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Article ; Online: Tumor analysis of MMR genes in Lynch-like syndrome: Challenges associated with results interpretation.

Rofes, Paula / Dueñas, Núria / Del Valle, Jesús / Navarro, Matilde / Balmaña, Judith / Ramón Y Cajal, Teresa / Tuset, Noemí / Castillo, Carmen / González, Sara / Brunet, Joan / Capellá, Gabriel / Lázaro, Conxi / Pineda, Marta

Cancer medicine

2024 Volume 13, Issue 7, Page(s) e7041

Abstract: Background: Up to 70% of suspected Lynch syndrome patients harboring MMR deficient tumors lack identifiable germline pathogenic variants in MMR genes, being referred to as Lynch-like syndrome (LLS). Previous studies have reported biallelic somatic MMR ... ...

Abstract	Background: Up to 70% of suspected Lynch syndrome patients harboring MMR deficient tumors lack identifiable germline pathogenic variants in MMR genes, being referred to as Lynch-like syndrome (LLS). Previous studies have reported biallelic somatic MMR inactivation in a variable range of LLS-associated tumors. Moreover, translating tumor testing results into patient management remains controversial. Our aim is to assess the challenges associated with the implementation of tumoral MMR gene testing in routine workflows. Methods: Here, we present the clinical characterization of 229 LLS patients. MMR gene testing was performed in 39 available tumors, and results were analyzed using two variant allele frequency (VAF) thresholds (≥5% and ≥10%). Results and discussion: More biallelic somatic events were identified at VAF ≥ 5% than ≥10% (35.9% vs. 25.6%), although the rate of nonconcordant results regarding immunohistochemical pattern increased (30.8% vs. 20.5%). Interpretation difficulties question the current utility of the identification of MMR somatic hits in the diagnostic algorithm of suspected LS cases.
MeSH term(s)	Humans ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis/diagnosis ; Colorectal Neoplasms, Hereditary Nonpolyposis/genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis/pathology ; Germ-Line Mutation ; Neoplastic Syndromes, Hereditary ; Brain Neoplasms ; DNA Mismatch Repair/genetics
Language	English
Publishing date	2024-04-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2659751-2
ISSN	2045-7634 ; 2045-7634
ISSN (online)	2045-7634
ISSN	2045-7634
DOI	10.1002/cam4.7041
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Article: Potential Involvement of

Quintana, Isabel / Mur, Pilar / Terradas, Mariona / García-Mulero, Sandra / Aiza, Gemma / Navarro, Matilde / Piñol, Virginia / Brunet, Joan / Moreno, Victor / Sanz-Pamplona, Rebeca / Capellá, Gabriel / Valle, Laura

Cancers

2022 Volume 14, Issue 3

Abstract: The ALFRED (Allelic Loss Featuring Rare Damaging) in silico method was developed to identify cancer predisposition genes through the identification of somatic second hits. By applying ALFRED to ~10,000 tumor exomes, 49 candidate genes were identified. We ...

Abstract	The ALFRED (Allelic Loss Featuring Rare Damaging) in silico method was developed to identify cancer predisposition genes through the identification of somatic second hits. By applying ALFRED to ~10,000 tumor exomes, 49 candidate genes were identified. We aimed to assess the causal association of the identified genes with colorectal cancer (CRC) predisposition. Of the 49 genes,
Language	English
Publishing date	2022-01-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14030699
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Article: Breast Cancer Patient with Li-Fraumeni Syndrome: A Case Report Highlighting the Importance of Multidisciplinary Management.

Cirauqui, Beatriz / Morán, Teresa / Estival, Anna / Quiroga, Vanesa / Etxaniz, Olatz / Balana, Carmen / Navarro, Matilde / Villà, Salvador / Ballester, Rosa / Margelí, Mireia

Case reports in oncology

2020 Volume 13, Issue 1, Page(s) 130–138

Abstract: Germline mutations in TP53, a tumor suppressor gene, are involved in the development of Li-Fraumeni syndrome, a rare disorder that predisposes carriers to multiple tumors. TP53 mutations have been associated with resistance to treatment and poor ... ...

Abstract	Germline mutations in TP53, a tumor suppressor gene, are involved in the development of Li-Fraumeni syndrome, a rare disorder that predisposes carriers to multiple tumors. TP53 mutations have been associated with resistance to treatment and poor prognosis. A young female with the pathogenic germline TP53 mutation c.844C > T (p.R282W) was diagnosed with two metachronous breast tumors, one HER2-negative and the other HER2-positive. She was later diagnosed with synchronous glioblastoma, epidermal growth factor receptor-mutated lung adenocarcinoma, and HER2-negative breast cancer metastases. The patient was treated with local therapies, including brain surgery and radiotherapy, lung surgery, and a bilateral mastectomy, as well as with targeted systemic treatment. She proved to be highly sensitive to systemic therapy, and 13 years after the initial diagnosis of breast cancer and 6 years after the diagnosis of the two new primary tumors and recurrence of a prior cancer, she is alive with an excellent performance status. This surprising positive evolution may well be partly due to the pronged multidisciplinary approach to managing her disease and her extraordinary response to treatment: the lung adenocarcinoma showed excellent response to erlotinib; the breast cancer responded extremely well to eribulin and pegylated liposomal doxorubicin; and the glioblastoma has remained in response to surgery and radiotherapy. Despite harboring a TP53 mutation and having multiple tumors, this patient has shown an unexpectedly favorable evolution. The coordinated participation of a multidisciplinary team and the patient's own extraordinarily high sensitivity to systemic treatment played a major role in this evolution.
Language	English
Publishing date	2020-02-13
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2458961-5
ISSN	1662-6575
ISSN	1662-6575
DOI	10.1159/000505684
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Article ; Online: Candidate genes for hereditary colorectal cancer: Mutational screening and systematic review.

Belhadj, Sami / Terradas, Mariona / Munoz-Torres, Pau M / Aiza, Gemma / Navarro, Matilde / Capellá, Gabriel / Valle, Laura

Human mutation

2020 Volume 41, Issue 9, Page(s) 1563–1576

Abstract: Genome-wide approaches applied for the identification of new hereditary colorectal cancer (CRC) genes, identified several potential causal genes, including RPS20, IL12RB1, LIMK2, POLE2, MRE11, POT1, FAN1, WIF1, HNRNPA0, SEMA4A, FOCAD, PTPN12, LRP6, POLQ, ...

Abstract	Genome-wide approaches applied for the identification of new hereditary colorectal cancer (CRC) genes, identified several potential causal genes, including RPS20, IL12RB1, LIMK2, POLE2, MRE11, POT1, FAN1, WIF1, HNRNPA0, SEMA4A, FOCAD, PTPN12, LRP6, POLQ, BLM, MCM9, and the epigenetic inactivation of PTPRJ. Here we attempted to validate the association between variants in these genes and nonpolyposis CRC by performing a mutational screening of the genes and PTPRJ promoter methylation analysis in 473 familial/early-onset CRC cases, a systematic review of the published cases, and assessment of allele frequencies in control population. In the studied cohort, 24 (5%) carriers of (predicted) deleterious variants in the studied genes and no constitutional PTPRJ epimutations were identified. Assessment of allele frequencies in controls compared with familial/early-onset patients with CRC showed association with increased nonpolyposis CRC risk of disruptive variants in RPS20, IL12RB1, POLE2, MRE11 and POT1, and of FAN1 c.149T>G (p.Met50Arg). Lack of association was demonstrated for LIMK2, PTPN12, LRP6, PTPRJ, POLQ, BLM, MCM9 and FOCAD variants. Additional studies are required to provide conclusive evidence for SEMA4A, WIF1, HNRNPA0 c.-110G>C, and FOCAD large deletions.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Cohort Studies ; Colorectal Neoplasms/genetics ; DNA Methylation ; DNA Mutational Analysis ; Early Detection of Cancer ; Genetic Predisposition to Disease ; Humans ; Middle Aged ; Promoter Regions, Genetic ; Receptor-Like Protein Tyrosine Phosphatases, Class 3/genetics ; Young Adult
Chemical Substances	PTPRJ protein, human (EC 3.1.3.48) ; Receptor-Like Protein Tyrosine Phosphatases, Class 3 (EC 3.1.3.48)
Language	English
Publishing date	2020-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Systematic Review
ZDB-ID	1126646-6
ISSN	1098-1004 ; 1059-7794
ISSN (online)	1098-1004
ISSN	1059-7794
DOI	10.1002/humu.24057
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Article ; Online: Contribution to colonic polyposis of recently proposed predisposing genes and assessment of the prevalence of NTHL1- and MSH3-associated polyposes.

Terradas, Mariona / Munoz-Torres, Pau M / Belhadj, Sami / Aiza, Gemma / Navarro, Matilde / Brunet, Joan / Capellá, Gabriel / Valle, Laura

Human mutation

2019 Volume 40, Issue 11, Page(s) 1910–1923

Abstract: Technological advances have allowed the identification of new adenomatous and serrated polyposis genes, and of several candidate genes that require additional supporting evidence of causality. Through an exhaustive literature review and mutational ... ...

Abstract	Technological advances have allowed the identification of new adenomatous and serrated polyposis genes, and of several candidate genes that require additional supporting evidence of causality. Through an exhaustive literature review and mutational screening of 177 unrelated polyposis patients, we assessed the involvement of MCM9, FOCAD, POLQ, and RNF43 in the predisposition to (nonserrated) colonic polyposis, as well as the prevalence of NTHL1 and MSH3 mutations among genetically unexplained polyposis patients. Our results, together with previously reported data and mutation frequency in controls, indicate that: MCM9 and POLQ mutations are not associated with polyposis; germline RNF43 mutations, with a prevalence of 1.5-2.5% among serrated polyposis patients, do not cause nonserrated polyposis; MSH3 biallelic mutations are highly infrequent among European polyposis patients, and the prevalence of NTHL1 biallelic mutations among unexplained polyposes is ~2%. Although nonsignificant, FOCAD predicted deleterious variants are overrepresented in polyposis patients compared to controls, warranting larger studies to provide definite evidence in favor or against their causal association with polyposis predisposition.
MeSH term(s)	Adenomatous Polyposis Coli/diagnosis ; Adenomatous Polyposis Coli/epidemiology ; Adenomatous Polyposis Coli/genetics ; Biomarkers ; DNA-Directed DNA Polymerase/genetics ; Deoxyribonuclease (Pyrimidine Dimer)/genetics ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; MutS Homolog 3 Protein/genetics ; Mutation ; Pharmacogenomic Variants ; Prevalence ; Tumor Suppressor Proteins/genetics ; Ubiquitin-Protein Ligases/genetics ; DNA Polymerase theta
Chemical Substances	Biomarkers ; FOCAD protein, human ; MSH3 protein, human ; MutS Homolog 3 Protein ; Tumor Suppressor Proteins ; RNF43 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; Deoxyribonuclease (Pyrimidine Dimer) (EC 3.1.25.1) ; NTHL1 protein, human (EC 3.1.25.1)
Language	English
Publishing date	2019-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1126646-6
ISSN	1098-1004 ; 1059-7794
ISSN (online)	1098-1004
ISSN	1059-7794
DOI	10.1002/humu.23853
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Article: Non-Lynch Familial and Early-Onset Colorectal Cancer Explained by Accumulation of Low-Risk Genetic Variants.

Mur, Pilar / Bonifaci, Nuria / Díez-Villanueva, Anna / Munté, Elisabet / Alonso, Maria Henar / Obón-Santacana, Mireia / Aiza, Gemma / Navarro, Matilde / Piñol, Virginia / Brunet, Joan / Tomlinson, Ian / Capellá, Gabriel / Moreno, Victor / Valle, Laura

Cancers

2021 Volume 13, Issue 15

Abstract: A large proportion of familial and/or early-onset cancer patients do not carry pathogenic variants in known cancer predisposing genes. We aimed to assess the contribution of previously validated low-risk colorectal cancer (CRC) alleles to familial/early- ... ...

Abstract	A large proportion of familial and/or early-onset cancer patients do not carry pathogenic variants in known cancer predisposing genes. We aimed to assess the contribution of previously validated low-risk colorectal cancer (CRC) alleles to familial/early-onset CRC (fCRC) and to serrated polyposis. We estimated the association of CRC with a 92-variant-based weighted polygenic risk score (wPRS) using 417 fCRC patients, 80 serrated polyposis patients, 1077 hospital-based incident CRC patients, and 1642 controls. The mean wPRS was significantly higher in fCRC than in controls or sporadic CRC patients. fCRC patients in the highest (20th) wPRS quantile were at four-fold greater CRC risk than those in the middle quantile (10th). Compared to low-wPRS fCRC, a higher number of high-wPRS fCRC patients had developed multiple primary CRCs, had CRC family history, and were diagnosed at age ≥50. No association with wPRS was observed for serrated polyposis. In conclusion, a relevant proportion of mismatch repair (MMR)-proficient fCRC cases might be explained by the accumulation of low-risk CRC alleles. Validation in independent cohorts and development of predictive models that include polygenic risk score (PRS) data and other CRC predisposing factors will determine the implementation of PRS into genetic testing and counselling in familial and early-onset CRC.
Language	English
Publishing date	2021-07-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13153857
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Article ; Online: Lessons learnt from the implementation of a colorectal cancer screening programme for lynch syndrome in a tertiary public hospital.

Dueñas, Nuria / Navarro, Matilde / Sanjuán, Xavier / Ruiz, Núria / Iglesias, Silvia / Matias-Guiu, Xavier / Guardiola, Jordi / Kreisler, Esther / Biondo, Sebastiano / González, Sara / Legido, Raquel / Blanco, Ana / Navarro, Silvia / Asiain, Leyre / Santos, Cristina / Capellá, Gabriel / Pineda, Marta / Brunet, Joan

Cancer epidemiology

2022 Volume 82, Page(s) 102291

Abstract: Background: Lynch syndrome (LS) is the first cause of inherited colorectal cancer (CRC), being responsible for 2-4% of all diagnoses. Identification of affected individuals is important as they have an increased lifetime risk of multiple CRC and other ... ...

Abstract	Background: Lynch syndrome (LS) is the first cause of inherited colorectal cancer (CRC), being responsible for 2-4% of all diagnoses. Identification of affected individuals is important as they have an increased lifetime risk of multiple CRC and other neoplasms, however, LS is consistently underdiagnosed at the population level. We aimed to evaluate the yield of LS screening in CRC in a single-referral centre and to identify the barriers to its effective implementation. Methods: LS screening programme included individuals with CRC < 70 years, multiple CRC, or endometrial cancer at any age. Mismatch repair (MMR) protein immunohistochemistry (IHC) analysis was performed in routine practice on the surgical specimen and, if MLH1 IHC was altered, MLH1 gene promoter methylation was analysed. Results were collected in the CRC multidisciplinary board database. LS suspected individuals (altered MMR IHC without MLH1 promoter methylation) were referred to the Cancer Genetic Counselling Unit (CGCU). If accepted, a genetic study was performed. Two checkpoints were included: review of the pathology data and verification of patient referral by a genetic counsellor. Results: Between 2016 and 2019, 381 individuals were included. MMR IHC analysis was performed in 374/381 (98.2 %) CRC cases and MLH1 promoter methylation in 18/21 (85.7 %). Seventeen of the 20 LS suspected individuals were invited for referral at the CGCU. Two cases were not invited and the remaining patient died of cancer before completion of tumour screening. Fifteen individuals attended and a genetic analysis was performed in 15/20 (75 %) LS suspected individuals. Ten individuals were diagnosed with LS, in concordance with the IHC profile (2.7 % of the total cohort). This led to cascade testing in 58/75 (77.3 %) of the available adult relatives at risk, identifying 26 individuals with LS. Conclusions: Establishing a standardized institutional LS screening programme with checkpoints in the workflow is key to increasing the yield of LS identification.
MeSH term(s)	Adult ; Female ; Humans ; Colorectal Neoplasms, Hereditary Nonpolyposis/diagnosis ; Colorectal Neoplasms, Hereditary Nonpolyposis/genetics ; Early Detection of Cancer/methods ; Colorectal Neoplasms/diagnosis ; Colorectal Neoplasms/epidemiology ; Colorectal Neoplasms/genetics ; Endometrial Neoplasms/diagnosis ; DNA Methylation ; Hospitals, Public ; DNA Mismatch Repair/genetics ; Microsatellite Instability
Language	English
Publishing date	2022-11-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2508729-0
ISSN	1877-783X ; 1877-7821
ISSN (online)	1877-783X
ISSN	1877-7821
DOI	10.1016/j.canep.2022.102291
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Zs.A 1427: Show issues

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Article ; Online: Delineating the Phenotypic Spectrum of the NTHL1-Associated Polyposis.

Belhadj, Sami / Mur, Pilar / Navarro, Matilde / González, Sara / Moreno, Victor / Capellá, Gabriel / Valle, Laura

Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association

2016 Volume 15, Issue 3, Page(s) 461–462

MeSH term(s)	Adenomatous Polyposis Coli/genetics ; Adenomatous Polyposis Coli/pathology ; Deoxyribonuclease (Pyrimidine Dimer)/genetics ; Genotyping Techniques ; Humans
Chemical Substances	Deoxyribonuclease (Pyrimidine Dimer) (EC 3.1.25.1) ; NTHL1 protein, human (EC 3.1.25.1)
Language	English
Publishing date	2016-10-05
Publishing country	United States
Document type	Case Reports ; Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2119789-1
ISSN	1542-7714 ; 1542-3565
ISSN (online)	1542-7714
ISSN	1542-3565
DOI	10.1016/j.cgh.2016.09.153
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Zs.A 5836: Show issues

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Article ; Online: Characteristics of Adrenocortical Carcinoma Associated With Lynch Syndrome.

Domènech, Marta / Grau, Elia / Solanes, Ares / Izquierdo, Angel / Del Valle, Jesús / Carrato, Cristina / Pineda, Marta / Dueñas, Nuria / Pujol, Magda / Lázaro, Conxi / Capellà, Gabriel / Brunet, Joan / Navarro, Matilde

The Journal of clinical endocrinology and metabolism

2020 Volume 106, Issue 2, Page(s) 318–325

Abstract: Context: Lynch syndrome (LS) is the most common inherited colorectal and endometrial cancer syndrome, caused by germline mutations in DNA mismatch repair (MMR) genes. It is also characterized by an increased risk of other tumors with lower prevalence, ... ...

Abstract	Context: Lynch syndrome (LS) is the most common inherited colorectal and endometrial cancer syndrome, caused by germline mutations in DNA mismatch repair (MMR) genes. It is also characterized by an increased risk of other tumors with lower prevalence, such as adrenal cortical carcinoma (ACC), an endocrine tumor with an incidence of <2 cases/million individuals/year. Most ACC developed during childhood are associated with hereditary syndromes. In adults, this association is not as well established as in children. Previous studies showed a 3.2% prevalence of LS among patients with ACC. Evidence acquisition: The objective of this study is to determine the prevalence of ACC in a Spanish LS cohort and their molecular and histological characteristics. This retrospective study includes 634 patients from 220 LS families registered between 1999 and 2018. Evidence synthesis: During the follow-up period, 3 patients were diagnosed with ACC (0.47%); all were carriers of a MSH2 germline mutation. The 3 ACC patients presented loss of expression of MSH2 and MSH6 proteins. One tumor analysis showed loss of heterozygosity of the MSH2 wildtype allele. Our findings support previous data that considered ACC as a LS spectrum tumor. Conclusion: MMR protein immunohistochemistry screening could be an efficient strategy to detect LS in patients with ACC.
Language	English
Publishing date	2020-11-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgaa833
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Article: Correction: Dueñas et al. Assessing Effectiveness of Colonic and Gynecological Risk Reducing Surgery in Lynch Syndrome Individuals.

Dueñas, Nuria / Navarro, Matilde / Teulé, Àlex / Solanes, Ares / Salinas, Mònica / Iglesias, Sílvia / Munté, Elisabet / Ponce, Jordi / Guardiola, Jordi / Kreisler, Esther / Carballas, Elvira / Cuadrado, Marta / Matias-Guiu, Xavier / de la Ossa, Napoleón / Lop, Joan / Lázaro, Conxi / Capellá, Gabriel / Pineda, Marta / Brunet, Joan

Cancers

2021 Volume 13, Issue 13

Abstract: In the original article, there was a mistake in Figure 3 as published [ ... ]. ...

Abstract	In the original article, there was a mistake in Figure 3 as published [...].
Language	English
Publishing date	2021-06-22
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13133104
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