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SUMMARY:Dissertation Defended: Jasmin Kaivola
DESCRIPTION:\n\nJasmin Kaivola from the Ivaska lab successfully defended he
 r PhD thesis "Biomechanical Tumour Matrix" on Friday the 29th of November 
 2024. Her opponent was Professor Rachel Lennon from the Cell-Matrix Resear
 ch Center\, University of Manchester\, UK.\n\nSummary of the Dissertation:
 \n\nThe interplay between mechanical forces and the tumour microenvironmen
 t is critical in cancer progression\, influencing tumour growth\, metastas
 is and therapy resistance. Integrins\, which mediate cell adhesion to the 
 extracellular matrix (ECM)\, transmit mechanical signals that regulate key
  cellular processes including proliferation and migration. These mechanica
 l forces modulate integrin activity\, altering the cytoskeleton and signal
 ling networks\, thereby promoting cancer invasiveness and metastasis. The 
 tumour matrix's physical properties\, such as stiffness\, further drive ca
 ncer progression. Cancer-associated fibroblasts remodel the ECM\, increasi
 ng matrix stiffness and enhancing mechanotransduction pathways. Moreover\,
  cancer-associated adipocytes contribute to metabolic reprogramming and in
 flammation\, creating a feedback loop that accelerates tumour growth. Unde
 rstanding these molecular mechanisms is crucial for developing therapies t
 hat disrupt these pathways to inhibit cancer progression and metastasis.\n
 \nIn this thesis\, I have explored how reintroducing mechanical forces los
 t in cancer\, owing to increased tissue rigidity\, can downregulate oncoge
 nic signalling activity. Specifically\, stretching and vibrating vocal fol
 d cancer cells lead to nucleocytoplasmic localisation of the oncogenic tra
 nscription factors YAP/TAZ and β-catenin. Additionally\, I have investiga
 ted the role of healthy adipocytes in the breast tumour microenvironment\,
  demonstrating that secretion of the adipocrine factor IGFBP2 can act as a
  protective barrier against breast cancer progression. Lastly\, I examined
  the role of the integrin inactivator SHANK3 in KRAS-driven cancers\, show
 ing that disrupting the SHANK3-KRAS interaction can induce cell death in K
 RAS-mutant cancer cells through hyperactivation of the MAPK-ERK pathway. C
 ollectively\, these findings offer novel strategies to inhibit and target 
 cancer progression across different cancer types.\n\nDownload Doctoral Dis
 sertation at UTUPub: https://urn.fi/URN:ISBN:978-951-29-9938-5
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