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Patients with familial adenomatous polyposis harbor colonic biofilms containing tumorigenic bacteria.
Dejea CM, Fathi P, Craig JM, Boleij A, Taddese R, Geis AL, Wu X, DeStefano Shields CE, Hechenbleikner EM, Huso DL, Anders RA, Giardiello FM, Wick EC, Wang H, Wu S, Pardoll DM, Housseau F, Sears CL
(2018) Science 359: 592-597
MeSH Terms: Adenomatous Polyposis Coli, Animals, Bacterial Toxins, Bacteroides fragilis, Biofilms, Carcinogenesis, Colon, Colonic Neoplasms, DNA Damage, Escherichia coli, Gastrointestinal Microbiome, Humans, Interleukin-17, Intestinal Mucosa, Metalloendopeptidases, Mice, Peptides, Polyketides, Precancerous Conditions
Show Abstract · Added March 20, 2018
Individuals with sporadic colorectal cancer (CRC) frequently harbor abnormalities in the composition of the gut microbiome; however, the microbiota associated with precancerous lesions in hereditary CRC remains largely unknown. We studied colonic mucosa of patients with familial adenomatous polyposis (FAP), who develop benign precursor lesions (polyps) early in life. We identified patchy bacterial biofilms composed predominately of and Genes for colibactin () and toxin (), encoding secreted oncotoxins, were highly enriched in FAP patients' colonic mucosa compared to healthy individuals. Tumor-prone mice cocolonized with (expressing colibactin), and enterotoxigenic showed increased interleukin-17 in the colon and DNA damage in colonic epithelium with faster tumor onset and greater mortality, compared to mice with either bacterial strain alone. These data suggest an unexpected link between early neoplasia of the colon and tumorigenic bacteria.
Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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19 MeSH Terms
Motivation for Launching a Cancer Metastasis Inhibition (CMI) Program.
Pulley JM, Jerome RN, Ogletree ML, Bernard GR, Lavieri RR, Zaleski NM, Hong CC, Shirey-Rice JK, Arteaga CL, Mayer IA, Holroyd KJ, Cook RS
(2018) Target Oncol 13: 61-68
MeSH Terms: Early Detection of Cancer, Humans, Motivation, Neoplasm Metastasis, Quality of Life
Show Abstract · Added January 2, 2018
Metastatic cancers impose significant burdens on patients, affecting quality of life, morbidity, and mortality. Even during remission, microscopic metastases can lurk, but few therapies directly target tumor cell metastasis. Agents that interfere with this process would represent a new paradigm in cancer management, changing the 'waiting game' into a time of active prevention. These therapies could take multiple forms based on the pathways involved in the metastatic process. For example, a phenome-wide association study showed that a single nucleotide polymorphism in the gene TBXA2R is associated with increased metastasis in multiple primary cancers (P = 0.003), suggesting clinical applicability of TBXA2R antagonists. Emerging data related to the role of platelets in metastasis are concordant with our sense that these pathways present significant opportunities for therapeutic development. However, before real progress can be made toward clinical targeting of the metastatic process, foundational work is needed to define informative measures of critical elements such as circulating tumor cells and tumor DNA, and circulatory vs. lymphatic spread. These challenges require an expansion of team science and composition to obtain competitive funding. At our academic medical center, we have implemented a Cancer Metastasis Inhibition (CMI) program investigating this approach across multiple cancers.
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5 MeSH Terms
New terminology-noninvasive follicular neoplasm with papillary-like nuclear features (NIFTP) and its effect on the rate of malignancy at a single institution.
Kiernan CM, Weiss VL, Mehrad M, Ely K, Baregamian N, Solórzano CC
(2018) Surgery 163: 55-59
MeSH Terms: Adult, Carcinoma, Papillary, Diagnosis, Differential, Female, Humans, Male, Middle Aged, Retrospective Studies, Terminology as Topic, Thyroid Cancer, Papillary, Thyroid Gland, Thyroid Neoplasms
Show Abstract · Added April 15, 2019
BACKGROUND - The cytologic qualities of noninvasive follicular neoplasm with papillary-like nuclear features mimic papillary thyroid carcinoma (PTC) on fine-needle aspiration, leading to difficulty in distinguishing the 2 preoperatively. The aim of this study was to determine the impact of reclassification of noninvasive follicular neoplasm with papillary-like nuclear features at our practice.
METHODS - We searched 1,046 patient charts for those cases with preoperative cytology and subsequent follicular-variant papillary thyroid carcinoma diagnosis on resection. Endocrine pathologists reviewed the cases to determine the reclassification of noninvasive follicular neoplasm with papillary-like nuclear features.
RESULTS - Sixty (6%) follicular-variant papillary thyroid carcinomas were identified, 4% (44) in the index nodule. Of the 44 patients, 84% (37) met the criteria for evaluation. Of these, 46% (17) were noninvasive follicular neoplasm with papillary-like nuclear features. After reclassification of noninvasive follicular-variant papillary thyroid carcinoma to noninvasive follicular neoplasm with papillary-like nuclear features, the overall cancer rate changed from 31% to 29%. Malignancy rates across Bethesda cytologic categories changed as follows: benign (n = 419) from 3.5% to 3.3%; atypia of undetermined significance/follicular lesion of undetermined significance (n = 240) from 17% to 15%; suspicious for follicular neoplasm (n = 104) from 23% to 21%; suspicious for malignancy (n = 85) from 68% to 60%, and malignant (n = 198) from 93% to 92%.
CONCLUSION - Reclassification of noninvasive follicular neoplasm with papillary-like nuclear features led to a small decrease in the overall malignancy rate. The most affected Bethesda category was suspicious for malignancy. Because the majority of noninvasive follicular neoplasm with papillary-like nuclear features will be indeterminate lesions by cytology/molecular testing, thyroidectomy will remain a common treatment modality. Noninvasive follicular neoplasm with papillary-like nuclear features classification will primarily affect decision making to avoid excessive treatment/monitoring.
Copyright © 2017 Elsevier Inc. All rights reserved.
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MeSH Terms
Cancer-associated fibroblasts promote directional cancer cell migration by aligning fibronectin.
Erdogan B, Ao M, White LM, Means AL, Brewer BM, Yang L, Washington MK, Shi C, Franco OE, Weaver AM, Hayward SW, Li D, Webb DJ
(2017) J Cell Biol 216: 3799-3816
MeSH Terms: Cancer-Associated Fibroblasts, Cell Communication, Cell Line, Tumor, Cell Movement, Coculture Techniques, Extracellular Matrix, Fibronectins, Humans, Integrin alpha5beta1, Male, Mechanotransduction, Cellular, Neoplasm Invasiveness, Nonmuscle Myosin Type IIA, Prostatic Neoplasms, RNA Interference, Receptor, Platelet-Derived Growth Factor alpha, Time Factors, Transfection, Tumor Cells, Cultured, Tumor Microenvironment
Show Abstract · Added March 14, 2018
Cancer-associated fibroblasts (CAFs) are major components of the carcinoma microenvironment that promote tumor progression. However, the mechanisms by which CAFs regulate cancer cell migration are poorly understood. In this study, we show that fibronectin (Fn) assembled by CAFs mediates CAF-cancer cell association and directional migration. Compared with normal fibroblasts, CAFs produce an Fn-rich extracellular matrix with anisotropic fiber orientation, which guides the cancer cells to migrate directionally. CAFs align the Fn matrix by increasing nonmuscle myosin II- and platelet-derived growth factor receptor α-mediated contractility and traction forces, which are transduced to Fn through α5β1 integrin. We further show that prostate cancer cells use αv integrin to migrate efficiently and directionally on CAF-derived matrices. We demonstrate that aligned Fn is a prominent feature of invasion sites in human prostatic and pancreatic carcinoma samples. Collectively, we present a new mechanism by which CAFs organize the Fn matrix and promote directional cancer cell migration.
© 2017 Erdogan et al.
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20 MeSH Terms
Evaluating Molecular Biomarkers for the Early Detection of Lung Cancer: When Is a Biomarker Ready for Clinical Use? An Official American Thoracic Society Policy Statement.
Mazzone PJ, Sears CR, Arenberg DA, Gaga M, Gould MK, Massion PP, Nair VS, Powell CA, Silvestri GA, Vachani A, Wiener RS, ATS Assembly on Thoracic Oncology
(2017) Am J Respir Crit Care Med 196: e15-e29
MeSH Terms: Biomarkers, Tumor, Early Detection of Cancer, Humans, Lung Neoplasms, Societies, Medical, United States
Show Abstract · Added January 29, 2018
BACKGROUND - Molecular biomarkers have the potential to improve the current state of early lung cancer detection. The goal of this project was to develop a policy statement that provides guidance about the level of evidence required to determine that a molecular biomarker, used to support early lung cancer detection, is appropriate for clinical use.
METHODS - An ad hoc project steering committee was formed, to include individuals with expertise in the early detection of lung cancer and molecular biomarker development, from inside and outside of the Assembly on Thoracic Oncology. Key questions, generated from the results of a survey of the project steering committee, were discussed at an in-person meeting. Results of the discussion were summarized in a policy statement that was circulated to the steering committee and revised multiple times to achieve consensus.
RESULTS - With a focus on the clinical applications of lung cancer screening and lung nodule evaluation, the policy statement outlines categories of results that should be reported in the early phases of molecular biomarker development, discusses the level of evidence that would support study of the clinical utility, describes the outcomes that should be proven to consider a molecular biomarker clinically useful, and suggests study designs capable of assessing these outcomes.
CONCLUSIONS - The application of molecular biomarkers to assist with the early detection of lung cancer has the potential to substantially improve our ability to select patients for lung cancer screening, and to assist with the characterization of indeterminate lung nodules. We have described relevant considerations and have suggested standards to apply when determining whether a molecular biomarker for the early detection of lung cancer is ready for clinical use.
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6 MeSH Terms
Grounding Cardio-Oncology in Basic and Clinical Science.
Moslehi J, Amgalan D, Kitsis RN
(2017) Circulation 136: 3-5
MeSH Terms: Biomedical Research, Cancer Survivors, Cardiovascular Diseases, Humans, Neoplasms
Added December 2, 2017
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5 MeSH Terms
Dynamics of infection as a determinant of progression of gastric precancerous lesions: 16-year follow-up of an eradication trial.
Mera RM, Bravo LE, Camargo MC, Bravo JC, Delgado AG, Romero-Gallo J, Yepez MC, Realpe JL, Schneider BG, Morgan DR, Peek RM, Correa P, Wilson KT, Piazuelo MB
(2018) Gut 67: 1239-1246
MeSH Terms: Adult, Aged, Anti-Bacterial Agents, Disease Progression, Drug Administration Schedule, Female, Follow-Up Studies, Helicobacter Infections, Helicobacter pylori, Humans, Male, Metaplasia, Middle Aged, Precancerous Conditions, Risk Factors, Stomach Neoplasms
Show Abstract · Added June 29, 2017
OBJECTIVE - To evaluate the long-term effect of cumulative time exposed to infection on the progression of gastric lesions.
DESIGN - 795 adults with precancerous gastric lesions were randomised to receive anti- treatment at baseline. Gastric biopsies were obtained at baseline and at 3, 6, 12 and 16 years. A total of 456 individuals attended the 16-year visit. Cumulative time of exposure was calculated as the number of years infected during follow-up. Multivariable logistic regression models were used to estimate the risk of progression to a more advanced diagnosis (versus no change/regression) as well as gastric cancer risk by intestinal metaplasia (IM) subtype. For a more detailed analysis of progression, we also used a histopathology score assessing both severity and extension of the gastric lesions (range 1-6). The score difference between baseline and 16 years was modelled by generalised linear models.
RESULTS - Individuals who were continuously infected with for 16 years had a higher probability of progression to a more advanced diagnosis than those who cleared the infection and remained negative after baseline (p=0.001). Incomplete-type IM was associated with higher risk of progression to cancer than complete-type (OR, 11.3; 95% CI 1.4 to 91.4). The average histopathology score increased by 0.20 units/year (95% CI 0.12 to 0.28) among individuals continuously infected with . The effect of cumulative time of infection on progression in the histopathology score was significantly higher for individuals with atrophy (without IM) than for individuals with IM (p<0.001).
CONCLUSIONS - Long-term exposure to infection was associated with progression of precancerous lesions. Individuals infected with with these lesions may benefit from eradication, particularly those with atrophic gastritis without IM. Incomplete-type IM may be a useful marker for the identification of individuals at higher risk for cancer.
© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
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16 MeSH Terms
Clinical and Genome-Wide Analysis of Cisplatin-Induced Peripheral Neuropathy in Survivors of Adult-Onset Cancer.
Dolan ME, El Charif O, Wheeler HE, Gamazon ER, Ardeshir-Rouhani-Fard S, Monahan P, Feldman DR, Hamilton RJ, Vaughn DJ, Beard CJ, Fung C, Kim J, Fossa SD, Hertz DL, Mushiroda T, Kubo M, Einhorn LH, Cox NJ, Travis LB, Platinum Study Group
(2017) Clin Cancer Res 23: 5757-5768
MeSH Terms: Adolescent, Adult, Age Factors, Age of Onset, Aged, Cancer Survivors, Cell Cycle Proteins, Cisplatin, Gene Expression Regulation, Neoplastic, Genome-Wide Association Study, Genotype, Humans, Hypertension, Male, Middle Aged, Neoplasm Proteins, Peripheral Nervous System Diseases, Polymorphism, Single Nucleotide, Risk Factors, Testicular Neoplasms
Show Abstract · Added October 27, 2017
Our purpose was to characterize the clinical influences, genetic risk factors, and gene mechanisms contributing to persistent cisplatin-induced peripheral neuropathy (CisIPN) in testicular cancer survivors (TCSs). TCS given cisplatin-based therapy completed the validated EORTC QLQ-CIPN20 questionnaire. An ordinal CisIPN phenotype was derived, and associations with age, smoking, excess drinking, hypertension, body mass index, diabetes, hypercholesterolemia, cumulative cisplatin dose, and self-reported health were examined for 680 TCS. Genotyping was performed on the Illumina HumanOmniExpressExome chip. Following quality control and imputation, 5.1 million SNPs in 680 genetically European TCS formed the input set. GWAS and PrediXcan were used to identify genetic variation and genetically determined gene expression traits, respectively, contributing to CisIPN. We evaluated two independent datasets for replication: Vanderbilt's electronic health database (BioVU) and the CALGB 90401 trial. Eight sensory items formed a subscale with good internal consistency (Cronbach α = 0.88). Variables significantly associated with CisIPN included age at diagnosis (OR per year, 1.06; = 2 × 10), smoking (OR, 1.54; = 0.004), excess drinking (OR, 1.83; = 0.007), and hypertension (OR, 1.61; = 0.03). CisIPN was correlated with lower self-reported health (OR, 0.56; = 2.6 × 10) and weight gain adjusted for years since treatment (OR per Δkg/m, 1.05; = 0.004). PrediXcan identified lower expressions of and and higher expression as associated with CisIPN ( value for each < 5 × 10) with replication of meeting significance criteria (Fisher combined = 0.0089). CisIPN is associated with age, modifiable risk factors, and genetically determined expression level of Further study of implicated genes could elucidate the pathophysiologic underpinnings of CisIPN. .
©2017 American Association for Cancer Research.
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20 MeSH Terms
Increased expression of deleted in malignant brain tumors (DMBT1) gene in precancerous gastric lesions: Findings from human and animal studies.
Garay J, Piazuelo MB, Lopez-Carrillo L, Leal YA, Majumdar S, Li L, Cruz-Rodriguez N, Serrano-Gomez SJ, Busso CS, Schneider BG, Delgado AG, Bravo LE, Crist AM, Meadows SM, Camargo MC, Wilson KT, Correa P, Zabaleta J
(2017) Oncotarget 8: 47076-47089
MeSH Terms: Animals, Disease Models, Animal, Ethnic Groups, Gastric Mucosa, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genetic Association Studies, Helicobacter Infections, Humans, Mice, Mice, Knockout, Neoplasm Staging, Precancerous Conditions, Receptors, Cell Surface, Stomach Neoplasms
Show Abstract · Added June 29, 2017
Helicobacter pylori infection triggers a cascade of inflammatory stages that may lead to the appearance of non-atrophic gastritis, multifocal atrophic, intestinal metaplasia, dysplasia, and cancer. Deleted in malignant brain tumors 1 (DMBT1) belongs to the group of secreted scavenger receptor cysteine-rich proteins and is considered to be involved in host defense by binding to pathogens. Initial studies showed its deletion and loss of expression in a variety of tumors but the role of this gene in tumor development is not completely understood. Here, we examined the role of DMBT1 in gastric precancerous lesions in Caucasian, African American and Hispanic individuals as well as in the development of gastric pathology in a mouse model of H. pylori infection. We found that in 3 different populations, mucosal DMBT1 expression was significantly increased (2.5 fold) in individuals with dysplasia compared to multifocal atrophic gastritis without intestinal metaplasia; the increase was also observed in individuals with advanced gastritis and positive H. pylori infection. In our animal model, H. pylori infection of Dmbt1-/- mice resulted in significantly higher levels of gastritis, more extensive mucous metaplasia and reduced Il33 expression levels in the gastric mucosa compared to H. pylori-infected wild type mice. Our data in the animal model suggest that in response to H. pylori infection DMBT1 may mediate mucosal protection reducing the risk of developing gastric precancerous lesions. However, the increased expression in human gastric precancerous lesions points to a more complex role of DMBT1 in gastric carcinogenesis.
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15 MeSH Terms
Myc enhances B-cell receptor signaling in precancerous B cells and confers resistance to Btk inhibition.
Moyo TK, Wilson CS, Moore DJ, Eischen CM
(2017) Oncogene 36: 4653-4661
MeSH Terms: Agammaglobulinaemia Tyrosine Kinase, Animals, B-Lymphocytes, CD79 Antigens, Cell Proliferation, Flow Cytometry, Humans, Lymphoma, Non-Hodgkin, Male, Mice, Mice, Inbred C57BL, Mitogen-Activated Protein Kinase 3, Phosphatidylinositol 3-Kinases, Phospholipase C gamma, Phosphorylation, Precancerous Conditions, Protein-Tyrosine Kinases, Proto-Oncogene Proteins c-myc, Pyrazoles, Pyrimidines, Receptors, Antigen, B-Cell, Splenic Neoplasms, Syk Kinase
Show Abstract · Added April 6, 2017
Dysregulation of the oncogenic transcription factor MYC induces B-cell transformation and is a driver for B-cell non-Hodgkin lymphoma (B-NHL). MYC overexpression in B-NHL is associated with more aggressive phenotypes and poor prognosis. Although genomic studies suggest a link between MYC overexpression and B-cell receptor (BCR) signaling molecules in B-NHL, signaling pathways essential to Myc-mediated B-cell transformation have not been fully elucidated. We utilized intracellular phospho-flow cytometry to investigate the relationship between Myc and BCR signaling in pre-malignant B cells. Utilizing the Eμ-myc mouse model, where Myc is overexpressed specifically in B cells, both basal and stimulated BCR signaling were increased in precancerous B lymphocytes from Eμ-myc mice compared with wild-type littermates. B cells overexpressing Myc displayed constitutively higher levels of activated CD79α, Btk, Plcγ2 and Erk1/2. Notably, Myc-overexpressing B cells maintained elevated BCR signaling despite treatment with ibrutinib, a Bruton's tyrosine kinase inhibitor. Furthermore, PI3K/Akt pathway signaling was also increased in Eμ-myc B cells, and this increase was partially suppressed with ibrutinib. In addition, experiments with Btk-null B cells revealed off-target effects of ibrutinib on BCR signaling. Our data show that in pre-malignant B cells, Myc overexpression is sufficient to activate BCR and PI3K/Akt signaling pathways and further enhances signaling following BCR ligation. Therefore, our results indicate that precancerous B cells have already acquired enhanced survival and growth capabilities before transformation, and that elevated MYC levels confer resistance to pharmacologic inhibitors of BCR signaling, which has significant implications for B-NHL treatment.
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23 MeSH Terms