Search Results
Graduate Program in Microbiology, Immunology, and Cancer Biology, University of Minnesota, Minneapolis, Minnesota, USA
Search for other papers by Mark Daniel in
Google Scholar
PubMed
Search for other papers by Todd P Knutson in
Google Scholar
PubMed
Carbone Cancer Center, University of Wisconsin-Madison, Madison, Wisconsin, USA
Search for other papers by Jamie M Sperger in
Google Scholar
PubMed
Search for other papers by Yingming Li in
Google Scholar
PubMed
Search for other papers by Anupama Singh in
Google Scholar
PubMed
Carbone Cancer Center, University of Wisconsin-Madison, Madison, Wisconsin, USA
Search for other papers by Charlotte N Stahlfeld in
Google Scholar
PubMed
Search for other papers by Courtney Passow in
Google Scholar
PubMed
Search for other papers by Benjamin Auch in
Google Scholar
PubMed
Carbone Cancer Center, University of Wisconsin-Madison, Madison, Wisconsin, USA
Search for other papers by Joshua M Lang in
Google Scholar
PubMed
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota, USA
Department of Urology, University of Minnesota, Minneapolis, Minnesota, USA
Search for other papers by Scott M Dehm in
Google Scholar
PubMed
are challenging and a high burden for patients. As a result, assessing CRPC genomic alterations via blood-based 'liquid biopsy' is an attractive alternative. One common liquid biopsy approach involves the examination of circulating tumor cells (CTCs
Search for other papers by Adly Yacoub in
Google Scholar
PubMed
Search for other papers by Anna Miller in
Google Scholar
PubMed
Search for other papers by Ruben W Caron in
Google Scholar
PubMed
Search for other papers by Liang Qiao in
Google Scholar
PubMed
Search for other papers by David A Curiel in
Google Scholar
PubMed
Search for other papers by Paul B Fisher in
Google Scholar
PubMed
Search for other papers by Michael P Hagan in
Google Scholar
PubMed
Search for other papers by Steven Grant in
Google Scholar
PubMed
Search for other papers by Paul Dent in
Google Scholar
PubMed
. Expression of activated forms of RAS family members and alterations in p53 mutational status were noted to regulate radiosensitivity in isogenic cells, in part, by modulating the expression of ERBB receptors and ERBB receptor paracrine ligands. These
Search for other papers by L Fugazzola in
Google Scholar
PubMed
Search for other papers by E Puxeddu in
Google Scholar
PubMed
Search for other papers by N Avenia in
Google Scholar
PubMed
Search for other papers by C Romei in
Google Scholar
PubMed
Search for other papers by V Cirello in
Google Scholar
PubMed
Search for other papers by A Cavaliere in
Google Scholar
PubMed
Search for other papers by P Faviana in
Google Scholar
PubMed
Search for other papers by D Mannavola in
Google Scholar
PubMed
Search for other papers by S Moretti in
Google Scholar
PubMed
Search for other papers by S Rossi in
Google Scholar
PubMed
Search for other papers by M Sculli in
Google Scholar
PubMed
Search for other papers by V Bottici in
Google Scholar
PubMed
Search for other papers by P Beck-Peccoz in
Google Scholar
PubMed
Search for other papers by F Pacini in
Google Scholar
PubMed
Search for other papers by A Pinchera in
Google Scholar
PubMed
Search for other papers by F Santeusanio in
Google Scholar
PubMed
Search for other papers by R Elisei in
Google Scholar
PubMed
terminators and run on an ABI PRISM 310 genetic analyzer (PE Applied Biosystems, Foster City, CA, USA). The cycle-sequencing conditions consisted of 25 cycles of 96°C for 30 s, 50°C for 15 s and 60°C for 4 min. One sequence read from each direction across the
Search for other papers by Sarah E McClelland in
Google Scholar
PubMed
chromosome segregation errors ( Fig. 1A ) increase genetic heterogeneity between tumour cells at each cell cycle, allowing rapid evolution of tumour genomes and presenting a challenge to cancer patient treatment (see below). Chromosome segregation errors can
Cancer Epigenetics Group, School of Allied Health Sciences (ESTSP), Department of Pathology, Department of Epidemiology, Department of Urology, Department of Pathology and Molecular Immunology, Portuguese Oncology Institute, Research Center, Rua Dr António Bernardino Almeida, 4200-072 Porto, Portugal
Search for other papers by Filipa Quintela Vieira in
Google Scholar
PubMed
Search for other papers by Pedro Costa-Pinheiro in
Google Scholar
PubMed
Search for other papers by João Ramalho-Carvalho in
Google Scholar
PubMed
Search for other papers by Andreia Pereira in
Google Scholar
PubMed
Search for other papers by Francisco Duarte Menezes in
Google Scholar
PubMed
Search for other papers by Luís Antunes in
Google Scholar
PubMed
Cancer Epigenetics Group, School of Allied Health Sciences (ESTSP), Department of Pathology, Department of Epidemiology, Department of Urology, Department of Pathology and Molecular Immunology, Portuguese Oncology Institute, Research Center, Rua Dr António Bernardino Almeida, 4200-072 Porto, Portugal
Search for other papers by Isa Carneiro in
Google Scholar
PubMed
Search for other papers by Jorge Oliveira in
Google Scholar
PubMed
Cancer Epigenetics Group, School of Allied Health Sciences (ESTSP), Department of Pathology, Department of Epidemiology, Department of Urology, Department of Pathology and Molecular Immunology, Portuguese Oncology Institute, Research Center, Rua Dr António Bernardino Almeida, 4200-072 Porto, Portugal
Cancer Epigenetics Group, School of Allied Health Sciences (ESTSP), Department of Pathology, Department of Epidemiology, Department of Urology, Department of Pathology and Molecular Immunology, Portuguese Oncology Institute, Research Center, Rua Dr António Bernardino Almeida, 4200-072 Porto, Portugal
Search for other papers by Rui Henrique in
Google Scholar
PubMed
Cancer Epigenetics Group, School of Allied Health Sciences (ESTSP), Department of Pathology, Department of Epidemiology, Department of Urology, Department of Pathology and Molecular Immunology, Portuguese Oncology Institute, Research Center, Rua Dr António Bernardino Almeida, 4200-072 Porto, Portugal
Search for other papers by Carmen Jerónimo in
Google Scholar
PubMed
methylation, alterations in chromatin modification patterns, due to histones post-translational modifications (PTMs), were implicated in carcinogenesis and have emerged as potential key regulators of cancer-related pathways ( Miremadi et al . 2007
Search for other papers by D Führer in
Google Scholar
PubMed
Search for other papers by A Tannapfel in
Google Scholar
PubMed
Search for other papers by O Sabri in
Google Scholar
PubMed
Search for other papers by P Lamesch in
Google Scholar
PubMed
Search for other papers by R Paschke in
Google Scholar
PubMed
In a 59-year-old patient, thyroid follicular cancer was diagnosed in two right-sided toxic thyroid nodules, which had presented clinically as unilateral thyroid autonomy. In addition, the patient had histologically proven lung metastases of thyroid cancer; however, these failed to exhibit iodine uptake and were resistant to radioiodine treatment. The functional activity of the thyroid nodules prompted us to screen for TSH receptor (TSHR) mutations, and the histological diagnosis of follicular carcinoma led us to search for the PAX8-PPARgamma1 rearrangement and mutations in the ras genes. Each thyroid nodule harboured a different TSHR mutation (large nodule, Asp633Tyr; small nodule, Phe631Ile). Presence of both mutations in one sample suggestive of local invasion of a thyroid carcinoma could not be demonstrated, although several specimens from different nodule locations were screened. Only the wild-type TSHR sequence was identified in the histologically normal left thyroid lobe, and no genetic alterations were found in the other investigated genes. No TSHR mutations were detected in the pulmonary metastases. This is the first case report of a patient with toxic follicular thyroid carcinoma harbouring two different TSHR mutations and presenting with non-functional lung metastases.
Search for other papers by Kensey Bergdorf in
Google Scholar
PubMed
Search for other papers by Donna C Ferguson in
Google Scholar
PubMed
Search for other papers by Mitra Mehrad in
Google Scholar
PubMed
Search for other papers by Kim Ely in
Google Scholar
PubMed
Search for other papers by Thomas Stricker in
Google Scholar
PubMed
Search for other papers by Vivian L Weiss in
Google Scholar
PubMed
The prevalence of thyroid carcinoma is increasing and represents the most common endocrine malignancy, with papillary thyroid carcinoma (PTC) being the most frequent subtype. The genetic alterations identified in PTCs fail to distinguish tumors with different clinical behaviors, such as extra-thyroidal extension and lymph node metastasis. We hypothesize that the immune microenvironment may play a critical role in tumor invasion and metastasis. Computational immunogenomic analysis was performed on 568 PTC samples in The Cancer Genome Atlas using CIBERSORT, TIMER and TIDE deconvolution analytic tools for characterizing immune cell composition. Immune cell infiltrates were correlated with histologic type, mutational type, tumor pathologic T stage and lymph node N stage. Dendritic cells (DCs) are highly associated with more locally advanced tumor T stage (T3/T4, odds ratio (OR) = 2.6, CI = 1.4–4.5, P = 5.4 × 10−4). Increased dendritic cells (OR = 3.4, CI = 1.9–6.3, P = 5.5 × 10−5) and neutrophils (OR = 10.5, CI = 2.7–44, P = 8.7 × 10−4) significantly correlate with lymph node metastasis. In addition, dendritic cells positively correlate with tall cell morphology (OR = 4.5, CI = 1.6–13, P = 4.9 × 10−3) and neutrophils negatively correlate with follicular morphology (OR = 1.3 × 10−3, CI = 5.3 × 10−5–0.031, P = 4.1 × 10−5). TIDE analysis indicates an immune-exclusive phenotype that may be mediated by increased galectin-3 found in PTCs. Thus, characterization of the PTC immune microenvironment using three computational platforms shows that specific immune cells correlate with mutational type, histologic type, local tumor extent and lymph node metastasis. Immunologic evaluation of PTCs may provide a better indication of biologic behavior, resulting in the improved diagnosis and treatment of thyroid cancer.
Search for other papers by G P Risbridger in
Google Scholar
PubMed
Search for other papers by J J Bianco in
Google Scholar
PubMed
Search for other papers by S J Ellem in
Google Scholar
PubMed
Search for other papers by S J McPherson in
Google Scholar
PubMed
Androgens are essential for stimulating normal development, growth and secretory activities of the prostate whereas oestrogens are generally regarded as inhibitors of growth. Evidence for the local synthesis of oestrogens includes the detection of aromatase mRNA and protein in the stroma of human non-malignant tissues and in malignant tissue, where it is detected in epithelial tumour cells. As well, aromatase activity was measured by biochemical assay and protein was detected in prostatic non-malignant and tumour cell lines. Taken together with the identification of direct oestrogenic actions on the prostate, these results suggest that alterations in local oestrogen synthesis may have significant consequences in malignancy of these organs. Genetically modified mouse models were studied in order to evaluate the action of oestrogens alone or in combination with androgens on the prostate gland. Hypogonadal (hpg) mice are deficient in gonadotrophins and androgens but showed direct proliferative responses to oestradiol. The responses were characterised by discrete lobe-specific changes including smooth-muscle regression, fibroblast proliferation, inflammation, and basal epithelial cell proliferation and metaplasia. The aromatase knockout (ArKO) mouse, deficient in oestrogens due to a non-functional aromatase enzyme, developed prostatic hyperplasia during the lifelong exposure to elevated androgens, however, no malignant changes were detected in the prostate at any time. In contrast, combined androgen and oestrogen treatment has been shown to induce prostatic dysplasia and adenocarcinoma. These results demonstrate that malignant changes to the prostate gland are dependent upon both androgenic and oestrogenic responses and that neither hormone alone is sufficient to evoke aberrant patterns of growth, resulting in malignancy.
Search for other papers by Greta Gandolfi in
Google Scholar
PubMed
Laboratory of Translational Research, Arcispedale S. Maria Nuova – IRCCS, Department of Pharmacology and Biotechnology (FaBiT), University of Bologna, 40139, Pathology Unit, Department of Oncology, Arcispedale S. Maria Nuova – IRCCS, Department of Medicine (DIMES) – Anatomic Pathology Unit, Bellaria Hospital, University of Bologna, Viale Risorgimento 80, Reggio Emilia, 42123, Italy
Search for other papers by Dario de Biase in
Google Scholar
PubMed
Search for other papers by Valentina Sancisi in
Google Scholar
PubMed
Search for other papers by Moira Ragazzi in
Google Scholar
PubMed
Search for other papers by Giorgia Acquaviva in
Google Scholar
PubMed
Search for other papers by Annalisa Pession in
Google Scholar
PubMed
Search for other papers by Simonetta Piana in
Google Scholar
PubMed
Search for other papers by Giovanni Tallini in
Google Scholar
PubMed
Search for other papers by Alessia Ciarrocchi in
Google Scholar
PubMed
metastases and death among the overall PTC cases, and hence the difficulty in collecting large cohorts of PTCs that developed distant metastases (DM-PTCs), has been an important limitation for studies that attempted to correlate genetic alterations with
Division of Biomedical Informatics & Personalized Medicine, Department of Medicine, University of Colorado School of Medicine at Colorado Anschutz Medical Campus Aurora, Aurora, Colorado, USA
Search for other papers by Nikita Pozdeyev in
Google Scholar
PubMed
Division of Biomedical Informatics & Personalized Medicine, Department of Medicine, University of Colorado School of Medicine at Colorado Anschutz Medical Campus Aurora, Aurora, Colorado, USA
Search for other papers by Lauren Fishbein in
Google Scholar
PubMed
Search for other papers by Laurie M Gay in
Google Scholar
PubMed
Search for other papers by Ethan S Sokol in
Google Scholar
PubMed
Search for other papers by Ryan Hartmaier in
Google Scholar
PubMed
Departments of Pathology and Urology, Upstate Medical University, Syracuse, New York, USA
Search for other papers by Jeffrey S Ross in
Google Scholar
PubMed
Search for other papers by Sourat Darabi in
Google Scholar
PubMed
Translational Genomics Research Institute, Phoenix, Arizona, USA
Search for other papers by Michael J Demeure in
Google Scholar
PubMed
Search for other papers by Adwitiya Kar in
Google Scholar
PubMed
Search for other papers by Lindsey J Foust in
Google Scholar
PubMed
Search for other papers by Katrina Koc in
Google Scholar
PubMed
Search for other papers by Daniel W Bowles in
Google Scholar
PubMed
Search for other papers by Stephen Leong in
Google Scholar
PubMed
Research Service Veterans Affairs Medical Center, Aurora, Colorado, USA
Search for other papers by Margaret E Wierman in
Google Scholar
PubMed
Research Service Veterans Affairs Medical Center, Aurora, Colorado, USA
Search for other papers by Katja Kiseljak-Vassiliades in
Google Scholar
PubMed
identifying novel genetic alterations and understanding the percent targetable alterations for therapeutic intervention. Our analysis confirmed the commonly known pathway alterations in ACC and identified several novel somatic alterations. Importantly, we
