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.

Prevalence of bullying victimization and its association with self-perceived health, psychopathology, and suicidality: A nationwide population-based survey in Taiwan.

&lt;div&gt;Abstract&lt;p&gt;Chimeric antigen receptor (CAR) T-cell therapy can lead to dramatic clinical responses in B-cell malignancies. However, early clinical trials with CAR T-cell therapy in non–B-cell malignancies have been disappointing to date, suggesting that tumor-intrinsic features contribute to resistance. To investigate tumor-intrinsic modes of resistance, we performed genome scale CRISPR-Cas9 screens in mesothelin (MSLN)-expressing pancreatic cancer cells. Co-culture with MSLN-targeting CAR T cells identified both antigen-dependent and antigen-independent modes of resistance. In particular, loss of the majority of the genes involved in the pathway responsible for GPI-anchor biosynthesis and attachment abrogated the ability of CAR T cells to target pancreatic cancer cells, suggesting that disruption of this pathway may permit MSLN CAR T-cell evasion in the clinic. Antigen-independent mediators of CAR T-cell response included members of the death receptor pathway as well as genes that regulate tumor transcriptional responses, including &lt;i&gt;TFAP4&lt;/i&gt; and &lt;i&gt;INTS12&lt;/i&gt;. TFAP4-mediated CAR T resistance depended on the NFκB transcription factor p65, indicating that tumor resistance to CAR T-cell therapy likely involves alterations in tumor-intrinsic states. Overall, this study uncovers multiple antigen-dependent and -independent mechanisms of CAR T-cell evasion by pancreatic cancer, paving the way for overcoming resistance in this disease that is notoriously refractory to immunotherapy.&lt;/p&gt;Significance:&lt;p&gt;The identification and validation of key determinants of CAR T-cell response in pancreatic cancer provide insights into the landscape of tumor cell intrinsic resistance mechanisms and into approaches to improve therapeutic efficacy.&lt;/p&gt;&lt;/div&gt; 

/pdf/data-from-systematic-interrogation-of-tumor-cell-resistance-lqtn2qg4.pdf

Data from Systematic Interrogation of Tumor Cell Resistance to Chimeric Antigen Receptor T-cell Therapy in Pancreatic Cancer

Mp58-07 clinically significant prostate cancer detection rate by pi-rads score and psa-density: a descriptive analysis


 Cancer genome alterations that cause cancer cells to grow also confer vulnerabilities, which normal cells lack. The challenge is that, for the majority of cancers, we do not understand the relationship between the genetic alterations and the dependencies they cause. To solve this problem, we are creating a Cancer Dependency Map (DepMap) by systematically identifying genetic dependencies and small molecule sensitivities as well as discovering the biomarkers that predict them. Since its inception, DepMap has compiled data for over eighteen hundred cell line models, performed more than a thousand CRISPR screens, and drug sensitivity profiles using PRISM in over 500 cell lines as well as developed new analytic methods for the identification of cancer vulnerabilities. DepMap is being used by researchers around the world and numerous potential therapeutic targets have been identified using this resource. However, we are still in the early stages of having a complete map and we will discuss our ongoing work towards making the Cancer Dependency Map more powerful. The next generation DepMap will include more complex cellular models including 3D models, representing pediatric and rare cancers, and expanding the perturbation space to include combinations. Additionally, we are performing novel types of omics characterization and building new computational and visualizations tools. These new scientific directions will help make progress towards our identification of the landscape of cancer vulnerabilities and create a roadmap for cancer therapeutics.
 Citation Format: Kirsty Wienand, Samantha Stokes, Philip G. Montgomery, Kelly Sullivan, Joshua M. Dempster, William C. Hahn, Jennifer A. Roth, Francisca Vazquez. Towards the next generation cancer dependency map [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 2 (Clinical Trials and Late-Breaking Research); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(8_Suppl):Abstract nr LB074.

William C. Hahn

Papers

Prevalence of bullying victimization and its association with self-perceived health, psychopathology, and suicidality: A nationwide population-based survey in Taiwan.

Data from Systematic Interrogation of Tumor Cell Resistance to Chimeric Antigen Receptor T-cell Therapy in Pancreatic Cancer

Mp58-07 clinically significant prostate cancer detection rate by pi-rads score and psa-density: a descriptive analysis

Abstract LB074: Towards the next generation cancer dependency map

Mp58-02 psa-density determines the need for systematic biopsy in men with pi-rads 4/5 mri