https://cancerbiologyprogram.med.wayne.edu/pdfs/hallmarks_cancer_article.pdf

Hallmarks of cancer: the next generation.

The hallmarks of cancer.

WHO CLASSIFICATION OF TUMOURS OF HAEMATOPOIETIC AND LYMPHOID TISSUES , WHO CLASSIFICATION OF TUMOURS OF HAEMATOPOIETIC AND LYMPHOID TISSUES , کتابخانه مرکزی دانشگاه علوم پزشکی تهران

WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues

Background: Currently, a lack of consensus exists on how best to perform and interpret quantitative real-time PCR (qPCR) experiments. The problem is exacerbated by a lack of sufficient experimental detail in many publications, which impedes a reader’s ability to evaluate critically the quality of the results presented or to repeat the experiments.

Content: The Minimum Information for Publication of Quantitative Real-Time PCR Experiments (MIQE) guidelines target the reliability of results to help ensure the integrity of the scientific literature, promote consistency between laboratories, and increase experimental transparency. MIQE is a set of guidelines that describe the minimum information necessary for evaluating qPCR experiments. Included is a checklist to accompany the initial submission of a manuscript to the publisher. By providing all relevant experimental conditions and assay characteristics, reviewers can assess the validity of the protocols used. Full disclosure of all reagents, sequences, and analysis methods is necessary to enable other investigators to reproduce results. MIQE details should be published either in abbreviated form or as an online supplement.

Summary: Following these guidelines will encourage better experimental practice, allowing more reliable and unequivocal interpretation of qPCR results.

/pdf/the-miqe-guidelines-minimum-information-for-publication-of-27m8n04lrd.pdf

The MIQE Guidelines: Minimum Information for Publication of Quantitative Real-Time PCR Experiments

The 2016 World Health Organization Classification of Tumors of the Central Nervous System is both a conceptual and practical advance over its 2007 predecessor. For the first time, the WHO classification of CNS tumors uses molecular parameters in addition to histology to define many tumor entities, thus formulating a concept for how CNS tumor diagnoses should be structured in the molecular era. As such, the 2016 CNS WHO presents major restructuring of the diffuse gliomas, medulloblastomas and other embryonal tumors, and incorporates new entities that are defined by both histology and molecular features, including glioblastoma, IDH-wildtype and glioblastoma, IDH-mutant; diffuse midline glioma, H3 K27M-mutant; RELA fusion-positive ependymoma; medulloblastoma, WNT-activated and medulloblastoma, SHH-activated; and embryonal tumour with multilayered rosettes, C19MC-altered. The 2016 edition has added newly recognized neoplasms, and has deleted some entities, variants and patterns that no longer have diagnostic and/or biological relevance. Other notable changes include the addition of brain invasion as a criterion for atypical meningioma and the introduction of a soft tissue-type grading system for the now combined entity of solitary fibrous tumor / hemangiopericytoma-a departure from the manner by which other CNS tumors are graded. Overall, it is hoped that the 2016 CNS WHO will facilitate clinical, experimental and epidemiological studies that will lead to improvements in the lives of patients with brain tumors.

/pdf/the-2016-world-health-organization-classification-of-tumors-1rt6cpzcew.pdf

The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary.

Cell state (phenotypic) plasticity is a carefully regulated feature of adult epithelial cells that enables adaptive responses to injury, inflammation, and other forms of stress. Aberrant expansion of the normally restricted capability for cell state plasticity to escape terminal differentiation is a critical aspect of neoplasia. The nongenetic factors and specific programs that mediate aberrant cell state plasticity and impaired differentiation require deeper characterization to understand this elusive aspect of cancer pathogenesis. Using genetically engineered and carcinogen-induced murine models of intestinal neoplasia, we demonstrate that impaired differentiation is a conserved event preceding cancer development. Single cell RNA-sequencing (scRNA-seq) of neoplastic intestinal lesions from both mouse models and a patient with familial adenomatous polyposis revealed that cancer initiates by adopting an aberrant transcriptional state characterized by nonoverlapping expression of a regenerative pathway, marked by Ly6a (Sca-1), and a fetal intestinal program, positive for Tacstd2 (Trop2). Genetic inactivation of Sox9 prevented adenoma formation in Apc KO mice, obstructed emergence of aberrant regenerative and fetal intestinal programs, and restored multi-lineage differentiation by scRNA-seq. Expanded chromatin accessibility at regeneration and fetal genes upon Apc inactivation was reduced by concomitant Sox9 suppression. These studies indicate that cancer initiation requires aberrant cell state plasticity mediated by unabated regenerative activity and developmental reprogramming.

Developmental reprogramming mediates aberrant cell state plasticity in colorectal cancer initiation

Sensitizing shRNA Screen for Molecular Targets in CDK4/CDK6-Based Combination Therapy in Multiple Myeloma

Telomeres are nucleoprotein structures that compose the ends of eukaryotic chromosomes and that regulate chromosome integrity and cell proliferative lifespan. Stabilization of telomere length correlates with cell immortalization, and constitutive activation of telomerase is observed in most human cancers, suggesting that telomere maintenance plays an important role in malignant transformation and possibly aging. However, several lines of evidence indicate that alterations in telomere biology both suppress and facilitate malignant transformation. Moreover, recent observations indicate that telomerase expression plays important regulatory functions beyond the maintenance of telomere length in both normal and malignant cells. Understanding these additional functions of telomerase promise to provide further insight into both normal and malignant cell physiology.

/pdf/new-functions-for-telomerase-3yb6tg4z0d.pdf

New Functions for Telomerase.

Structure of Tank-Binding Kinase 1

The present invention provides methods of screening for compounds that interfere with interaction between ERG, ETV1, ETV4 or ETV5 and mSWI/SNF (BAF) chromatin remodeling complex proteins. Included are methods of screening for compounds that interfere with interaction between ERG, ETV1, ETV4 or ETV5 and BAF155. Methods of treating prostate cancer with compounds that interfere with interaction between ERG, ETV1, ETV4 or ETV5 and mSWI/SNF (BAF) chromatin remodeling complex proteins are also provided.

William C. Hahn

Papers

Developmental reprogramming mediates aberrant cell state plasticity in colorectal cancer initiation

Sensitizing shRNA Screen for Molecular Targets in CDK4/CDK6-Based Combination Therapy in Multiple Myeloma

New Functions for Telomerase.

Structure of Tank-Binding Kinase 1

Methods of identifying compounds that interfere with erg-driven misguidance of baf complexes in tmprss2-erg driven prostate cancers