240601 Flashcards
Acute myeloid leukemia (AML) is an aggressive hematopoietic malignancy for which there is
an unmet need for novel treatment strategies. There is evidence that the growth arrest and DNA
damage-inducible gene gamma (GADD45g) is a novel tumor suppressor in AML. This finding
may have important clinical implications for cancer therapy. In the laboratory you work, you
have access to different AML cell lines, bone marrow specimens collected from patients with
newly diagnosed AML, human cord blood obtained from healthy volunteers, and NOD/SCID
mice.
A. What type of preliminary experimental evidence would support your initial hypothesis
that the gene GADD45g is involved in AML? Provide at least three examples of
experimental evidence and briefly describe the methodological procedure.
Acute myeloid leukemia (AML) is an aggressive hematopoietic malignancy for which there is
an unmet need for novel treatment strategies. There is evidence that the growth arrest and DNA
damage-inducible gene gamma (GADD45g) is a novel tumor suppressor in AML. This finding
may have important clinical implications for cancer therapy. In the laboratory you work, you
have access to different AML cell lines, bone marrow specimens collected from patients with
newly diagnosed AML, human cord blood obtained from healthy volunteers, and NOD/SCID
mice.
B. What does the Figure 1 present regarding the GADD45g expression? What is the name
of such plot and what is it used for in cancer research? What is the probability
(approximately) that patients with GADD45g-high will survive beyond 30 months?
What is the probability (approximately) that patients with GADD45g-low will survive
beyond 20 months?
How do you understand the heterogeneity of cancer (definition of tumor heterogeneity)? How
does cancer heterogeneity arise?
Figure 2 presents a model of carcinogenesis. Describe the presented model of carcinogenesis
and use it to illustrate the difference between the hereditary and sporadic form of cancer.
Figure 3 presents a chemical modification of DNA. Describe the mechanism of this process,
subcellular occurrence as well as role of this process in cancer diagnostics.
What are the molecular mechanisms that lead to the conversion of a proto-oncogene into an
active oncogene? Give example of three known oncogenes and describe their oncogenic mode
of action.
A. What is the major role of cancer stem cells in cancer development?
B. Name and describe two experimental approaches for the study of human cancer stem
cells.
C. Describe three mechanisms mediating the resistance of cancer stem cells to anti-cancer
therapy.
The apoptosis mechanism is often altered in cancer cells. Give two examples of regulatory
proteins that are often altered in tumours and describe how they affect the apoptosis
mechanism.
What is a Vogelstein model and what can we learn from this model?
Describe the two major mechanisms that tumour cells employ to maintain their telomeres.
Tumours are classified into broad classes based on their cell of origin. Describe 3 of these broad
classes of tumours, cell from which they arise and list two examples of specific tumour types
that belong to each tumour class.
