1. סרטן היא תחלואה המכילה שפה בפני עצמה ועולם רפואי בפני עצמו...
סרטן היא תחלואה המכילה שפה בפני עצמה ועולם רפואי בפני עצמו...
ספרות, פילוסופיה, אמונות, מדע, טכנולוגיה, כלכלה...

2. Concepts Change on genomic level- DNA sequence Evolutionary process
Cell clone
Additional genomic processes diversify the population
Environmental effectors
Immunology
Angiogenesis
Tissue response

3. Changes on DNA level are involved and define cancer
Cancer can be caused by environmental factors:
Chemicals
Physical exposures
Biological metabolites
Viruses (Hep. viruses, papilloma V )
Cellular intrinsic changes and mishaps
Point mut, translocations, LOH…
SOLID VS. NON-SOLID TUMORS
Carcinoma-Epithelial,
Sarcoma- Muscle
Glioma- Glia (neuron supporting cells)
Leukemia
Lymphoma

4. Staging and grading
I- differentiated tissue, markers IV- No differentiation markers, marked invasiveness Stage 1-4: involvement of other tissues usually with Lymph nodes (Stage 3- invasiveness) Neoplasia: Cell growth, increased proportion of cell divisions, differentiation malignant NEOPLASMS Benign growth--- Tumor, Angiogenesis, metastasis

5. The process is exhibited through the development

7. Cancer Causing genes
Oncogenes: GOF, dominant, de-novo (cell signaling to cycling)
Tumor suppressors: LOF, both alleles, de-novo/inherited, 2hit?
Maintenance/ metabolic functions/cellular communication
Reduced DNA repair, increased metabolism, reduced contact
Founder mutation
Driver Mutations- give advantage to the cell, evidence that implicate them with the cancerous process
Gate Keeper Genes
Passenger Mutations- no proof for functionality or contribution
Clonallity and heterogeneity
Signature: typical transcriptome, mutated genes, proteome

8. Current tumor mutational evolution is very simplistic
Current tumor mutational evolution is very simplistic. The one above asses diversity in the cell population without the genomic landscape.
Do subgroups always contain the mutational history of their evolution?
Analysis methods/ importance?

9. The most prevalent gene
Why more than one gene

10. AML as an example

11. Mutation burden and cancer incidence.
Mutation burden and cancer incidence. (A) Comparison of the mean number of non-coding mutations per genome in tumours of different tissues (raw data from Lawrence et al., 2013). Error bars show the standard error of the mean. (B) UK annual incidence of various malignancies [Cancer Registry Statistics, 2011; ( and the Cancer Research UK website ( An asterisk (*) signifies that the incidence data refer to the tissue of origin, rather than the specific cancer subtype shown in A (e.g. lung cancer rather than lung squamous cell or adenocarcinoma). CLL, chronic lymphocytic leukaemia; DLBCL, diffuse large B-cell lymphoma.
Carolyn S. Grove, and George S. Vassiliou Dis. Model. Mech. 2014;7:

12. Open q. Why certain tissues are more prone to tumor- genesis?
Why certain people are more prone to tumor- genesis?
Are certain cells/ genes/tissues chronological ages more prone to tumor- genesis?
? Half of the coding driver mutations occur outside of known
cancer genes