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Article ; Online: miRNA analysis in pancreatic cancer: the Dartmouth experience.

Abreu, Francine B de / Liu, Xiaoying / Tsongalis, Gregory J

Clinical chemistry and laboratory medicine

2017 Volume 55, Issue 5, Page(s) 755–762

Abstract: Pancreatic cancer is considered one of the most lethal cancers being the fourth leading cause of cancer deaths in adults in the United States because of the lack of early signs and symptoms and the lack of early detection. Pancreatic ductal ... ...

Abstract	Pancreatic cancer is considered one of the most lethal cancers being the fourth leading cause of cancer deaths in adults in the United States because of the lack of early signs and symptoms and the lack of early detection. Pancreatic ductal adenocarcinoma (PDAC) is the most common histological type among pancreatic cancers, representing 80%-90% of all solid tumors of the pancreas. The majority of PDAC develops from three precursor lesions: pancreatic intraepithelial neoplasia, intraductual papillary mucinous neoplasm and mucinous cystic neoplasm. Although histologic tissue evaluation remains the gold standard for diagnosis, endoscopic ultrasound-guided fine needle aspiration has become the preferred modality for obtaining pathologic confirmation. At Dartmouth-Hitchcock Medical Center (DHMC),we have developed and validated a microRNA (miRNA) panel for patients with pancreatic diseases that can be used in association with the gold standard method for diagnosis. miRNAs have an important role in biological processes, such as apoptosis, metabolism, cell growth and differentiation. In cancer, miRNAs can be classified as either oncogenic or tumor suppressor according to their function in the carcinogenic process. In this study, we describe the expression of many miRNA in benign and malignant pancreatic tissues as well as their clinical significance. For this reason, miRNAs have been considered potential biomarkers of pancreatic diseases that could potentially contribute to an early diagnosis, predict disease progression, accurately monitor disease, contribute to better treatment strategies and reduce mortality by improving disease management.
MeSH term(s)	Humans ; MicroRNAs/analysis ; Molecular Targeted Therapy ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Prognosis
Chemical Substances	MicroRNAs
Language	English
Publishing date	2017-05-01
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1418007-8
ISSN	1437-4331 ; 1434-6621 ; 1437-8523
ISSN (online)	1437-4331
ISSN	1434-6621 ; 1437-8523
DOI	10.1515/cclm-2017-0046
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Article ; Online: Impact of Molecular Sequencing Information as Related to 2008 and 2016 World Health Organization Classification of Acute Myeloid Leukemia and Myelodysplasia.

Toth, Laura N / de Abreu, Francine B / Peterson, Jason D / Loo, Eric Y

Archives of pathology & laboratory medicine

2018 Volume 142, Issue 9, Page(s) 1017

MeSH term(s)	Humans ; Leukemia, Myeloid, Acute/classification ; Leukemia, Myeloid, Acute/genetics ; Myelodysplastic Syndromes/classification ; Myelodysplastic Syndromes/genetics ; World Health Organization
Language	English
Publishing date	2018-08-30
Publishing country	United States
Document type	Letter
ZDB-ID	194119-7
ISSN	1543-2165 ; 0363-0153 ; 0096-8528 ; 0003-9985
ISSN (online)	1543-2165
ISSN	0363-0153 ; 0096-8528 ; 0003-9985
DOI	10.5858/arpa.2017-0577-LE
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Article ; Online: Non-small cell lung cancers with isocitrate dehydrogenase 1 or 2 (IDH1/2) mutations.

Toth, Laura N / de Abreu, Francine B / Tafe, Laura J

Human pathology

2018 Volume 78, Page(s) 138–143

Abstract: Isocitrate dehydrogenases 1 and 2 (IDH1/2) are important metabolic enzymes that convert isocitrate to α-ketoglutarate. IDH1/2 mutations are associated with the development of multiple malignancies. In this study, we examine the prevalence and features of ...

Abstract	Isocitrate dehydrogenases 1 and 2 (IDH1/2) are important metabolic enzymes that convert isocitrate to α-ketoglutarate. IDH1/2 mutations are associated with the development of multiple malignancies. In this study, we examine the prevalence and features of non-small cell lung cancers (NSCLC) with IDH1/2 mutations. From May 2013 to March 2017, 800 lung cancer samples were successfully sequenced for somatic mutations on the Ion Torrent PGM with the 50-gene AmpliSeq Cancer Hotspot Panel v2 on the Ion Torrent PGM (318 chip). Variants were identified using the Ion Torrent Variant Caller Plugin and reference genome hg19. Golden Helix's SVS software was used for variant annotation and prediction of significance. Nine samples (1.1%) from 8 patients harbored an IDH1 (3 p.R132C and 2 p.R132L) or IDH2 mutation (p.R140W, p.R172S, and p.R172T). All patients' tumors had adenocarcinoma histology, and all patients had a smoking history. Eighty-eight percent of patients' tumors had a coexisting KRAS mutation and 6 of 8 were diagnosed at greater than 70 years of age. Five patients presented with stage IV disease and 3 with stage I. After comparison to a cohort of KRAS-mutated NSCLC with a history of smoking, IDH-mutated cases were significantly older but presented with similar rates of advanced-stage disease and sex distribution. Additional studies are needed to understand the role of IDH1/2 mutations in the development of NSCLC, but such patients who have poor prognostic indicators (KRAS mutation and advanced stage at presentation) may benefit from IDH1/2-directed therapies.
MeSH term(s)	Aged ; Aged, 80 and over ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Carcinoma, Non-Small-Cell Lung/diagnosis ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Female ; Humans ; Isocitrate Dehydrogenase/genetics ; Male ; Middle Aged ; Mutation/genetics ; Oncogenes/genetics ; Prognosis
Chemical Substances	IDH2 protein, human (EC 1.1.1.41) ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; IDH1 protein, human (EC 1.1.1.42.)
Language	English
Publishing date	2018-05-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	207657-3
ISSN	1532-8392 ; 0046-8177
ISSN (online)	1532-8392
ISSN	0046-8177
DOI	10.1016/j.humpath.2018.04.014
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Zs.A 722: Show issues

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Article ; Online: Central xanthoma of the jaw in association with Noonan syndrome.

Olson, Nicholas J / Addante, Rocco R / de Abreu, Francine B / Memoli, Vincent A

Human pathology

2018 Volume 82, Page(s) 202–205

Abstract: Xanthomas are histiocytic lesions of the skin, soft tissue, and bone and are generally considered to be reactive in nature. When they arise in the bones of the jaw, they are referred to as central xanthomas. New evidence supports the hypothesis that ... ...

Abstract	Xanthomas are histiocytic lesions of the skin, soft tissue, and bone and are generally considered to be reactive in nature. When they arise in the bones of the jaw, they are referred to as central xanthomas. New evidence supports the hypothesis that central xanthomas are a separate and distinct entity from their extragnathic counterparts. Noonan syndrome (NS) is an autosomal dominant disorder that has been associated with giant cell lesions, which also commonly occur in the jaw. We present a case of a 15-year-old boy with NS who presented with a radiolucent lesion of the mandible that on excision was found to be a central xanthoma. Although giant cell lesions have been well described in NS, xanthomas of the jaw have not been reported. We will also discuss the entities that must be excluded before making a diagnosis of central xanthoma, as this can affect both treatment and follow-up.
MeSH term(s)	Adolescent ; Biopsy ; Diagnosis, Differential ; Humans ; Immunohistochemistry ; Male ; Mandibular Diseases/diagnosis ; Mandibular Diseases/etiology ; Mandibular Diseases/surgery ; Noonan Syndrome/complications ; Noonan Syndrome/diagnosis ; Predictive Value of Tests ; Tomography, X-Ray Computed ; Xanthomatosis/diagnosis ; Xanthomatosis/etiology ; Xanthomatosis/surgery
Language	English
Publishing date	2018-05-01
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	207657-3
ISSN	1532-8392 ; 0046-8177
ISSN (online)	1532-8392
ISSN	0046-8177
DOI	10.1016/j.humpath.2018.04.020
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Article ; Online: Synchronous Pulmonary Adenofibroma and Solitary Fibrous Tumor: Case Report and Review of the Literature.

Olson, Nicholas J / Czum, Julianna M / de Abreu, Francine B / Linos, Konstantinos / Black, Candice C

International journal of surgical pathology

2018 Volume 27, Issue 3, Page(s) 322–327

Abstract: Pulmonary adenofibroma (PAF) is a rare neoplasm that may be related to solitary fibrous tumor (SFT). A subset of PAFs harbor the NAB2-STAT6 fusion that is typical of SFT, but a significant proportion do not. Their distinction is clinically important as ... ...

Abstract	Pulmonary adenofibroma (PAF) is a rare neoplasm that may be related to solitary fibrous tumor (SFT). A subset of PAFs harbor the NAB2-STAT6 fusion that is typical of SFT, but a significant proportion do not. Their distinction is clinically important as SFTs can potentially have an aggressive clinical course, while there has been no report of a PAF behaving in a malignant fashion. We report a case of a 60-year-old male who developed a SFT and PAF in the same lung. The SFT harbored a NAB2-STAT6 fusion, while the PAF did not have any identifiable fusion. This case represents the first instance of a single patient with both of these tumors occurring simultaneously in the same lung.
MeSH term(s)	Adenofibroma/diagnostic imaging ; Adenofibroma/genetics ; Adenofibroma/pathology ; Adenofibroma/surgery ; Biomarkers, Tumor/genetics ; Humans ; Lung/diagnostic imaging ; Lung/pathology ; Lung/surgery ; Lung Neoplasms/diagnostic imaging ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Lung Neoplasms/surgery ; Male ; Middle Aged ; Neoplasms, Multiple Primary/diagnostic imaging ; Neoplasms, Multiple Primary/genetics ; Neoplasms, Multiple Primary/pathology ; Neoplasms, Multiple Primary/surgery ; Oncogene Proteins, Fusion/genetics ; Pneumonectomy ; Repressor Proteins/genetics ; STAT6 Transcription Factor/genetics ; Solitary Fibrous Tumors/diagnostic imaging ; Solitary Fibrous Tumors/genetics ; Solitary Fibrous Tumors/pathology ; Solitary Fibrous Tumors/surgery ; Tomography, X-Ray Computed
Chemical Substances	Biomarkers, Tumor ; NAB2 protein, human ; Oncogene Proteins, Fusion ; Repressor Proteins ; STAT6 Transcription Factor ; STAT6 protein, human
Language	English
Publishing date	2018-10-26
Publishing country	United States
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	1336393-1
ISSN	1940-2465 ; 1066-8969
ISSN (online)	1940-2465
ISSN	1066-8969
DOI	10.1177/1066896918807302
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Zs.A 4500: Show issues

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Article ; Online: Variant allele frequencies do not correlate well with myeloblast counts in a clinically validated gene sequencing panel for routine acute myeloid leukemia workup.

Toth, Laura N / Green, Donald / Peterson, Jason / Deharvengt, Sophie J / de Abreu, Francine B / Loo, Eric Y

Leukemia & lymphoma

2019 Volume 60, Issue 10, Page(s) 2415–2422

Abstract: Next generation sequencing (NGS) has introduced new types of data, such as variant allele frequencies (VAFs), into the workup of acute myeloid leukemias (AML). There is interest in using NGS to prognosticate disease behavior and monitor residual disease, ...

Abstract	Next generation sequencing (NGS) has introduced new types of data, such as variant allele frequencies (VAFs), into the workup of acute myeloid leukemias (AML). There is interest in using NGS to prognosticate disease behavior and monitor residual disease, but the attribution of sequencing data entirely to the leukemic clone may be confounded by VAF contribution from background non-leukemic populations and undetected copy number aberrations. Sixty-eight patients with AML were evaluated by a clinically validated gene sequencing panel at our institution from 2015 to 2018. No correlation was found with a direct comparison of blast counts and VAFs in both primary- and secondary-AML (
MeSH term(s)	Alleles ; Biomarkers, Tumor ; Bone Marrow/pathology ; Gene Frequency ; Genetic Variation ; Granulocyte Precursor Cells/pathology ; High-Throughput Nucleotide Sequencing ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Neoplasms, Second Primary/diagnosis ; Neoplasms, Second Primary/etiology
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2019-04-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2019.1587757
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Zs.A 2997: Show issues

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Article ; Online: Frequency of Somatic TP53 Mutations in Combination with Known Pathogenic Mutations in Colon Adenocarcinoma, Non-Small Cell Lung Carcinoma, and Gliomas as Identified by Next-Generation Sequencing.

Shajani-Yi, Zahra / de Abreu, Francine B / Peterson, Jason D / Tsongalis, Gregory J

Neoplasia (New York, N.Y.)

2018 Volume 20, Issue 3, Page(s) 256–262

Abstract: The tumor suppressor gene TP53 is the most frequently mutated gene in human cancer. It encodes p53, a DNA-binding transcription factor that regulates multiple genes involved in DNA repair, metabolism, cell cycle arrest, apoptosis, and senescence. TP53 is ...

Abstract	The tumor suppressor gene TP53 is the most frequently mutated gene in human cancer. It encodes p53, a DNA-binding transcription factor that regulates multiple genes involved in DNA repair, metabolism, cell cycle arrest, apoptosis, and senescence. TP53 is associated with human cancer by mutations that lead to a loss of wild-type p53 function as well as mutations that confer alternate oncogenic functions that enable them to promote invasion, metastasis, proliferation, and cell survival. Identifying the discrete TP53 mutations in tumor cells may help direct therapies that are more effective. In this study, we identified the frequency of individual TP53 mutations in patients with colon adenocarcinoma (48%), non-small cell lung carcinoma (NSCLC) (36%), and glioma/glioblastoma (28%) at our institution using next-generation sequencing. We also identified the occurrence of somatic mutations in numerous actionable genes including BRAF, EGFR, KRAS, IDH1, and PIK3CA that occurred concurrently with these TP53 mutations. Of the 480 tumors examined that contained one or more mutations in the TP53 gene, 219 were colon adenocarcinomas, 215 were NSCLCs, and 46 were gliomas/glioblastomas. Among the patients positive for TP53 mutations diagnosed with colon adenocarcinoma, 50% also showed at least one mutation in pathogenic genes of which 14% were BRAF, 33% were KRAS, and 3% were NRAS. Forty-seven percent of NSCLC patients harboring TP53 mutations also had a mutation in at least one actionable pathogenic variant with the following frequencies: BRAF: 4%, EGFR: 10%, KRAS: 28%, and PIK3CA: 4%. Fifty-two percent of patients diagnosed with glioma/glioblastoma with a positive TP53 mutation had at least one concurrent mutation in a known pathogenic gene of which 9% were CDKN2A, 41% were IDH1, and 11% were PIK3CA.
MeSH term(s)	Adenocarcinoma/genetics ; Carcinoma, Non-Small-Cell Lung/genetics ; Colonic Neoplasms/genetics ; Glioma/genetics ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Lung Neoplasms/genetics ; Mutation/genetics ; Tumor Suppressor Protein p53/genetics
Chemical Substances	TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2018-02-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2017.12.005
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Zs.A 5203: Show issues

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Article ; Online: Undifferentiated Sarcoma as Intermediate Step in the Progression of Malignant Melanoma to Rhabdomyosarcoma: Histologic, Immunohistochemical, and Molecular Studies of a New Case of Malignant Melanoma With Rhabdomyosarcomatous Differentiation.

Tran, Tien Anh N / Linos, Konstantinos / de Abreu, Francine B / Carlson, John Andrew

The American Journal of dermatopathology

2018 Volume 41, Issue 3, Page(s) 221–229

Abstract: Malignant melanoma (MM) may display highly variable phenotypic diversity, sometimes associated with loss of immunohistochemical melanocytic markers and acquisition of nonmelanocytic lineage of differentiation. Primary cutaneous MM with ... ...

Abstract	Malignant melanoma (MM) may display highly variable phenotypic diversity, sometimes associated with loss of immunohistochemical melanocytic markers and acquisition of nonmelanocytic lineage of differentiation. Primary cutaneous MM with rhabdomyosarcomatous differentiation is extremely rare with only 5 reported cases in the literature. To date, a chronological progression of a MM to rhabdomyosarcoma has not been conclusively documented. A 96-year-old man underwent a re-excision of an "atypical fibroxanthoma" of the forearm, which revealed a small lentigo maligna melanoma associated with a dominant dermal high-grade spindle cell nodule admixed with a population of malignant polygonal epithelioid cells. On immunohistochemical studies, the spindle cells were completely negative for all melanocytic markers, whereas a small population of polygonal neoplastic cells at the periphery was positive for Desmin and Myo-D1, supporting early rhabdomyosarcomatous transformation. Several subsequent re-excisions demonstrated merely nodules of malignant pleomorphic epithelioid cells with rhabdomyosarcomatous differentiation and devoid of melanocytic markers. In addition, both rhabdomyosarcomatous component and original MM displayed identical mutations. Therefore, the histologic, immunohistochemical, and molecular findings documented for the first time a chronological progression from an invasive MM to a pleomorphic rhabdomyosarcoma through an intermediate stage of undifferentiated sarcoma/atypical fibroxanthoma. Interestingly, subsequent recurrences of pure rhabdomyosarcomatous component displayed skip lesions/microsatellitosis, marked tumor-infiltrative lymphocytes, and rare junctional nests of rhabdomyosarcomatous cells in the epidermis, histologic features that were not described in primary cutaneous rhabdomyosarcoma and therefore could serve as morphologic clues to the diagnosis of rhabdomyosarcomatous transformation in an MM.
MeSH term(s)	Aged, 80 and over ; Biomarkers, Tumor/analysis ; Biomarkers, Tumor/genetics ; Biopsy ; Cell Differentiation ; DNA Mutational Analysis ; Disease Progression ; Genetic Predisposition to Disease ; Humans ; Immunohistochemistry ; Male ; Melanoma/chemistry ; Melanoma/genetics ; Melanoma/pathology ; Melanoma/surgery ; Mutation ; Phenotype ; Rhabdomyosarcoma/chemistry ; Rhabdomyosarcoma/genetics ; Rhabdomyosarcoma/pathology ; Rhabdomyosarcoma/surgery ; Sarcoma/chemistry ; Sarcoma/genetics ; Sarcoma/pathology ; Sarcoma/surgery ; Skin Neoplasms/chemistry ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Skin Neoplasms/surgery
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2018-09-30
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	448469-1
ISSN	1533-0311 ; 0193-1091
ISSN (online)	1533-0311
ISSN	0193-1091
DOI	10.1097/DAD.0000000000001236
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Article: Molecular matching and treatment strategies for advanced stage lung cancer at Dartmouth-Hitchcock Medical Center: A three-year review of a Molecular Tumor Board.

Bernhardt, Erica B / Chamberlin, Mary D / Gorlov, Ivan P / de Abreu, Francine B / Bloch, Katarzyna J / Peterson, Jason D / Tsongalis, Gregory J / Shirai, Keisuke / Dragnev, Konstantin H / Miller, Todd W / Tafe, Laura J

Practical laboratory medicine

2020 Volume 21, Page(s) e00174

Abstract: Matching of actionable tumor mutations with targeted therapy increases response rates and prolongs survival in lung cancer patients. Drug development and trials targeting genetic alterations are expanding rapidly. We describe the role of a Molecular ... ...

Abstract	Matching of actionable tumor mutations with targeted therapy increases response rates and prolongs survival in lung cancer patients. Drug development and trials targeting genetic alterations are expanding rapidly. We describe the role of a Molecular Tumor Board (MTB) in the design of molecularly informed treatment strategies in our lung cancer patient population. Tumor DNA was sequenced using a 50-gene targeted next-generation sequencing panel. Cases were evaluated by a multidisciplinary MTB who suggested a course of treatment based on each patient's molecular findings. During a three-year period, 21 lung cancer patients were presented at the MTB. All patients lacked common activating
Language	English
Publishing date	2020-06-12
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2834973-8
ISSN	2352-5517
ISSN	2352-5517
DOI	10.1016/j.plabm.2020.e00174
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Article ; Online: Triple-Negative Breast Cancer: Next-Generation Sequencing for Target Identification.

Marotti, Jonathan D / de Abreu, Francine B / Wells, Wendy A / Tsongalis, Gregory J

The American journal of pathology

2017 Volume 187, Issue 10, Page(s) 2133–2138

Abstract: Presently, the ability to study disease at the most fundamental molecular level has led to a reclassification of human cancers into numerous subtypes that vary in disease progression and response to therapy. Similar to most solid tumors, breast cancer is ...

Abstract	Presently, the ability to study disease at the most fundamental molecular level has led to a reclassification of human cancers into numerous subtypes that vary in disease progression and response to therapy. Similar to most solid tumors, breast cancer is a heterogeneous disease with considerable variation in histologic and biological features. Triple-negative breast cancer (TNBC) is a subtype of breast cancer in which the estrogen receptor and progesterone receptor are not expressed, and human epidermal growth factor-receptor 2 is not amplified or overexpressed. Data derived from highly complex molecular technologies, such as microarrays and next-generation sequencing, have identified gene expression and somatic mutation profile subsets of TNBC that reflect biological behavior more accurately and may lead to further effective therapeutic targets, better prognosis, and improved outcomes. Herein, we review the genomic findings of TNBC and discuss current efforts in precision medicine as they relate to TNBC.
MeSH term(s)	Clinical Trials as Topic ; DNA Mutational Analysis ; Female ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Triple Negative Breast Neoplasms/classification ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology ; Triple Negative Breast Neoplasms/therapy
Language	English
Publishing date	2017-07-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2017.05.018
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