I have completed my Ph.D. studies in Medical Sciences and Biotechnology at Università del Piemonte Orientale (Laboratory of Molecular Pathology, Department of Health Sciences, Novara) under the mentorship of Prof. Ciro Isidoro. Our laboratory's main research focuses on autophagy, a lysosome-mediated catabolic process essential for cellular homeostasis and macromolecular turnover. This process degrades damaged, aged, or excess cellular components and eliminates intracellular pathogens. In cancer, autophagy often becomes dysregulated, playing dual roles in tumorigenesis and progression. Initially, basal autophagy acts as a tumor suppressor by mitigating cellular damage and genomic instability, thereby preventing malignant transformation. However, depending on the advanced stages or severity of cancer, autophagy supports tumor cell survival by counteracting therapeutic stress and enabling adaptation to adverse conditions such as hypoxia, nutrient depletion, and limited growth factor availability. During my studies, I focused on the role and regulation of autophagy in hematological malignancies, particularly in Diffuse large B cell lymphoma and Acute myeloid leukemia and their cancer progression focusing on glycolysis and therapy resistance. I co-authored two original articles dealing with these topics, one was published in the journal Cells, and the other one in the International Journal of Molecular Sciences (which are reported in the section Results). In addition, I participated in other ongoing lab projects dealing with the functional role of Autophagy in regulating several aspects of ovarian cancer progression (therapy response, cancer cell migration, cell dormancy, and metabolic rewiring mechanisms). Furthermore, I also contributed to other projects of the lab related to other tumors like neuroblastoma, colorectal cancer, and cholangiocarcinoma. Altogether, I co-authored nine papers that are appended at the end of this thesis (the reader may refer to the section
BECLIN-1 dependent autophagy predicts good prognosis in hematological malignancies: mechanistic insights
AMREEN, Salwa
2025
Abstract
I have completed my Ph.D. studies in Medical Sciences and Biotechnology at Università del Piemonte Orientale (Laboratory of Molecular Pathology, Department of Health Sciences, Novara) under the mentorship of Prof. Ciro Isidoro. Our laboratory's main research focuses on autophagy, a lysosome-mediated catabolic process essential for cellular homeostasis and macromolecular turnover. This process degrades damaged, aged, or excess cellular components and eliminates intracellular pathogens. In cancer, autophagy often becomes dysregulated, playing dual roles in tumorigenesis and progression. Initially, basal autophagy acts as a tumor suppressor by mitigating cellular damage and genomic instability, thereby preventing malignant transformation. However, depending on the advanced stages or severity of cancer, autophagy supports tumor cell survival by counteracting therapeutic stress and enabling adaptation to adverse conditions such as hypoxia, nutrient depletion, and limited growth factor availability. During my studies, I focused on the role and regulation of autophagy in hematological malignancies, particularly in Diffuse large B cell lymphoma and Acute myeloid leukemia and their cancer progression focusing on glycolysis and therapy resistance. I co-authored two original articles dealing with these topics, one was published in the journal Cells, and the other one in the International Journal of Molecular Sciences (which are reported in the section Results). In addition, I participated in other ongoing lab projects dealing with the functional role of Autophagy in regulating several aspects of ovarian cancer progression (therapy response, cancer cell migration, cell dormancy, and metabolic rewiring mechanisms). Furthermore, I also contributed to other projects of the lab related to other tumors like neuroblastoma, colorectal cancer, and cholangiocarcinoma. Altogether, I co-authored nine papers that are appended at the end of this thesis (the reader may refer to the sectionFile | Dimensione | Formato | |
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https://hdl.handle.net/20.500.14242/218049
URN:NBN:IT:UNIUPO-218049