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Dive into the research topics where Mariana Niell-Swiller is active.

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Featured researches published by Mariana Niell-Swiller.


Frontiers in Oncology | 2015

Clinical Application of Multigene Panels: Challenges of Next-Generation Counseling and Cancer Risk Management

Thomas P. Slavin; Mariana Niell-Swiller; Ilana Solomon; Bita Nehoray; Christina Rybak; Kathleen R. Blazer; Jeffrey N. Weitzel

Background Multigene panels can be a cost- and time-effective alternative to sequentially testing multiple genes, especially with a mixed family cancer phenotype. However, moving beyond our single-gene testing paradigm has unveiled many new challenges to the clinician. The purpose of this article is to familiarize the reader with some of the challenges, as well as potential opportunities, of expanded hereditary cancer panel testing. Methods We include results from 348 commercial multigene panel tests ordered from January 1, 2014, through October 1, 2014, by clinicians associated with the City of Hope’s Clinical Cancer Genetics Community of Practice. We also discuss specific challenging cases that arose during this period involving abnormalities in the genes: CDH1, TP53, PMS2, PALB2, CHEK2, NBN, and RAD51C. Results If historically high risk genes only were included in the panels (BRCA1, BRCA2, MSH6, PMS2, TP53, APC, CDH1), the results would have been positive only 6.2% of the time, instead of 17%. Results returned with variants of uncertain significance (VUS) 42% of the time. Conclusion These figures and cases stress the importance of adequate pre-test counseling in anticipation of higher percentages of positive, VUS, unexpected, and ambiguous test results. Test result ambiguity can be limited by the use of phenotype-specific panels; if found, multiple resources (the literature, reference laboratory, colleagues, national experts, and research efforts) can be accessed to better clarify counseling and management for the patient and family. For pathogenic variants in low and moderate risk genes, empiric risk modeling based on the patient’s personal and family history of cancer may supersede gene-specific risk. Commercial laboratory and patient contributions to public databases and research efforts will be needed to better classify variants and reduce clinical ambiguity of multigene panels.


Genetic Testing and Molecular Biomarkers | 2015

Next-Generation Testing for Cancer Risk: Perceptions, Experiences, and Needs Among Early Adopters in Community Healthcare Settings

Kathleen R. Blazer; Bita Nehoray; Ilana Solomon; Mariana Niell-Swiller; Julie O. Culver; Gwen Uman; Jeffrey N. Weitzel

BACKGROUND Advances in next-generation sequencing (NGS) technologies are driving a shift from single-gene to multigene panel testing for clinical genetic cancer risk assessment (GCRA). This study explored perceptions, experiences, and challenges with NGS testing for GCRA among U.S. community-based clinicians. METHODS Surveys delivered at initial and 8-month time points, and 12-month tracking of cases presented in a multidisciplinary web-based case conference series, were conducted with GCRA providers who participated in a 235-member nationwide community of practice. RESULTS The proportion of respondents ordering panel tests rose from 29% at initial survey (27/94) to 44% (46/107) within 8 months. Respondents reported significantly less confidence about interpreting and counseling about NGS compared with single-gene test results (p < 0.0001 for all comparisons). The most cited reasons for not ordering NGS tests included concerns about clinical utility, interpreting and communicating results, and lack of knowledge/skills. Multigene panels were used in 204/668 cases presented during 2013, yielding 37 (18%) deleterious (7% in low/moderate-penetrance genes), 88 (43%) with ≥1 variant of uncertain significance, 77 (38%) uninformative negative, and 2 (1%) inconclusive results. CONCLUSIONS Despite concerns about utility and ability to interpret/counsel about NGS results, a rapidly increasing uptake of NGS testing among community clinicians was documented. Challenges identified in case discussions point to the need for ongoing education, practice-based support, and opportunities to partner in research that contributes to characterization of lesser known genes.


Journal of the National Cancer Institute | 2018

Prospective Study of Cancer Genetic Variants: Variation in Rate of Reclassification by Ancestry

Thomas P. Slavin; Lily Ravel Van Tongeren; Carolyn E Behrendt; Ilana Solomon; Christina Rybak; Bita Nehoray; Lili Kuzmich; Mariana Niell-Swiller; Kathleen R. Blazer; Shu Tao; Kai Yang; Julie O. Culver; Sharon Sand; Danielle Castillo; Josef Herzog; Stacy W. Gray; Jeffrey N. Weitzel

Background In germline genetic testing, variants from understudied ancestries have been disproportionately classified as being of uncertain significance. We hypothesized that the rate of variant reclassification likewise differs by ancestry. Methods Nonbenign variants in actionable genes were collected from consenting subjects undergoing genetic testing at two Southern California sites from September 1996 through December 2016. Variant reclassifications were recorded as they were received, until February 2017 or reclassification to benign. Excluding duplicate variants (same ancestry, laboratory, classification), generalized linear models for the hereditary breast cancer genes (BRCA1/2) and other variants investigated whether rate of reclassification differed for seven categories of ancestry compared with non-Hispanic European. Models took into account laboratory, year, gene, sex, and current classification (handled as a time-dependent covariate) and were adjusted for multiple hypothesis testing. Results Among 1483 nonbenign variants, 693 (46.7%) involved BRCA1/2. Overall, 268 (18.1%) variants were reclassified at least once. Few (9.7%) reclassified variants underwent a net upgrade in pathogenicity. For BRCA1/2 variants, reclassification rates varied by ancestry and increased over time, more steeply for ancestries with lower initial rates (African, Ashkenazi, Chinese) than for ancestries whose initial rates were high (Middle Eastern) or similar to non-Hispanic European (non-Chinese Asian, Native American, Hispanic). In contrast, reclassification rates of non-BRCA1/2 variants did not vary over time but were elevated for most minority ancestries except non-Chinese Asian and Native American. Conclusions For nonbenign variants in cancer-related genes, the rates at which reclassifications are issued vary by ancestry in ways that differ between BRCA1/2 and other genes.


Cancer Genetics and Cytogenetics | 2017

Genetic Gastric Cancer Susceptibility in the International Clinical Cancer Genomics Community Research Network

Thomas P. Slavin; Susan L. Neuhausen; Christina Rybak; Ilana Solomon; Bita Nehoray; Kathleen R. Blazer; Mariana Niell-Swiller; Aaron Adamson; Yate-Ching Yuan; Kai Yang; Sharon Sand; Danielle Castillo; Josef Herzog; Xiwei Wu; Shu Tao; Tanya Chavez; Yanghee Woo; Joseph Chao; Pamela Mora; Darling Horcasitas; Jeffrey N. Weitzel

Few susceptibility genes for gastric cancer have been identified. We sought to identify germline susceptibility genes from participants with gastric cancer from an international hereditary cancer research network. Adults with gastric cancer of any histology, and with a germline DNA sample (n = 51), were retrospectively selected. For those without previously identified germline mutations (n = 43), sequencing was performed for 706 candidate genes. Twenty pathogenic or likely pathogenic variants were identified among 18 participants. Eight of the 18 participants had previous positive clinical testing, including six with CDH1 pathogenic or likely pathogenic variants, and two with pathogenic MSH2 and TP53 variants. Of the remaining 10, six were in BRCA1 DNA damage response pathway genes (ATM, ATR, BRCA2, BRIP1, FANCC, TP53), other variants were identified in CTNNA1, FLCN, SBDS, and GNAS. Participants identified with pathogenic or likely pathogenic variants were younger at gastric cancer diagnosis than those without, 39.1 versus 48.0 years, and over 50% had a close family member with gastric cancer (p-values < 0.0001). In conclusion, many participants were identified with mutations in clinically-actionable genes. Age of onset and family history of gastric cancer were mutation status predictors. Our findings support multigene panels in identifying gastric cancer predisposition.


Genetics in Medicine | 2018

Somatic TP53 variants frequently confound germ-line testing results

Jeffrey N. Weitzel; Elizabeth C. Chao; Bita Nehoray; Lily Ravel Van Tongeren; Holly LaDuca; Kathleen R. Blazer; Thomas P. Slavin; D A B M D Facmg; Tina Pesaran; Christina Rybak; Ilana Solomon; Mariana Niell-Swiller; Jill S. Dolinsky; Danielle Castillo; Aaron M. Elliott; Chia-Ling Gau; Virginia Speare; Kory Jasperson

PurposeBlood/saliva DNA is thought to represent the germ line in genetic cancer-risk assessment. Cases with pathogenic TP53 variants detected by multigene panel testing are often discordant with Li-Fraumeni syndrome, raising concern about misinterpretation of acquired aberrant clonal expansions (ACEs) with TP53 variants as germ-line results.MethodsPathogenic TP53 variants with abnormal next-generation sequencing metrics (e.g., decreased ratio (<25%) of mutant to wild-type allele, more than two detected alleles) were selected from a CLIA laboratory testing cohort. Alternate tissues and/or close relatives were tested to distinguish between ACE and germ-line status. Clinical data and Li-Fraumeni syndrome testing criteria were examined.ResultsAmong 114,630 multigene panel tests and 1,454 TP53 gene-specific analyses, abnormal next-generation sequencing metrics were observed in 20% of 353 TP53-positive results, and ACE was confirmed for 91% of cases with ancillary materials, most of these due to clonal hematopoiesis. Only four met Chompret criteria. Individuals with ACE were older (50 years vs. 33.7; P = 0.02) and were identified more frequently in multigene panel tests (66/285; 23.2%) than in TP53 gene-specific tests (6/68; 8.8%, P = 0.005).ConclusionACE confounds germ-line diagnosis, may portend hematologic malignancy, and may provoke unwarranted clinical interventions. Ancillary testing to confirm germ-line status should precede Li-Fraumeni syndrome management.


Journal of Cancer Education | 2018

Experience Gained from the Development and Execution of a Multidisciplinary Multi-syndrome Hereditary Colon Cancer Family Conference

Ilana Solomon; Christina Rybak; Lily Ravel Van Tongeren; Lili Kuzmich; Kathleen R. Blazer; Bita Nehoray; Mariana Niell-Swiller; Shawnie Bray; Travis Bray; Karen Hurley; Jeffrey N. Weitzel; Thomas P. Slavin

Genetic healthcare professionals provide genetic cancer risk assessment and follow-up care for patients facing hereditary cancers. To meet the needs of those affected by hereditary colorectal cancer, City of Hope and the Hereditary Colon Cancer Foundation collaborated to develop a “Family Day” conference. We describe the development of our conference based upon the Hereditary Colon Cancer Foundation’s “Family Day” program model, with refinements completed using the Participatory Action Research theoretical framework, which incorporated input from conference participants and researchers. Thirty-one participants attended the conference, representing patients with, or families, friends, and caregivers of those with, multiple colorectal cancer predisposition syndromes, including Lynch, familial adenomatous polyposis, and juvenile polyposis. Participants who completed the feedback surveys (n = 22) were highly satisfied with the presentation content, ranking the keynote lecture on family communication the highest of the conference events. Participants also provided feedback regarding how to improve future conferences. In conclusion, we share our experience and provide guidance for developing a successful hereditary colon cancer predisposition patient and family conference.


Cancer Research | 2017

Abstract 4273: Variant reclassifications in hereditary cancer genetics and their implications for clinical care

Thomas P. Slavin; Stacy W. Gray; Lily Ravel Van Tongeren; Ilana Solomon; Christina Rybak; Bita Nehoray; Lili Kuzmich; Mariana Niell-Swiller; Kathleen R. Blazer; Kai Yang; Julie O. Culver; Sharon Sand; Danielle Castillo; Josef Herzog; Jeffrey N. Weitzel

BACKGROUND: Clinicians who provide genetic cancer risk assessment (GCRA) are dependent on laboratory reporting of germline results to inform cancer screening and treatment recommendations. Efforts to enhance variant classification and harmonization, such as ClinVar, will lead to an increase in the number of variants being reclassified. Given that the impact of variant reclassification on care is unknown, we evaluated the frequency and clinical impact of variant reclassification on individuals seen for GCRA. METHODS: We retrospectively evaluated data on 7,356 participants enrolled through the Clinical Cancer Genomics Community Research Network (CCGCRN) at City of Hope and Olive View Medical Center from September 1996- October 2016. RESULTS: 4,969 commercial genetic tests yielded a total of 1,610 variants of any category, of which 181 unique variants in 20 genes were reclassified. BRCA1 and BRCA2 (BRCA) and mismatch repair genes comprised 73.5% and 5.5% of the genes reclassified, respectively. Reclassification impacted 225 individuals (97% women) from 217 families; 89% of these individuals (n=201) had a personal history of cancer. The interval between initial report and variant reclassification averaged 3 years (17 days- 13 years). Minorities had higher reclassification rates as compared to non-Hispanic white participants (P = 0.0149). Of the 181 unique reclassifications, 164 (90.6%) of variants were downgraded. Sixteen reclassifications led to changes in clinical care. Thirteen variants carried by 15 individuals were upgraded from a variant of uncertain significance (VUS) to likely pathogenic or pathogenic (10 BRCA, 3 MLH1 or MSH2). These reclassifications prompted additional prophylactic surgical interventions (i.e., bilateral salpingo-oophorectomy), specialist referrals, and surveillance recommendations for at risk patients and family members. Three variants (NBN p.Arg215Trp, PTEN p.Ala79Thr, and MET c.1200+2T>C) were downgraded from likely pathogenic or pathogenic to VUS. Prior to downgrade to VUS, 2 cases had unnecessary surveillance procedures. CONCLUSIONS: Since many genomic variants will be reclassified over time, it is critical that laboratories deliver prompt notification of reclassifications, and that providers involved in GCRA discuss the possibility of variant reclassification with patients and family members and collect patient/proxy information during informed consent so that re-contact is possible. Given the non-trivial effort required for variant reclassification and patient/participant re-contact, system-level interventions are needed to facilitate genomic reinterpretation and the return of results to individuals over time. Citation Format: Thomas P. Slavin, Stacy W. Gray, Lily R. Van Tongeren, Ilana Solomon, Christina Rybak, Bita Nehoray, Lili Kuzmich, Mariana Niell-Swiller, Kathleen R. Blazer, Kai Yang, Julie Culver, Sharon Sand, Danielle Castillo, Josef Herzog, Jeffrey N. Weitzel. Variant reclassifications in hereditary cancer genetics and their implications for clinical care [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4273. doi:10.1158/1538-7445.AM2017-4273


Cancer Research | 2016

Abstract 2551: Identifying hereditary gastric cancer predisposition in the clinical cancer genomics community research network

Thomas P. Slavin; Kai Yang; Sharon Sand; Tanya Chavez; Danielle Castillo; Joseph Herzog; Ilana Solomon; Christina Rybak; Mariana Niell-Swiller; Bita Nehoray; Aaron Adamson; Kathleen R. Blazer; Susan L. Neuhausen; Jeffrey N. Weitzel

Genetic Cancer Risk Assessment (GCRA) clinical referral and testing guidelines are limited for individuals and families with gastric cancer. In part, this is due to a lack of knowledge regarding hereditary gastric cancer susceptibility. The Clinical Cancer Genomics Community Research Network registry includes over 15,000 families seen for GCRA at City of Hope and 45 other collaborating sites. The purpose of this research was to identify variants conferring inherited gastric cancer susceptibility for individuals and families in our registry without previously known genetic predisposition. Adult research participants from our IRB-approved registry with a DNA sample and a personal history of gastric cancer were selected. Those with a previously identified genetic predisposition were excluded (n = 8). In families with more than one eligible individual, the individual with earliest onset of disease was selected. All histologies were included (i.e., intestinal and diffuse adenocarcinomas, as well as, gastrointestinal stromal tumors). Of 47 eligible participants, 22 had previously uninformative clinical testing. Germline sequencing was completed using a novel 706 candidate cancer gene panel, which included genes involved in DNA damage response, cell cycle regulation, apoptosis, and the Fanconi anemia, mTOR, JAK-STAT, and RAS-MAPK pathways; known cancer susceptibility genes; and genes frequently mutated in gastric tumors (data from the Catalog of Somatic Variants in Cancer database). Based on 2015 American College of Medical Genetics and Genomics and the Association for Molecular Pathology Standards and Guidelines, 18 out of 47 research participants had pathogenic or likely pathogenic germline variants. Of the 18, 11 had a first- or second-degree relative with gastric cancer. Variants were identified in established cancer susceptibility genes, such as BRCA2, BRIP1, RAD51C, ATM, FLCN, as well as in genes from rare autosomal recessive conditions, such as FANCC. In conclusion, using a 706 gene panel to test a GCRA cohort, we were able to identify potentially pathogenic variants in 38% of participants with gastric cancer, with nearly half of these variants in clinically actionable genes. The variants identified in this study will need to be further evaluated using segregation studies, tumor studies, and in larger cohorts to establish causality. Citation Format: Thomas P. Slavin, Kai Yang, Sharon Sand, Tanya Chavez, Danielle Castillo, Joseph Herzog, Ilana Solomon, Christina Rybak, Mariana Niell-Swiller, Bita Nehoray, Aaron Adamson, Kathleen Blazer, Susan Neuhausen, Jeffrey Weitzel, Clinical Cancer Genomics Community Research Network. Identifying hereditary gastric cancer predisposition in the clinical cancer genomics community research network. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2551.


Cancer Research | 2016

Abstract PD7-02: Multiplex Identification of genetic etiologies among women with bilateral breast cancer using a 25-gene hereditary cancer panel

Jeffrey N. Weitzel; Kathleen R. Blazer; Bita Nehoray; J Kidd; Thomas P. Slavin; Ilana Solomon; Mariana Niell-Swiller; Christina Rybak; J Saam; J Lancaster

Background: Multiple primary cancers within an individual is one of the hallmarks of hereditary cancer predisposition. Technical advances in sequencing and identification of additional cancer susceptibility genes have led to multi-gene panel approaches to determine if patient cancers have a heritable cause. Simultaneous testing of multiple breast cancer associated genes to determine the prevalence, spectrum and combinations of mutations has not yet been evaluated in a large set of patients with two breast cancers. Methods: Patients with two breast cancer diagnoses were identified from 80,748 consecutive cases that underwent a 25-gene hereditary cancer panel test at a commercial diagnostic laboratory. Patient clinical data were obtained by healthcare provider report on test requisition forms. Results: Of 3,182 patients with two breast cancers, 13.3 % (n=424) had a pathogenic variant (PV) in at least one of 19 genes on the panel. PVs were most prevalent within BRCA1, representing 26.3% of the PVs, followed by BRCA2 (21.9%), CHEK2 (13.5%), PALB2 (11%) and ATM (11%). Fourteen patients had PVs in two different genes, including five with CHEK2/PALB2 in combination, which was the only combination observed more than once. PVs were more common among the 33.8% of patients with synchronous breast cancers compared to those with metachronous diagnoses (10.8% vs. 15%) and in the 58.4% who were first diagnosed younger than 50 years old (15.7% vs. 10%). Conclusion: Multiplex testing in women with two primary breast cancers identifies a relatively high percentage with a PV, including those whose first diagnosis was older than 50. While still the most prevalent and clear cause, fewer than half of the PVs identified were in BRCA1 or BRCA2. The observation of 5 cases with double CHEK2/PALB2 PVs is statistically unexpected given their individual prevalence in other studies of high risk women with breast cancer, suggesting a possible synergistic or additive effect. This study adds to our understanding of susceptibility to multiple primary breast cancers, and reaffirms the importance of this circumstance as a prompt for genetic testing. Nonetheless, as 66% of cases had metachronous tumors, it would be preferable to identify those at risk with heritable cancer syndromes at their first diagnosis and enable subsequent prevention or early detection. Citation Format: Weitzel JN, Blazer KR, Nehoray B, Kidd J, Slavin Jr TP, Solomon I, Niell-Swiller M, Rybak C, Saam J, Lancaster J. Multiplex Identification of genetic etiologies among women with bilateral breast cancer using a 25-gene hereditary cancer panel. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr PD7-02.


Cancer Epidemiology, Biomarkers & Prevention | 2015

Abstract A36: Exploring the climate, barriers, and possible approaches to implementing genetic cancer risk assessment in Latin America: A roundtable discussion

Tanya Chavez; Bita Nehoray; Alexandra Obregon-Tito; Charite Ricker; Ilana Solomon; Mariana Niell-Swiller; Christina Ryback; J. Abugattas; Yasser Sullcahuaman; María F. Noriega; Ana I. Orduz; Jorge M. Melo; Ana Chaves; Lenny Gallardo; Cynthia Villarreal; Robin Shaw; Rosa M. Álvarez; Eunice F. Morales; Alicia Cock-Rada; Azucena Del Toro; Pamela Mora; Marcia Cruz; Maria E. Fernandez; Kathleen R. Blazer; Jeffrey N. Weitzel

Genetic cancer risk assessment (GCRA) is an interdisciplinary medical subspecialty practice that employs a growing arsenal of genetic and genomic tools to identify individuals and families with increased risk for cancer, often prior to the onset of disease, when early detection or prevention strategies are most effective. Access to GCRA is a standard of care in most developed countries, but is not available in most of Latin America. In March of 2014, City of Hope in Duarte, CA, conducted a roundtable discussion forum with 16 Latin American physicians representing Brazil, Colombia, Mexico, Peru, and Puerto Rico. The purpose of the roundtable was to explore the current state of GCRA services, including policy, resources, and barriers, in the respective Latin American countries. Thirteen participants attended in-person and 3 via web conference. The session was moderated by a team comprised of 4 bilingual cancer genetics clinicians. Participants were prompted with open-ended discussion questions eliciting perceived needs and the current status of GCRA services in their country, barriers to GCRA practice, and possible approaches to address access barriers. The session was largely conducted in Spanish, recorded, and transcribed. The transcript was coded and thematically analyzed. Preliminary analysis identified barriers to GCRA implementation, including: (1) limited patient and provider knowledge about GCRA, (2) lack of insurance coverage and high patient out-of-pocket costs for GCRA testing, (3) long turnaround time for genetic test results, (4) absence of readily available provider training or expertise, and (5) lack of institutional infrastructure or policy to support the development of GCRA programs. Participants emphasized the importance of collecting evidence to support the efficacy of GCRA in their own populations as an essential step toward building GCRA services in their countries. The findings also point to the need for a multi-level approach that addresses the need for education and training and cost-effective genetic testing, as well as the creation of an evidence-based foundation for the development of policy, infrastructure and resources to implement and sustain GCRA services in Latin America. Citation Format: Tanya Chavez, Bita Nehoray, Alexandra Obregon-Tito, Charite Ricker, Ilana Solomon, Mariana Niell-Swiller, Christina Ryback, Julio E. Abugattas, Yasser Sullcahuaman, Maria F. Noriega, Ana I. Orduz, Jorge M. Melo, Ana Chaves, Lenny Gallardo, Cynthia Villarreal, Robin Shaw, Rosa M. Alvarez, Eunice F. Morales, Alicia M. Cock-Rada, Azucena Del Toro, Pamela Mora, Marcia Cruz, Maria E. Fernandez, Kathleen R. Blazer, Jeffrey N. Weitzel. Exploring the climate, barriers, and possible approaches to implementing genetic cancer risk assessment in Latin America: A roundtable discussion. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr A36.

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Bita Nehoray

City of Hope National Medical Center

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Ilana Solomon

City of Hope National Medical Center

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Jeffrey N. Weitzel

City of Hope National Medical Center

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Kathleen R. Blazer

City of Hope National Medical Center

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Christina Rybak

City of Hope National Medical Center

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Thomas P. Slavin

City of Hope National Medical Center

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Danielle Castillo

City of Hope National Medical Center

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Kai Yang

City of Hope National Medical Center

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Sharon Sand

City of Hope National Medical Center

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Josef Herzog

City of Hope National Medical Center

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