This document provides a tutorial for searching the IntOGen database to find information on altered genes and biological processes in different cancer types. It demonstrates how to search for breast cancer, sort the results to find the most significantly downregulated or mutated genes, and view module and experiment details for specific genes like CDKN2A. The tutorial explains how to navigate between genes, tumor types, modules, and experiments to discover knowledge on cancer alterations.
Risk of exposure to Campylobacter through consumption of ready-to-eat roast b...ILRI
Poster prepared by E. Mahundi, K. Makita, H. Toyomaki, D. Grace and L.R. Kurwijila at the 13th conference of the International Society for Veterinary Epidemiology and Economics, Maastricht, the Netherlands, 20-24 August 2012.
Analysis of primary breast tumour stromal cells and their potential role in d...Marion Hartmann
Although malignant epithelial cells are the origin of breast cancer and the main focus of research, evidence is increasing that the tumour microenvironment plays an important role in disease progression. Cellular interactions within the breast cancer microenvironment promote tumour growth, invasion, metastasis and resistance to therapy. Breast tumour stroma consists of various cell types including immunocytes, pericytes, endothelial cells and carcinoma associated fibroblasts. Stromal cells are the predominant cell type in the tumour microenvironment. Tumour stromal cells actively secrete growth factors, chemokines and cytokines that support tumourigenesis. Although the tumour promoting effect of stromal-epithelial interactions is recognized, the precise mechanisms involved are poorly understood. Further characterisation of tumour stromal cells will facilitate elucidation of these interactions.
Exploring the power and benefits of using WordPress plugins, how to build a WordPress plugin in a few simple steps, plus a good solid list of plugin resources.
Risk of exposure to Campylobacter through consumption of ready-to-eat roast b...ILRI
Poster prepared by E. Mahundi, K. Makita, H. Toyomaki, D. Grace and L.R. Kurwijila at the 13th conference of the International Society for Veterinary Epidemiology and Economics, Maastricht, the Netherlands, 20-24 August 2012.
Analysis of primary breast tumour stromal cells and their potential role in d...Marion Hartmann
Although malignant epithelial cells are the origin of breast cancer and the main focus of research, evidence is increasing that the tumour microenvironment plays an important role in disease progression. Cellular interactions within the breast cancer microenvironment promote tumour growth, invasion, metastasis and resistance to therapy. Breast tumour stroma consists of various cell types including immunocytes, pericytes, endothelial cells and carcinoma associated fibroblasts. Stromal cells are the predominant cell type in the tumour microenvironment. Tumour stromal cells actively secrete growth factors, chemokines and cytokines that support tumourigenesis. Although the tumour promoting effect of stromal-epithelial interactions is recognized, the precise mechanisms involved are poorly understood. Further characterisation of tumour stromal cells will facilitate elucidation of these interactions.
Exploring the power and benefits of using WordPress plugins, how to build a WordPress plugin in a few simple steps, plus a good solid list of plugin resources.
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We will illustrate the benefits of adding a community forum to your WordPress blog/site. We will show you how easy it is to add forum plugins/widgets, integrate SSO (single-sign-on), and take advantage of the Vanilla API. We will also look at real world examples of high traffic WordPress communities that benefit from these features.
Evolutionary theories are critical for understanding cancer development at the level of species as well as at the level of cells and tissues, and for developing effective therapies.
Comparative genomic hybridization is a molecular cytogenetic method for analysing copy number variations (CNVs) relative to ploidy level in the DNA of a test sample compared to a reference sample, without the need for culturing cells
Clinical Assessment In Incorporating a Personal GenomeDiego Herrera
This presentation goes in-depth in the growing field of personal genome sequencing. The advances in high-throughput DNA sequencing has made the process of mapping structural deviations in an individual's genetic totality more economical. The advantages in health care makes this technology more like to be fully integrated in medicine within the next ten years.
Unfortunately several cancers are not predictable with simple tests .pdfaquastore223
Unfortunately several cancers are not predictable with simple tests rather required much
intensive diagnosis. The whole genome sequence in determining the entire DNA in normal cells
as well as in tumor cells provide the facility to compare and pin point the mutations occurring in
the oncogenes or tumor suppressor genes responsible for causing the cancer seems to be a better
approach. But such approaches are highly expensive and require expertise.
Though, the whole genome sequencing is carried out pin pointing of specific driver mutations
responsible for cancer phenotype would be a question. Some critical mutations can be identified
in some cancer genome sequences while others are hard to find among the thousands of
possibilities. The mutations like missense, nonsense frameshift, rearrangements may alter the
coding sequences of any gene must be checked. The regulatory mutations that increase the
transcription of oncogenes or decrease that of tumor suppressor genes are potentially important
but are very difficult to find in a whole genome sequence.
The catalogs of regulatory elements in human genomes provide list of certain potential
sequences to be targeted. But the catalogs are rudimentary or incomplete. Therefore, the whole
genome sequencing is not a panacea that will lead to immediate cures of all cancers. Recent
studies have shown that the whole genome sequences of cells derived from different regions of
same tumor have suggested an important reason for cancer reference. Certain cancers are
heterogenous and cells within the tumor have different genomes. Certain mutations in oncogens
or tumor suppressor genes are common to all cells in the tumor but some are not.
These findings make a sense that accumulation of mutations in clone of cells cause cancer.
Therefore, designing drug targeting specific cells protecting adult stem cells cannot be
accomplished. Thus, effective cancer treatments would be directed against the common
mutations but is difficult to identify the specific mutations without sequencing of genomes of
many cells throughout the tumor. Cancer landscape is a large scale cancer genome sequencing
project (cancer genome atlas) funded by National Institute of Health (NIH). In this project the
whole genomes or exomex of several hundreds of cancer are being characterized. The recurrent
patterns of mutations are subdivided cancers in to groups with probable clinical relevance.
For example, 4 groups of breast cancers have been identified. Almost 178 lung squamous cell
carcinoma’s genomes have been characterized and matched with DNA of normal cells from
same patients. Mutations in certain tumor suppressor genes like p53 and certain oncogenes have
shown relatively high frequencies among these cancers. The mutations of certain cancers
resemble cancers in some other organs. For example, pattern of mutation in breast cancer
resembles many ovarian cancers more than other types of breast cancers. These findings may
help in designing the drugs .
Rare events or not i want to know about themMehis Pold
Clinical exome sequencing studies produce diagnostic yields in approximately 30% of hereditary disease cases. As also demonstrated, a re-analysis of exome data helps explain previously inconclusive data. Increased diagnostic yields are usually attributed to either novel disease-gene associations, better parental data, resequencing of patient samples or updated variant interpretation (summarized here). One more important factor, however, contributes to resolving previously unexplained cases – genomics software. This article provides an example how independently-developed novel genomics tools can improve diagnostic yields in hereditary disease.
Cell-free DNA Levels Serum Patients with Benign and Malignant Epithelial Ovar...inventionjournals
An elevated level of cell-free DNA (cfDNA) in the blood circulation has detected in cancer patients in comparison with healthy controls. CfDNA circulation in plasma and serum extensively studied and the results are highly variable due to many factors influence the test results that was preanalytic factors as well as analytic factors. Objectives: Is there any difference in the concentration of serum DNA among patients with benign epithelial ovarian tumors and malignant epithelial ovarian tumors? What is the clinicopathological variable that influences the cfDNA circulation? Method: Venous blood drawn with plain vacutainer, centrifuged at 1,000 rpm for 30 minutes, serum kept in -800 C freezer. The cfDNA extracted used NaI method.Results: Collected 30 cases of the benign ovarian tumor and 54 cases of malignant ovarian tumors. The average level serum cfDNA of benign epithelial ovarian tumors and malignant epithelial ovarian tumors were 24.6 ng/mL and 22:29 ng/mL respectively and statistically was not significantly different (p = 0.64). In multivariable analysis with linear regression, there were no clinicopathological variables that statistically significant influence the cfDNA levels in patients with epithelial ovarian tumors where p > 0.05. Conclusion: Concentration of cfDNA circulation of benign epithelial ovarian tumors a little bit higher than malignant epithelial ovarian tumors, but statistically was not significantly different. There was no clinicopathological variable influence the concentration of cfDNA circulation of ovarian tumors.
Cell-free DNA Levels Serum Patients with Benign and Malignant Epithelial Ovar...inventionjournals
An elevated level of cell-free DNA (cfDNA) in the blood circulation has detected in cancer patients in comparison with healthy controls. CfDNA circulation in plasma and serum extensively studied and the results are highly variable due to many factors influence the test results that was preanalytic factors as well as analytic factors. Objectives: Is there any difference in the concentration of serum DNA among patients with benign epithelial ovarian tumors and malignant epithelial ovarian tumors? What is the clinicopathological variable that influences the cfDNA circulation? Method: Venous blood drawn with plain vacutainer, centrifuged at 1,000 rpm for 30 minutes, serum kept in -800 C freezer. The cfDNA extracted used NaI method.Results: Collected 30 cases of the benign ovarian tumor and 54 cases of malignant ovarian tumors. The average level serum cfDNA of benign epithelial ovarian tumors and malignant epithelial ovarian tumors were 24.6 ng/mL and 22:29 ng/mL respectively and statistically was not significantly different (p = 0.64). In multivariable analysis with linear regression, there were no clinicopathological variables that statistically significant influence the cfDNA levels in patients with epithelial ovarian tumors where p > 0.05. Conclusion: Concentration of cfDNA circulation of benign epithelial ovarian tumors a little bit higher than malignant epithelial ovarian tumors, but statistically was not significantly different. There was no clinicopathological variable influence the concentration of cfDNA circulation of ovarian tumors.
Synonymous mutations as drivers in human cancer genomes.Fran Supek
Synonymous mutations change the sequence of a gene without directly altering the sequence of the encoded protein. Here, we present evidence that these "silent" mutations frequently contribute to human cancer. Selection on synonymous mutations in oncogenes is cancer-type specific, and although the functional consequences of cancer-associated synonymous mutations may be diverse, they recurrently alter exonic motifs that regulate splicing and are associated with changes in oncogene splicing in tumors. The p53 tumor suppressor (TP53) also has recurrent synonymous mutations, but, in contrast to those in oncogenes, these are adjacent to splice sites and inactivate them. We estimate that between one in two and one in five silent mutations in oncogenes have been selected, equating to ~6%- 8% of all selected single-nucleotide changes in these genes. In addition, our analyses suggest that dosage-sensitive oncogenes have selected mutations in their 3' UTRs.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
4. NOTE
Cancer type annotations
are based on International
Classification of Disease
(ICD)
ICD-10
nomenclature is
used to indicate
the topography or
site of the tumor
ICD-O
nomenclature is
used to indicate
the tumor
morphology or
subtype.
5. STEP 3
In this case we will select
breast cancer, and we will
leave blank the
morphology type.
6. We are in the page for all
experiments of Breast
Cancer, and all
genes/modules
This table summarizes
the evidence for the
involvement of each
gene in breast cancer
Note that you can
get the data in table
format by clicking on
‘CSV file’ under
‘Export”
7. This part gives summary
information of the
alterations found in each
gene in the cancer type
selected given a number
of experiments
combined
These colors indicate
significance. Colors
toward red means
that this gene is
significantly altered
in this tumor type
Color scale of corrected p-
values:
Gray = no significantly
altered
Red/Yellow = significantly
altered
Gray means that this White means that
gene is not there is no data for
significantly altered this gene in this
in this tumor type. tumor type
8. These values are based
on predictions by CGPrio
method. Genes with
higher probability rank are
more likely to be involved
in cancer.
See Furney et al., NAR
2008
9. STEP 4
You can sort the table by
clicking to the title of any
column. For example click
Down.
10. Now the genes in the Note that some
top are those genes are both
significantly significantly lost and
downregulated in downregulated.
breast cancer.
With these links you
can navigate to the
next pages to see the
rest of the genes
11. STEP 5
Now we will sort the
table to find the
genes with more
mutations known in
breast cancer
12. The first number is the number of
samples with mutations in this
Now the genes in the gene, and the second number is
top are those with the number of samples analyzed.
higher number of This information is based on
mutations known in COSMIC.
breast cancer.
We are browsing the
information for genes in
Breast cancer. But we
can also browse other
information.
This column informs whether
the gene is in the Cancer
Gene Census of the Sanger
Center and which type of
mutations are known in
cancer samples.
13. STEP 6
Select GO process from
Modules tab to
discover the most
altered biological
processes in breast
cancer.
15. STEP 7
If we click to the Up title, we will
sort by the pathways that have
the highest enrichment of genes
up-regulated in breast cancer.
Here, the red color
indicates that the
module (GO process) is
enriched for altered
(up-regulated) genes in
Gray means that the breast cancer.
number of genes in
this pathway that are
altered are not higher
than expected by
chance
19. Note that now we are
in the page of
CDKN2A for breast
cancer
STEP 11
Click on Tumor types
Tab
This box shows details of
This box shows the p- mutations of CDKN2A in
value for up-regulation breast cancer: The
and down-regulation of number of samples with
This box shows details of
CDKN2A in breast mutations (46), the
the annotations of this
cancer. number of samples
gene in the Cancer Gene
analyzed (1003) and the
Census of the Sanger
link to COSMIC for this
Center.
gene.
20. STEP 12
Now click on
Experiments Tab
This table provides
information on the
alterations found in
CDKN2A in different
morphology types for
Breast Cancer.
21. This is the list of experiments STEP 13
that have analyzed CDKN2A Click Down to sort the
in breast cancer. table for those
experiments in which
this gene is more
significantly down-
regulated.
N = number
White cells means no
of samples
data. In this case analyzed
means that this
experiment has not
analyzed for
transcriptomic
alterations
Coloured cells indicate
that this gene is down-
regulated in a
significant number of
samples of the
STEP 14 experiment.
Click on Yu K et al to
see the details of the
experiment.
22. Note that now we are
in the page of
CDKN2A for a
particular experiment
of breast cancer
STEP 15
To see what is the involvement of
CDKN2A in other cancer types click “all”
in experiments and “all” in tumor types.
This box gives details of
This box shows details down-regulation of
of the experiment, CDKN2A in this
including authors, title experiment. 183 samples
and link to the have been analyzed, of
publication or original which 24 have this gene
source of data. down-regulated. The
expected number of
samples with down-
regulation by chance is
about 8. This is highly
significant down-
regulation.
23. Note that now we are
in the page of
CDKN2A for all tumor
types
Go to
the tab
“tumor
type”.
This table gives
information of known
cancer alterations
found in CDKN2A
gene
24. THANKS FOR USING INTOGEN
You will find more
tutorials and
documentation in
www.intogen.org