Does a family history of adenomatous colon polyp(s) in a first-degree relative pose an increased risk of developing colon cancer?

175 Background: There are few published reports of relative risk (RR) for LPC based on family history of prostate cancer (PC) lethality. This study provides LPC RR using complete LPC family history data obtained from a statewide Cancer Registry linked to a genealogy database. Methods: The Utah Population Data Base (UPDB), which includes a statewide SEER cancer registry, includes 1,192,768 individuals with at least 12 of their 14 immediate ancestors. All males (probands) with specific LPC constellations were identified in the UPDB, and the observed number of LPC cases among these probands was compared to the expected number of LPC cases using internal cohort-specific rates from Utah death certificates including all deceased males with no 1st, 2nd, or 3rd degree relatives with LPC. LPC Family history was estimated for 1st degree to 3rd degree relatives for: number of LPC relatives affected, paternal versus maternal family history, and age at first PC diagnosis. Results: 3,921 individuals in UPDB were diagnosed with histologically confirmed PC, and had a Utah death certificate indicating PC as a cause of death and were designated LPC. The RR for LPC was significantly elevated with each additional first-degree relative (FDR) with LPC; even in the absence of FDR family history of LPC, significantly increased risk for LPC was observed in the presence of at least 1 LPC affected second degree relative (SDR). In the absence of positive FDR and SDR family history for LPC, there was still increased risk for LPC for males with 2 or more third degree relatives with LPC. Early age PC diagnosis in the LPC relative did not appear to affect LPC RR. Higher risks of LPC were associated with the maternal compared to the paternal lineages. Conclusions: Examination of lethal prostate cancer family history (in FDRs through TDRs) may be useful in identifying the cohort of men with prostate cancer most at risk for death from prostate cancer. Focused screening and treatment of this cohort holds potential to decrease the rates of undertreatment of lethal disease while avoiding over diagnosis and overtreatment in inconsequential disease.

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COLON CANCER AND POLYPS IN ACROMEGALY: INCREASED RISK ASSOCIATED WITH FAMILY HISTORY OF COLON CANCER

Clinical Endocrinology ◽

10.1111/j.1365-2265.1990.tb03751.x ◽

1990 ◽

Vol 32 (1) ◽

pp. 65-71 ◽

Cited By ~ 60

Author(s):

JOHN E. BRUNNER ◽

CHRISTINE COLE JOHNSON ◽

SAEED ZAFAR ◽

EDWARD L. PETERSON ◽

JOHN F. BRUNNER ◽

...

Keyword(s):

Colon Cancer ◽

Family History ◽

Increased Risk ◽

History Of

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Differences in the Distribution of Cytogenetic Subtypes Between Multiple Myeloma Patients with and without a History of Familial MGUS and Multiple Myeloma

Blood ◽

10.1182/blood.v120.21.4000.4000 ◽

2012 ◽

Vol 120 (21) ◽

pp. 4000-4000

Author(s):

Alexandra Greenberg ◽

Margot Cousin ◽

Celine M Vachon ◽

Dirk Larson ◽

Colin L. Colby ◽

...

Keyword(s):

Multiple Myeloma ◽

Family History ◽

Research Funding ◽

Plasma Cells ◽

Statistical Significance ◽

Degree Relative ◽

First Degree Relatives ◽

Familial Tendency ◽

Increased Risk ◽

History Of

Abstract Abstract 4000 Background: We have previously reported that there is an increased risk of monoclonal gammopathy of undetermined significance (MGUS) in first-degree relatives of patients with multiple myeloma (Vachon CM. Blood 2009 114: 785–790). There are several cytogenetic subtypes of myeloma, and there are no data on whether certain cytogenetic subtypes of myeloma are more frequently associated with familial MGUS. Methods: We studied patients with myeloma who participated in the familial MGUS study in whom presence or absence of MGUS in the first-degree relatives had been ascertained (Vachon CM. Blood 2009 114: 785–790). Probands were seen at the Mayo Clinic Hematology/Oncology practice (Rochester, MN, USA) between February 2006 and September 2007. Cytogenetic data was acquired via electronic medical record abstraction of fluorescence in-situ hybridization (FISH) lab reports, and used to categorize patients into one of nine cytogenetic subgroups: trisomy(ies), t(6;14), t(11;14), t(4;14), t(14;16), t(14;20), Mixed (those with trisomy(ies) and an IgH translocation), other cytogenetic abnormalities (in the absence of trisomy(ies) or IgH translocation), and normal (Kumar S. Blood 2012;119:2100–2105). We examined whether a difference in the distribution of the six primary cytogenetic categories of myeloma existed between probands with a family history of MGUS and/or myeloma and those without. Results and Conclusions: Of the 248 patients invited to participate, FISH data (with sufficient plasma cells) was available on 119 participants to establish the primary molecular cytogenetic classification of myeloma. All had available information regarding family history of MGUS and multiple myeloma. 27 had an affected first-degree relative with MGUS, and 92 did not. Distributions of cytogenetic subtypes in the two groups are shown in Table 1. IgH translocated MM was more common in myeloma patients who lacked an affected first-degree relative compared to those with familial MGUS (19% vs 30%, P=0.32) Interestingly, the t(11;14) subtype was more common in myeloma patients without familial MGUS compared to those with an first-degree relative with MGUS (19.6% vs 7.4%, P=0.24). The differences in Table 1 did not reach statistical significance, possibly due to the small numbers of individuals with a family history in this sample. However, the distribution (Table 1) suggests that the distribution of cytogenetic subtypes may be different in myeloma that is not associated with familial MGUS compared with myeloma in which a familial tendency is detected. IgH translocated MM appears to have a lower risk of familial tendency. Further investigation is needed to estimate the risk of familial MGUS within each cytogenetic subtype. Disclosures: Kumar: Merck: Consultancy, Honoraria; Millennium: Research Funding; Celgene: Consultancy, Research Funding; Novartis: Research Funding; Genzyme: Research Funding.

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ATM mutation carriers and family history of pancreatic cancer.

Journal of Clinical Oncology ◽

10.1200/jco.2020.38.15_suppl.1529 ◽

2020 ◽

Vol 38 (15_suppl) ◽

pp. 1529-1529

Author(s):

Jeannie Klavanian ◽

Dana Zakalik ◽

Anish S Konde ◽

Tara Rangarajan

Keyword(s):

Pancreatic Cancer ◽

Family History ◽

Gene Mutations ◽

Close Relative ◽

Degree Relative ◽

Mutation Carriers ◽

Increased Risk ◽

Age Of Diagnosis ◽

History Of ◽

Atm Gene

1529 Background: Multigene panel testing (MGT) is commonly utilized in patients with a personal or family history of cancer. One of the more common gene mutations identified is in the ATM gene, associated with a moderately increased risk of breast and other cancers. There are reports of an association with pancreatic cancer, however the exact risks are unclear. The aim of this study is to describe the family history of pancreatic cancer in a cohort of ATM mutation carriers, and to evaluate possible genotype/phenotype correlation. Methods: Patients who underwent MGT, between ‘13 and ‘19, and tested positive for a pathogenic/likely pathogenic ATM mutation were included in this study. Family history, with a focus on pancreatic cancer, and genetic testing results were analyzed. Results: A total of 114 patients were identified to carry an ATM mutation. Twenty-two (19.3%) individuals had a family history of pancreatic cancer in a close relative, and of those, 13 (11.4%) had an affected first degree relative, and 11 (9.6%) had an affected second degree relative. Among the families with pancreatic cancer, 20 close relatives had a personal history of pancreatic cancer, with the youngest diagnosed at age 40, the oldest diagnosed at age 91, and a mean age of diagnosis of 66.5 years. Thirteen unique variants were identified: 4 splice site, 3 missense, 3 frameshift, 1 nonsense, and 1 silent. Two families had the known high-penetrance ATM mutation, c.7271T > C (p.V2424G). Conclusions: This study describes the association of pancreatic cancer in individuals found to carry pathogenic ATM mutations. A significant proportion (19.3%) of patients had a family history of pancreatic cancer in a close relative, diagnosed as young as age 40. The mean age of diagnosis was slightly younger than the average age in the general population (age 70). As pancreatic cancer screening continues to improve, this information will be an important component to help guide cancer risk assessment and future screening recommendations for ATM mutation carriers. Additional larger studies are needed to further characterize pancreatic cancer risks in patients with ATM gene mutations.

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Family History of Cancer and Tobacco Exposure in Index Cases of Pancreatic Ductal Adenocarcinoma

Journal of Oncology ◽

10.1155/2011/215985 ◽

2011 ◽

Vol 2011 ◽

pp. 1-7 ◽

Cited By ~ 7

Author(s):

R. Lochan ◽

A. K. Daly ◽

H. L. Reeves ◽

R. M. Charnley

Keyword(s):

Pancreatic Cancer ◽

Family History ◽

Pancreatic Adenocarcinoma ◽

Ductal Adenocarcinoma ◽

Tobacco Exposure ◽

Degree Relative ◽

Family History Questionnaire ◽

Increased Risk ◽

History Of ◽

History Of Cancer

Aim. To examine interaction between history of cancer in first-degree relatives and tobacco smoking in index patients of pancreatic adenocarcinoma.Methods. We carried out a case-control involving 113 patients with pancreatic adenocarcinoma and 110 controls over a 12-month period at the Freeman Hospital, Newcastle upon Tyne, UK. They were all administered a detailed tobacco exposure questionnaire and a family history questionnaire. We calculated cumulative tobacco exposure and risk for pancreas cancer.Results. Both smokers (OR 3.01 (95% CI: 1.73 to 5.24)) and those with a family history of malignancy (OR 1.98 (95% CI: 1.15–3.38)) were more likely to develop pancreatic cancer. Having more than one first-degree relative with cancer did not significantly further increase the risk of pancreatic cancer. Amongst pancreatic cancer cases, cumulative tobacco exposure was significantly decreased () in the group of smokers (current and ex-smokers) who had a family history of malignancy [mean (SD): 30.00 (24.77) pack-years versus 44.69 (28.47) pack-years with no such history].Conclusions. Individuals with a family history of malignancy are at an increased risk of pancreatic cancer. Furthermore, individuals with a family history of malignancy and who smoke appear to require a lesser degree of tobacco exposure for the development of pancreatic cancer.

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Psychiatric disorder in young adults born very preterm: Role of family history

European Psychiatry ◽

10.1016/j.eurpsy.2008.06.004 ◽

2008 ◽

Vol 23 (7) ◽

pp. 527-531 ◽

Cited By ~ 26

Author(s):

M. Walshe ◽

L. Rifkin ◽

M. Rooney ◽

E. Healy ◽

C. Nosarti ◽

...

Keyword(s):

Young Adults ◽

Family History ◽

Psychiatric Disorder ◽

Psychiatric Illness ◽

Degree Relative ◽

Interview Schedule ◽

Very Preterm ◽

Increased Risk ◽

History Of

AbstractObjectiveTo investigate whether young adults born very preterm (VPT) (<33 weeks) are at increased risk for psychiatric illness in adulthood and whether a family history of psychiatric disorder further increases this risk.MethodsWe assessed 169 VPT and 101 term born individuals using the Clinical Interview Schedule – Revised.ResultsYoung adults born VPT had an increased risk for psychiatric disorder compared to controls (OR = 3.1, 95% CI = 1.1–8.6, p = 0.03). Those born VPT who had a history of psychiatric disorder in a first-degree relative, had an increase in risk for psychiatric disorder compared to those born VPT without a family history (OR = 5.2, 95% CI = 1.8–14.9, p = 0.002).ConclusionIndividuals born VPT are at increased risk of psychiatric illness in young adulthood compared to controls. In addition, a family history of psychiatric disorder in a first-degree relative may leave young adults born VPT particularly vulnerable to psychiatric illness.

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Risk of invasive breast cancer in relatives of patients with breast carcinoma in situ: a prospective cohort study

BMC Medicine ◽

10.1186/s12916-020-01772-x ◽

2020 ◽

Vol 18 (1) ◽

Author(s):

Trasias Mukama ◽

Mahdi Fallah ◽

Hermann Brenner ◽

Xing Xu ◽

Kristina Sundquist ◽

...

Keyword(s):

Breast Cancer ◽

Family History ◽

Breast Carcinoma ◽

Invasive Breast Cancer ◽

Carcinoma In Situ ◽

Degree Relative ◽

Breast Carcinoma In Situ ◽

Increased Risk ◽

History Of

Abstract Background Wide implementation of mammography screening has resulted in increased numbers of women diagnosed with breast carcinoma in situ. We aimed to determine the risk of invasive breast cancer in relatives of patients with breast carcinoma in situ in comparison to the risk in relatives of patients with invasive breast cancer. Methods We analyzed the occurrence of cancer in a nationwide cohort including all 5,099,172 Swedish women born after 1931 with at least one known first-degree relative. This was a record linkage study of Swedish family cancer datasets, including cancer registry data collected from January 1, 1958, to December 31, 2015. We calculated standardized incidence ratios (SIRs) and 10-year cumulative risk of breast cancer diagnosis for women with a family history of in situ and invasive breast cancer. Results Having one first-degree relative with breast carcinoma in situ was associated with 50% increased risk of invasive breast cancer (SIR = 1.5, 95% CI 1.4–1.7) when compared to those who had no family history of invasive breast cancer or breast carcinoma in situ in either first- or second-degree relatives. Similarly, having one first-degree relative with invasive breast cancer was associated with 70% (1.7, 1.7–1.8) increased risk. The 10-year cumulative risk for women at age 50 with a relative with breast carcinoma in situ was 3.5% (2.9–3.9%) and was not significantly different from 3.7% (3.6–3.8%) risk for 50-year-old women with a relative with invasive breast cancer (95% confidence intervals overlapped). Conclusions The risk of invasive breast cancer for women with a family history of breast carcinoma in situ was comparable to that for women with a family history of invasive breast cancer. Therefore, family history of breast carcinoma in situ should not be overlooked in recommendations for breast cancer prevention for women with a family history of breast cancer.

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Family History of Cancer and Risk of Lymphoma: Influence of IL8RB, GGH IVS7 and IL10 Polymorphisms.

Blood ◽

10.1182/blood.v112.11.1777.1777 ◽

2008 ◽

Vol 112 (11) ◽

pp. 1777-1777

Author(s):

Eva Domingo-Domènech ◽

Yolanda Benavente ◽

Carlos Montalbán ◽

Ramon Bosch ◽

Josep Gumà ◽

...

Keyword(s):

Family History ◽

Variant Allele ◽

Degree Relative ◽

Family History Of Cancer ◽

Increased Risk ◽

Inheritance Model ◽

History Of ◽

Additive Inheritance ◽

History Of Cancer

Abstract Background and aims: Family history of cancer in lymphoma patients has largely been described. On the other hand, genetic susceptibility associated to lymphoma risk is being investigated at the present time. However, single nucleotide polymorphisms (SNPs) associated to the entity among those reporting family history of cancer have yet not been identified. In a previous study of our group, we identified that the probability of having a first-degree relative with cancer was significantly higher among the patients with lymphoid neoplasm than among the control subjects (43% vs 35%, p<0.05). When analysing by lymphoma subtypes, B-cell lymphoma, chronic lymphocytic leukaemia (CLL) and multiple myeloma (MM) patients were significantly more likely to report a first-degree relative with any cancer, with a risk increase ranging from 1.4 up to 2.1 among CLL patients. Thus, a 2-to 4-fold increased risk of lymphoma has been identified in patients with a family history of hematologic disease or lymphoma in first-degree relatives, with CLL, MM and Hodgkin’s lymphoma (HL) being the three entities more consistently reported. The purpose of this study was to evaluate the role of genetic variants of several polymorphisms in the risk of developing a lymphoid neoplasm among subjects with family history of cancer in the case-control study Epilymph. Material and methods: Newly diagnosed cases of lymphoma were recruited between 1998–2002 in 4 Spanish centers. Controls were hospitalized patients matched to the cases by age, gender and study center. Personal interviews were conducted in order to collect data on demographics, environmental exposure, medical and family history, including cancer. The site of cancer, age at diagnosis, and status of any affected relatives with cancer were requested. In this analysis, we only included those subjects who reported a family history of cancer. 72 SNPs in 47 genes were included in the analysis. DNA of 503 cases and 569 controls were genotyped using the TaqmanTM platform. Odds Ratios (OR) and 95% confidence intervals (CI) for the association of the variants with the risk of lymphoma were calculated using unconditional logistic regression analysis, under the log additive inheritance model. Results: Family history of cancer was reported by 421 subjects (196 controls and 225 cases, p-value=0.001). Among those, 41 had an hematological origin. The two SNP genotyped in IL8RB gene were associated to an increase in risk of lymphoma for every extra variant allele (IL8RB +1235C>T OR=1.68, 95%CI=1.25–2.27 and IL8RB -1010A>G OR=1.59, 95%CI=1.17–2.17). The OR associated to an additional variant allele of Ggh IVS7-3001 polymorphism was 1.82 (95%CI=1.06–3.14). IL-1082 A>G was observed to decrease the risk of lymphoma (OR=0.72, 95%CI=0.54–0.96).Restricting the analysis to those with a familial cancer of hematological origin under a log-additive inheritance model, a statistical increase in the risk was found for every extra variant allele MTHFR +429A>C in the genotype (OR=21.52, 95%CI=2.42–191.08), whereas presenting at least one variant allele of IL10 -1082 A>G decreased the risk of lymphoma (OR=0.05, 95%CI=0.01–0.38). In order to evaluate the association between SNPs and lymphoma subtypes in subjects with family history of cancer, we explored the relation between all statistically significant SNPs reported above and non-Hodgkin lymphomas (NHL), Chronic lymphocytic leukemia (CLL), multiple myeloma (MM), and Hodgkin lymphoma (HL). We observe that the association of SNPs and all lymphoma is similar after stratifying by subtypes, although these results are based on few subjects. Interestingly, those SNPs related to low risk of lymphoma, were observed to have the lowest risk among HL cases (IL10 -1082 A>G OR=0.28, 95%CI=0.09– 0.82), whereas HL and MM seems to be at higher risk for those SNPs related to increased risk of lymphoma (IL8RB+1235 OR=2.29, 95%CI=1.29–4.05 and IL8RB-1010 OR=2.45, 95%CI=1.33–4.51 for MM and Ggh IVS7-3001 OR=5.47, 95%CI=1.33–22.52 for HL). Conclusions: These results suggest a potential role of IL8RB, GGH IVS7 and IL10 SNPs in the risk of lymphoid neoplasms among subjects with family history of cancer. HL and MM seem to be those entities in which these associations appear to be stronger, although the number of cases included is small.

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