 patients with mCRC enrolled on four first-line randomised trials testing chemotherapy with or without bevacizumab (2000-2007) were pooled. Association between sex and progression-free survival and overall survival (OS) was evaluated by stratified Cox regression model, adjusted for potential confounders. Predictive value was evaluated by interaction effect between sex and treatment. In a pre-planned secondary analysis, analyses were stratified using an age cut point of 60 years to evaluate the possible role of menopausal-related effects. Results: Bevacizumab was associated with an improved median OS in males and females, with a 2.3- and 0.6-months benefit, respectively. Stratified by age, bevacizumab resulted in improved OS in males at both age categories. In females at or above the age of 60 (n = 731), bevacizumab resulted in improved OS. However, in females below the age of 60 (n = 634), OS benefit did not reach statistical significance (adjusted hazard ratio = 0.94, 95% confidence interval 0.74-1.20). Conclusions: Our results confirmed the OS benefit from the addition of bevacizumab to first-line chemotherapy in mCRC in both sexes. Among females, the benefit was less than 1 month. For females under the age of 60, there was no survival benefit. These findings could be used to relieve financial toxicity or be redistributed within healthcare systems for other health-related purposes.
MeSH term(s)	Female ; Humans ; Male ; Middle Aged ; Antineoplastic Combined Chemotherapy Protocols ; Bevacizumab/therapeutic use ; Colorectal Neoplasms/drug therapy ; Randomized Controlled Trials as Topic
Chemical Substances	Bevacizumab (2S9ZZM9Q9V)
Language	English
Publishing date	2022-11-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	82061-1
ISSN	1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
ISSN (online)	1879-0852
ISSN	0277-5379 ; 0959-8049 ; 0964-1947
DOI	10.1016/j.ejca.2022.10.022
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Article ; Online: Localization of genes involved in the metabolic syndrome using multivariate linkage analysis.

Olswold, Curtis / de Andrade, Mariza

BMC genetics

2003 Volume 4 Suppl 1, Page(s) S57

Abstract: There are no well accepted criteria for the diagnosis of the metabolic syndrome. However, the metabolic syndrome is identified clinically by the presence of three or more of these five variables: larger waist circumference, higher triglyceride levels, ... ...

Abstract	There are no well accepted criteria for the diagnosis of the metabolic syndrome. However, the metabolic syndrome is identified clinically by the presence of three or more of these five variables: larger waist circumference, higher triglyceride levels, lower HDL-cholesterol concentrations, hypertension, and impaired fasting glucose. We use sets of two or three variables, which are available in the Framingham Heart Study data set, to localize genes responsible for this syndrome using multivariate quantitative linkage analysis. This analysis demonstrates the applicability of using multivariate linkage analysis and how its use increases the power to detect linkage when genes are involved in the same disease mechanism.
MeSH term(s)	Blood Pressure/genetics ; Blood Pressure/physiology ; Chromosome Mapping/statistics & numerical data ; Chromosomes, Human, Pair 17/genetics ; Chromosomes, Human, Pair 2/genetics ; Chromosomes, Human, Pair 5/genetics ; Chromosomes, Human, Pair 6/genetics ; Diabetes Mellitus, Type 2/genetics ; Female ; Gene Order/genetics ; Genetic Linkage/genetics ; Humans ; Lod Score ; Male ; Metabolic Syndrome/genetics ; Metabolic Syndrome/physiopathology ; Multivariate Analysis ; Quantitative Trait Loci/genetics ; Quantitative Trait, Heritable ; Software/statistics & numerical data
Language	English
Publishing date	2003-12-31
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
ISSN	1471-2156
ISSN (online)	1471-2156
DOI	10.1186/1471-2156-4-S1-S57
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Article ; Online: Comparison of longitudinal variance components and regression-based approaches for linkage detection on chromosome 17 for systolic blood pressure.

de Andrade, Mariza / Olswold, Curtis

BMC genetics

2003 Volume 4 Suppl 1, Page(s) S17

Abstract: We compare two methods to detect genetic linkage by using serial observations of systolic blood pressure in pedigree data from the Framingham Heart Study focusing on chromosome 17. The first method is a variance components (VC) approach that incorporates ...

Abstract	We compare two methods to detect genetic linkage by using serial observations of systolic blood pressure in pedigree data from the Framingham Heart Study focusing on chromosome 17. The first method is a variance components (VC) approach that incorporates longitudinal pedigree data, and the second method is a regression-based approach that summarizes all longitudinal measures in one single measure. No evidence of linkage was found either using the VC longitudinal approach or the regression-based approach, except when all time points were used from Cohorts 1 and 2 and only subjects aged 25 and 75 years were included.
MeSH term(s)	Adult ; Adult Children ; Aged ; Analysis of Variance ; Blood Pressure/genetics ; Blood Pressure/physiology ; Chromosome Mapping/methods ; Chromosome Mapping/statistics & numerical data ; Chromosomes, Human, Pair 17/genetics ; Cohort Studies ; Female ; Genetic Linkage/genetics ; Genetic Markers/genetics ; Humans ; Longitudinal Studies ; Male ; Quantitative Trait Loci/genetics ; Regression Analysis ; Systole
Chemical Substances	Genetic Markers
Language	English
Publishing date	2003-12-31
Publishing country	England
Document type	Comparative Study ; Journal Article
ISSN	1471-2156
ISSN (online)	1471-2156
DOI	10.1186/1471-2156-4-S1-S17
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Article: Risk of malignancy in first-degree relatives of patients with pancreatic carcinoma.

McWilliams, Robert R / Rabe, Kari G / Olswold, Curtis / De Andrade, Mariza / Petersen, Gloria M

Cancer

2005 Volume 104, Issue 2, Page(s) 388–394

Abstract: Background: Approximately 5-10% of pancreatic carcinoma (PC) patients report a family history of the disease. In some families, mutations of tumor suppressor genes have been elucidated, but for most the causative gene remains unidentified. Counseling ... ...

Abstract	Background: Approximately 5-10% of pancreatic carcinoma (PC) patients report a family history of the disease. In some families, mutations of tumor suppressor genes have been elucidated, but for most the causative gene remains unidentified. Counseling the families of PC patients regarding their risk of cancer remains problematic because little information is available. Methods: The authors analyzed family history questionnaires completed by 426 unselected, sequential Mayo Clinic patients with PC. The prevalence of malignancy reported among 3355 of their first-degree relatives was compared with the Surveillance, Epidemiology, and End Results Project (SEER) 9 (2000) registry. Age-adjusted and gender-adjusted standardized incidence ratios (SIRs) were generated. Results: Greater than 130,000 person-years at risk for cancer among the first-degree relatives were analyzed. The risk of PC was found to be increased among the first-degree relatives of patients with PC (SIR of 1.88; 95% confidence interval [95% CI], 1.27-2.68), as was the risk of liver carcinoma (SIR of 2.70; 95% CI, 1.51-4.46). Lymphoma (SIR of 0.28; 95% CI, 0.12-0.55), bladder carcinoma (SIR of 0.55; 95% CI, 0.31-0.89), breast carcinoma (SIR of 0.73; 95% CI, 0.57-0.92), lung carcinoma (SIR of 0.62; 95% CI, 0.47-0.80), and prostate carcinoma (SIR of 0.71; 95% CI, 0.54-0.92) were found to be underrepresented. When the proband was age < 60 years, the risk of PC to first-degree relatives was found to be increased further (SIR of 2.86; 95% CI, 1.15-5.89). In this subgroup, no other malignancies were found to be significantly increased, although the risks of melanoma (SIR of 1.73; 95% CI, 0.70-3.57), ovarian carcinoma (SIR of 2.20; 95% CI, 0.72-5.12), and colon carcinoma (SIR of 1.37; 95% CI, 0.80-2.19) were suggestive. Conclusions: There was a nearly twofold increased risk of PC in the first-degree relatives of PC probands. This risk was found to increase nearly threefold when patients were diagnosed before age 60 years. At the current time, in the absence of a pedigree suggestive of known familial cancer syndromes, the current study results do not support targeted screening for other malignancies in the first-degree relatives of patients with sporadic PC.
MeSH term(s)	Adult ; Family ; Family Health ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Neoplasms/epidemiology ; Pancreatic Neoplasms/genetics ; Registries ; Risk Assessment ; Smoking
Language	English
Publishing date	2005-07-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1429-1
ISSN	1097-0142 ; 0008-543X ; 1934-662X
ISSN (online)	1097-0142
ISSN	0008-543X ; 1934-662X
DOI	10.1002/cncr.21166
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Article ; Online: Identification of genes involved in alcohol consumption and cigarettes smoking.

de Andrade, Mariza / Olswold, Curtis L / Slusser, Joshua P / Tordsen, Larry A / Atkinson, Elizabeth J / Rabe, Kari G / Slager, Susan L

BMC genetics

2005 Volume 6 Suppl 1, Page(s) S112

Abstract: We compared the results of quantitative linkage analysis using single-nucleotide polymorphisms and microsatellite markers and introduced a new screening test for multivariate quantitative linkage analysis using the Collaborative Study on the Genetics of ... ...

Abstract	We compared the results of quantitative linkage analysis using single-nucleotide polymorphisms and microsatellite markers and introduced a new screening test for multivariate quantitative linkage analysis using the Collaborative Study on the Genetics of Alcoholism data. We analyzed 115 extended non-Hispanic White families and tested for linkage using two phenotypes: the maximum number of drinks in a 24-hour period and the number of packs smoked per day for one year. Our results showed that the linkage signal increased using single-nucleotide polymorphisms compared with microsatellite markers and that the screening test gave similar results to that of the bivariate analysis, suggesting its potential use in reducing overall analysis time.
MeSH term(s)	Alcohol Drinking/genetics ; Chromosomes, Human, Pair 1/genetics ; Genetic Linkage ; Humans ; Microsatellite Repeats/genetics ; Polymorphism, Single Nucleotide/genetics ; Smoking/genetics
Language	English
Publishing date	2005-12-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1471-2156
ISSN (online)	1471-2156
DOI	10.1186/1471-2156-6-S1-S112
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Article ; Online: Genetic variants associated with the risk of chronic obstructive pulmonary disease with and without lung cancer.

de Andrade, Mariza / Li, Yan / Marks, Randolph S / Deschamps, Claude / Scanlon, Paul D / Olswold, Curtis L / Jiang, Ruoxiang / Swensen, Stephen J / Sun, Zhifu / Cunningham, Julie M / Wampfler, Jason A / Limper, Andrew H / Midthun, David E / Yang, Ping

Cancer prevention research (Philadelphia, Pa.)

2011 Volume 5, Issue 3, Page(s) 365–373

Abstract: Chronic obstructive pulmonary disease (COPD) is a strong risk factor for lung cancer. Published studies about variations of genes encoding glutathione metabolism, DNA repair, and inflammatory response pathways in susceptibility to COPD were inconclusive. ...

Abstract	Chronic obstructive pulmonary disease (COPD) is a strong risk factor for lung cancer. Published studies about variations of genes encoding glutathione metabolism, DNA repair, and inflammatory response pathways in susceptibility to COPD were inconclusive. We evaluated 470 single-nucleotide polymorphisms (SNP) from 56 genes of these three pathways in 620 cases and 893 controls to identify susceptibility markers for COPD risk, using existing resources. We assessed SNP- and gene-level effects adjusting for sex, age, and smoking status. Differential genetic effects on disease risk with and without lung cancer were also assessed; cumulative risk models were established. Twenty-one SNPs were found to be significantly associated with risk of COPD (P < 0.01); gene-based analyses confirmed two genes (GCLC and GSS) and identified three additional genes (GSTO2, ERCC1, and RRM1). Carrying 12 high-risk alleles may increase risk by 2.7-fold; eight SNPs altered COPD risk without lung cancer by 3.1-fold and 4 SNPs altered the risk with lung cancer by 2.3-fold. Our findings indicate that multiple genetic variations in the three selected pathways contribute to COPD risk through GCLC, GSS, GSTO2, ERCC1, and RRM1 genes. Functional studies are needed to elucidate the mechanisms of these genes in the development of COPD, lung cancer, or both.
MeSH term(s)	Adenocarcinoma/genetics ; Aged ; Biomarkers, Tumor/genetics ; Case-Control Studies ; Female ; Genotype ; Humans ; Lung Neoplasms/genetics ; Male ; Polymorphism, Single Nucleotide/genetics ; Pulmonary Disease, Chronic Obstructive/genetics ; Risk Factors ; Smoking
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2011-11-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2434717-6
ISSN	1940-6215 ; 1940-6207
ISSN (online)	1940-6215
ISSN	1940-6207
DOI	10.1158/1940-6207.CAPR-11-0243
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