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1. Prognostic gene expression signature for high-grade serous ovarian cancer

Author

Millstein, J, Budden, T, Goode, EL, Anglesio, MS, Talhouk, A, Intermaggio, MP, Leong, HS, Chen, S, Elatre, W, Gilks, B, Nazeran, T, Volchek, M, Bentley, RC, Wang, C, Chiu, DS, Kommoss, S, Leung, SCY, Senz, J, Lum, A, Chow, V, Sudderuddin, H, Mackenzie, R, George, J, Fereday, S, Hendley, J, Traficante, N, Steed, H, Koziak, JM, Kobel, M, McNeish, IA, Goranova, T, Ennis, D, Macintyre, G, De Silva, DS, Ramon y Cajal, T, Garcia-Donas, J, Hernando Polo, S, Rodriguez, GC, Cushing-Haugen, KL, Harris, HR, Greene, CS, Zelaya, RA, Behrens, S, Fortner, RT, Sinn, P, Herpel, E, Lester, J, Lubinski, J, Oszurek, O, Toloczko, A, Cybulski, C, Menkiszak, J, Pearce, CL, Pike, MC, Tseng, C, Alsop, J, Rhenius, V, Song, H, Jimenez-Linan, M, Piskorz, AM, Gentry-Maharaj, A, Karpinskyj, C, Widschwendter, M, Singh, N, Kennedy, CJ, Sharma, R, Harnett, PR, Gao, B, Johnatty, SE, Sayer, R, Boros, J, Winham, SJ, Keeney, GL, Kaufmann, SH, Larson, MC, Luk, H, Hernandez, BY, Thompson, PJ, Wilkens, LR, Carney, ME, Trabert, B, Lissowska, J, Brinton, L, Sherman, ME, Bodelon, C, Hinsley, S, Lewsley, LA, Glasspool, R, Banerjee, SN, Stronach, EA, Haluska, P, Ray-Coquard, I, Mahner, S, Winterhoff, B, Slamon, D, Levine, DA, Kelemen, LE, Benitez, J, Chang-Claude, J, Gronwald, J, Wu, AH, Menon, U, Goodman, MT, Schildkraut, JM, Wentzensen, N, Brown, R, Berchuck, A, Chenevix-Trench, G, DeFazio, A, Gayther, SA, Garcia, MJ, Henderson, MJ, Rossing, MA, Beeghly-Fadiel, A, Fasching, PA, Orsulic, S, Karlan, BY, Konecny, GE, Huntsman, DG, Bowtell, DD, Brenton, JD, Doherty, JA, Pharoah, PDP, Ramus, SJ, Millstein, J, Budden, T, Goode, EL, Anglesio, MS, Talhouk, A, Intermaggio, MP, Leong, HS, Chen, S, Elatre, W, Gilks, B, Nazeran, T, Volchek, M, Bentley, RC, Wang, C, Chiu, DS, Kommoss, S, Leung, SCY, Senz, J, Lum, A, Chow, V, Sudderuddin, H, Mackenzie, R, George, J, Fereday, S, Hendley, J, Traficante, N, Steed, H, Koziak, JM, Kobel, M, McNeish, IA, Goranova, T, Ennis, D, Macintyre, G, De Silva, DS, Ramon y Cajal, T, Garcia-Donas, J, Hernando Polo, S, Rodriguez, GC, Cushing-Haugen, KL, Harris, HR, Greene, CS, Zelaya, RA, Behrens, S, Fortner, RT, Sinn, P, Herpel, E, Lester, J, Lubinski, J, Oszurek, O, Toloczko, A, Cybulski, C, Menkiszak, J, Pearce, CL, Pike, MC, Tseng, C, Alsop, J, Rhenius, V, Song, H, Jimenez-Linan, M, Piskorz, AM, Gentry-Maharaj, A, Karpinskyj, C, Widschwendter, M, Singh, N, Kennedy, CJ, Sharma, R, Harnett, PR, Gao, B, Johnatty, SE, Sayer, R, Boros, J, Winham, SJ, Keeney, GL, Kaufmann, SH, Larson, MC, Luk, H, Hernandez, BY, Thompson, PJ, Wilkens, LR, Carney, ME, Trabert, B, Lissowska, J, Brinton, L, Sherman, ME, Bodelon, C, Hinsley, S, Lewsley, LA, Glasspool, R, Banerjee, SN, Stronach, EA, Haluska, P, Ray-Coquard, I, Mahner, S, Winterhoff, B, Slamon, D, Levine, DA, Kelemen, LE, Benitez, J, Chang-Claude, J, Gronwald, J, Wu, AH, Menon, U, Goodman, MT, Schildkraut, JM, Wentzensen, N, Brown, R, Berchuck, A, Chenevix-Trench, G, DeFazio, A, Gayther, SA, Garcia, MJ, Henderson, MJ, Rossing, MA, Beeghly-Fadiel, A, Fasching, PA, Orsulic, S, Karlan, BY, Konecny, GE, Huntsman, DG, Bowtell, DD, Brenton, JD, Doherty, JA, Pharoah, PDP, and Ramus, SJ

Abstract

BACKGROUND: Median overall survival (OS) for women with high-grade serous ovarian cancer (HGSOC) is ∼4 years, yet survival varies widely between patients. There are no well-established, gene expression signatures associated with prognosis. The aim of this study was to develop a robust prognostic signature for OS in patients with HGSOC. PATIENTS AND METHODS: Expression of 513 genes, selected from a meta-analysis of 1455 tumours and other candidates, was measured using NanoString technology from formalin-fixed paraffin-embedded tumour tissue collected from 3769 women with HGSOC from multiple studies. Elastic net regularization for survival analysis was applied to develop a prognostic model for 5-year OS, trained on 2702 tumours from 15 studies and evaluated on an independent set of 1067 tumours from six studies. RESULTS: Expression levels of 276 genes were associated with OS (false discovery rate < 0.05) in covariate-adjusted single-gene analyses. The top five genes were TAP1, ZFHX4, CXCL9, FBN1 and PTGER3 (P < 0.001). The best performing prognostic signature included 101 genes enriched in pathways with treatment implications. Each gain of one standard deviation in the gene expression score conferred a greater than twofold increase in risk of death [hazard ratio (HR) 2.35, 95% confidence interval (CI) 2.02-2.71; P < 0.001]. Median survival [HR (95% CI)] by gene expression score quintile was 9.5 (8.3 to -), 5.4 (4.6-7.0), 3.8 (3.3-4.6), 3.2 (2.9-3.7) and 2.3 (2.1-2.6) years. CONCLUSION: The OTTA-SPOT (Ovarian Tumor Tissue Analysis consortium - Stratified Prognosis of Ovarian Tumours) gene expression signature may improve risk stratification in clinical trials by identifying patients who are least likely to achieve 5-year survival. The identified novel genes associated with the outcome may also yield opportunities for the development of targeted therapeutic approaches.

Published
2020

2. Interim Results from the IMPACT Study: Evidence for Prostate-specific Antigen Screening in BRCA2 Mutation Carriers

Author

Page, EC, Bancroft, EK, Brook, MN, Assel, M, Al Battat, MH, Thomas, S, Taylor, N, Chamberlain, A, Pope, J, Ni Raghallaigh, H, Evans, DG, Rothwell, J, Maehle, L, Grindedal, EM, James, P, Mascarenhas, L, McKinley, J, Side, L, Thomas, T, van Asperen, C, Vasen, H, Kiemeney, LA, Ringelberg, J, Jensen, TD, Osther, PJS, Helfand, BT, Genova, E, Oldenburg, RA, Cybulski, C, Wokolorczyk, D, Ong, K-R, Huber, C, Lam, J, Taylor, L, Salinas, M, Feliubadalo, L, Oosterwijk, JC, van Zelst-Stams, W, Cook, J, Rosario, DJ, Domchek, S, Powers, J, Buys, S, O'Toole, K, Ausems, MGEM, Schmutzler, RK, Rhiem, K, Izatt, L, Tripathi, V, Teixeira, MR, Cardoso, M, Foulkes, WD, Aprikian, A, van Randeraad, H, Davidson, R, Longmuir, M, Ruijs, MWG, Helderman van den Enden, ATJM, Adank, M, Williams, R, Andrews, L, Murphy, DG, Halliday, D, Walker, L, Liljegren, A, Carlsson, S, Azzabi, A, Jobson, I, Morton, C, Shackleton, K, Snape, K, Hanson, H, Harris, M, Tischkowitz, M, Taylor, A, Kirk, J, Susman, R, Chen-Shtoyerman, R, Spigelman, A, Pachter, N, Ahmed, M, Ramon y Cajal, T, Zgajnar, J, Brewer, C, Gadea, N, Brady, AF, van Os, T, Gallagher, D, Johannsson, O, Donaldson, A, Barwell, J, Nicolai, N, Friedman, E, Obeid, E, Greenhalgh, L, Murthy, V, Copakova, L, Saya, S, McGrath, J, Cooke, P, Ronlund, K, Richardson, K, Henderson, A, Teo, SH, Arun, B, Kast, K, Dias, A, Aaronson, NK, Ardern-Jones, A, Bangma, CH, Castro, E, Dearnaley, D, Eccles, DM, Tricker, K, Eyfjord, J, Falconer, A, Foster, C, Gronberg, H, Hamdy, FC, Stefansdottir, V, Khoo, V, Lindeman, GJ, Lubinski, J, Axcrona, K, Mikropoulos, C, Mitra, A, Moynihan, C, Rennert, G, Suri, M, Wilson, P, Dudderidge, T, Offman, J, Kote-Jarai, Z, Vickers, A, Lilja, H, Eeles, RA, Page, EC, Bancroft, EK, Brook, MN, Assel, M, Al Battat, MH, Thomas, S, Taylor, N, Chamberlain, A, Pope, J, Ni Raghallaigh, H, Evans, DG, Rothwell, J, Maehle, L, Grindedal, EM, James, P, Mascarenhas, L, McKinley, J, Side, L, Thomas, T, van Asperen, C, Vasen, H, Kiemeney, LA, Ringelberg, J, Jensen, TD, Osther, PJS, Helfand, BT, Genova, E, Oldenburg, RA, Cybulski, C, Wokolorczyk, D, Ong, K-R, Huber, C, Lam, J, Taylor, L, Salinas, M, Feliubadalo, L, Oosterwijk, JC, van Zelst-Stams, W, Cook, J, Rosario, DJ, Domchek, S, Powers, J, Buys, S, O'Toole, K, Ausems, MGEM, Schmutzler, RK, Rhiem, K, Izatt, L, Tripathi, V, Teixeira, MR, Cardoso, M, Foulkes, WD, Aprikian, A, van Randeraad, H, Davidson, R, Longmuir, M, Ruijs, MWG, Helderman van den Enden, ATJM, Adank, M, Williams, R, Andrews, L, Murphy, DG, Halliday, D, Walker, L, Liljegren, A, Carlsson, S, Azzabi, A, Jobson, I, Morton, C, Shackleton, K, Snape, K, Hanson, H, Harris, M, Tischkowitz, M, Taylor, A, Kirk, J, Susman, R, Chen-Shtoyerman, R, Spigelman, A, Pachter, N, Ahmed, M, Ramon y Cajal, T, Zgajnar, J, Brewer, C, Gadea, N, Brady, AF, van Os, T, Gallagher, D, Johannsson, O, Donaldson, A, Barwell, J, Nicolai, N, Friedman, E, Obeid, E, Greenhalgh, L, Murthy, V, Copakova, L, Saya, S, McGrath, J, Cooke, P, Ronlund, K, Richardson, K, Henderson, A, Teo, SH, Arun, B, Kast, K, Dias, A, Aaronson, NK, Ardern-Jones, A, Bangma, CH, Castro, E, Dearnaley, D, Eccles, DM, Tricker, K, Eyfjord, J, Falconer, A, Foster, C, Gronberg, H, Hamdy, FC, Stefansdottir, V, Khoo, V, Lindeman, GJ, Lubinski, J, Axcrona, K, Mikropoulos, C, Mitra, A, Moynihan, C, Rennert, G, Suri, M, Wilson, P, Dudderidge, T, Offman, J, Kote-Jarai, Z, Vickers, A, Lilja, H, and Eeles, RA

Abstract

BACKGROUND: Mutations in BRCA2 cause a higher risk of early-onset aggressive prostate cancer (PrCa). The IMPACT study is evaluating targeted PrCa screening using prostate-specific-antigen (PSA) in men with germline BRCA1/2 mutations. OBJECTIVE: To report the utility of PSA screening, PrCa incidence, positive predictive value of PSA, biopsy, and tumour characteristics after 3 yr of screening, by BRCA status. DESIGN, SETTING, AND PARTICIPANTS: Men aged 40-69 yr with a germline pathogenic BRCA1/2 mutation and male controls testing negative for a familial BRCA1/2 mutation were recruited. Participants underwent PSA screening for 3 yr, and if PSA > 3.0 ng/ml, men were offered prostate biopsy. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: PSA levels, PrCa incidence, and tumour characteristics were evaluated. Statistical analyses included Poisson regression offset by person-year follow-up, chi-square tests for proportion t tests for means, and Kruskal-Wallis for medians. RESULTS AND LIMITATIONS: A total of 3027 patients (2932 unique individuals) were recruited (919 BRCA1 carriers, 709 BRCA1 noncarriers, 902 BRCA2 carriers, and 497 BRCA2 noncarriers). After 3 yr of screening, 527 men had PSA > 3.0 ng/ml, 357 biopsies were performed, and 112 PrCa cases were diagnosed (31 BRCA1 carriers, 19 BRCA1 noncarriers, 47 BRCA2 carriers, and 15 BRCA2 noncarriers). Higher compliance with biopsy was observed in BRCA2 carriers compared with noncarriers (73% vs 60%). Cancer incidence rate per 1000 person years was higher in BRCA2 carriers than in noncarriers (19.4 vs 12.0; p = 0.03); BRCA2 carriers were diagnosed at a younger age (61 vs 64 yr; p = 0.04) and were more likely to have clinically significant disease than BRCA2 noncarriers (77% vs 40%; p = 0.01). No differences in age or tumour characteristics were detected between BRCA1 carriers and BRCA1 noncarriers. The 4 kallikrein marker model discriminated better (area under the curve [AUC] = 0.73) for clinically significant cancer at

Published
2019

3. Open-Source Bioinformatic Pipeline to Improve PMS2 Genetic Testing Using Short-Read NGS Data.

Author

Munté E, Feliubadaló L, Del Valle J, González S, Ramos-Muntada M, Balmaña J, Ramon Y Cajal T, Tuset N, Llort G, Cadiñanos J, Brunet J, Capellá G, Lázaro C, and Pineda M

Subjects
Humans, DNA Mutational Analysis methods, Germ-Line Mutation, Neoplastic Syndromes, Hereditary genetics, Neoplastic Syndromes, Hereditary diagnosis, Mismatch Repair Endonuclease PMS2 genetics, High-Throughput Nucleotide Sequencing methods, Computational Biology methods, Genetic Testing methods
Abstract

The molecular diagnosis of mismatch repair-deficient cancer syndromes is hampered by difficulties in sequencing the PMS2 gene, mainly owing to the PMS2CL pseudogene. Next-generation sequencing short reads cannot be mapped unambiguously by standard pipelines, compromising variant calling accuracy. This study aimed to provide a refined bioinformatic pipeline for PMS2 mutational analysis and explore PMS2 germline pathogenic variant prevalence in an unselected hereditary cancer (HC) cohort. PMS2 mutational analysis was optimized using two cohorts: 192 unselected HC patients for assessing the allelic ratio of paralogous sequence variants, and 13 samples enriched with PMS2 (likely) pathogenic variants screened previously by long-range genomic DNA PCR amplification. Reads were forced to align with the PMS2 reference sequence, except those corresponding to exon 11, where only those intersecting gene-specific invariant positions were considered. Afterward, the refined pipeline's accuracy was validated in a cohort of 40 patients and used to screen 5619 HC patients. Compared with our routine diagnostic pipeline, the PMS2&#95;vaR pipeline showed increased technical sensitivity (0.853 to 0.956, respectively) in the validation cohort, identifying all previously PMS2 pathogenic variants found by long-range genomic DNA PCR amplification. Fifteen HC cohort samples carried a pathogenic PMS2 variant (15 of 5619; 0.285%), doubling the estimated prevalence in the general population. The refined open-source approach improved PMS2 mutational analysis accuracy, allowing its inclusion in the routine next-generation sequencing pipeline streamlining PMS2 screening., Competing Interests: Disclosure Statement None declared., (Copyright © 2024 Association for Molecular Pathology and American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Published
2024
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4. Paired Somatic-Germline Testing of 15 Polyposis and Colorectal Cancer-Predisposing Genes Highlights the Role of APC Mosaicism in de Novo Familial Adenomatous Polyposis.

Author

Rofes P, González S, Navarro M, Moreno-Cabrera JM, Solanes A, Darder E, Carrasco E, Iglesias S, Salinas M, Gómez C, Velasco À, Tuset N, Varela M, Llort G, Ramon Y Cajal T, Grau È, Dueñas N, de la Ossa Merlano N, Matías-Guiu X, Rivera B, Balmaña J, Pineda M, Brunet J, Capellá G, Del Valle J, and Lázaro C

Subjects
Adenomatous Polyposis Coli pathology, Adult, Aged, Cohort Studies, Colorectal Neoplasms pathology, Female, High-Throughput Nucleotide Sequencing methods, Humans, Male, Middle Aged, Young Adult, Adenomatous Polyposis Coli genetics, Adenomatous Polyposis Coli Protein genetics, Colorectal Neoplasms genetics, Genes, APC, Genetic Predisposition to Disease genetics, Genetic Testing methods, Germ-Line Mutation, Mosaicism
Abstract

Familial adenomatous polyposis (FAP) is an autosomal dominant syndrome responsible for 1% of colorectal cancers (CRCs). Up to 90% of classic FAPs are caused by inactivating mutations in APC, and mosaicism has been previously reported in 20% of de novo cases, usually linked to milder phenotypic manifestations. This study aimed to explore the prevalence of mosaicism in 11 unsolved cases of classic FAP and to evaluate the diagnostic yield of somatic testing. Paired samples of colorectal polyps, tumors, and/or mucosa were analyzed using a custom next-generation sequencing panel targeting 15 polyposis and CRC-predisposing genes. Whenever possible, the extension of mosaicism to blood or sperm was also examined. Of 11 patients with classic adenomatous polyposis, a mosaic pathogenic variant in APC was identified in 7 (64%). No other altered genes were identified. In two of seven patients (29%), mosaicism was found restricted to colonic tissues, whereas in five of seven patients (71%), it was extended to the blood. Germline affectation was confirmed in one patient. We report the first analysis at a somatic level of 15 genes associated with CRC susceptibility, which highlights the role of APC mosaicism in classic FAP etiology. The results further reinforce the importance of testing target tissues when blood test results are negative., (Copyright © 2021 Association for Molecular Pathology and American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Published
2021
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5. Validity and Reliability of the Decision Regret Scale in Cancer Patients Receiving Adjuvant Chemotherapy.

Author

Calderon C, Ferrando PJ, Lorenzo-Seva U, Higuera O, Ramon Y Cajal T, Rogado J, Mut-Lloret M, Rodriguez-Capote A, Jara C, and Jimenez-Fonseca P

Subjects
Adult, Aged, Aged, 80 and over, Decision Making, Female, Humans, Male, Middle Aged, Psychometrics, Quality of Life, Reproducibility of Results, Surveys and Questionnaires, Chemotherapy, Adjuvant psychology, Conflict, Psychological, Emotions, Neoplasms drug therapy, Patient Satisfaction
Abstract

Objectives: Decisional regret is an indicator of satisfaction with the treatment decision and can help to identify those patients who need more support and evaluate the efficacy of decision support interventions. The objectives of this study are, 1) to evaluate the psychometric properties of the Decision Regret Scale and 2) to analyze the moderating effect of psychological distress on functional status and regret in patients with cancer following adjuvancy., Methods: A prospective, multicenter cohort of 403 patients who completed the Decision Regret Scale (DRS), Health-Related Quality of Life (EORTC QLQ-C30), and Brief Symptom Inventory (BSI). The evaluation was conducted six months after receiving adjuvant treatment in patients with resected cancer., Results: After treatment, most participants (51.9%) experienced no decision regret; 33.7% felt mild regret, and 14.4% exhibited high levels of regret. The Spanish version of the DRS demonstrated satisfactory properties: it had a strong, clear unidimensional factorial structure with substantial loadings. Decisional regret was related with lower scores on functional, symptom, and quality of life scales, and higher levels of psychological distress (all P = 0.001). Psychological distress was found to have a moderating effect on the relationship between functional state and decision regret., Conclusions: The Spanish version of the DRS is a reliable, valid tool to evaluate regret and post-decisional quality in clinical practice and further highlights the potential clinical implications of psychological distress for the relation between physical status and regret., (Copyright © 2018 American Academy of Hospice and Palliative Medicine. Published by Elsevier Inc. All rights reserved.)

Published
2019
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6. What factors may influence psychological well being at three months and one year post BRCA genetic result disclosure?

Author

Bosch N, Junyent N, Gadea N, Brunet J, Ramon y Cajal T, Torres A, Graña B, Velasco A, Darder E, Mensa I, and Balmaña J

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Female, Follow-Up Studies, Genetic Markers, Hereditary Breast and Ovarian Cancer Syndrome genetics, Humans, Logistic Models, Male, Middle Aged, Multivariate Analysis, Psychological Tests, Risk Factors, Spain, Surveys and Questionnaires, Time Factors, Young Adult, Anxiety etiology, Depression etiology, Genes, BRCA1, Genes, BRCA2, Genetic Predisposition to Disease psychology, Genetic Testing, Hereditary Breast and Ovarian Cancer Syndrome psychology
Abstract

Genetic testing for breast cancer predisposition has been available in the clinical practice for more than a decade. How the result of genetic testing affects the psychological well-being of the individuals is an under-researched area in many populations. Follow-up analysis of psychological well-being via HADS scale was performed in 364 individuals at 3 months and 1 year after the disclosure of BRCA1/2 genetic result. We analyzed potential predictors for pathological anxiety and variables associated to the variation of HADS scores over time. At pre-test only 16% and 4% of individuals presented symptoms of anxiety and depression, respectively. Having a prior diagnosis of cancer and presenting a pathological HADS-A score at the baseline were associated with clinically significant anxiety scores at one year, but the genetic test result was not. Thus, BRCA genetic testing does not influence short and long term anxiety and depression levels among those identified as mutation carriers. It is our task to demystify the allegedly negative impact of BRCA testing on psychological well being to increase the uptake of genetic testing and benefit those who are at high risk of developing breast, ovarian and prostate cancer., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Published
2012
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7. Risk factors associated with the occurrence of breast cancer after bilateral salpingo-oophorectomy in high-risk women.

Author

Ramon Y Cajal T, Torres A, Alonso C, Fisas D, Ojeda B, Boguña I, Prat J, Baiget M, and Barnadas A

Subjects
Adolescent, Adult, Aged, BRCA1 Protein genetics, BRCA2 Protein genetics, Breast Neoplasms genetics, Case-Control Studies, Female, Functional Laterality, Humans, Middle Aged, Mutation genetics, Prospective Studies, Risk Factors, Spain, Young Adult, Breast Neoplasms epidemiology, Ovariectomy, Salpingostomy
Abstract

Introduction: Bilateral salpingo-oophorectomy (BSO) is a common procedure for preventing breast and ovarian cancer in high-risk women. The goal of this study was to determine the incidence of subsequent breast cancer (BC) in a high-risk population and to identify clinical and epidemiological predictors of BC following BSO., Materials and Methods: One hundred and thirty-three consecutive high-risk women, tested for BRCA1 and BRCA2 mutations due to family history, underwent preventive or therapeutic BSO at one of the study hospitals. One hundred and three patients had breast tissue at risk and were considered evaluable for the event-free survival analysis. Twenty-five women harbored a deleterious mutation in BRCA1 and 25 in BRCA2 genes., Results: Fifteen cases of invasive BC were diagnosed with a median interval of 49 months after BSO. Multivariate analysis showed that a prior BC after 50 years of age (p=0.004), age over 50 years at the time of BSO (p=0.005), and prior replacement or contraceptive hormonal treatment (p=0.007) were significantly associated with a shorter event-free survival., Conclusion: In conclusion, age at prior diagnosis of cancer, age at BSO and prior hormonal treatment may be predictors of breast cancer after BSO., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Published
2011
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