Track: Molecular Pathways and Signaling

The session on Molecular Pathways and Signaling is a fundamental exploration into the intricate, corrupted regulatory network that defines cancer. Understanding these systems is the bedrock of rational drug design in precision oncology.

Oncogenic Activation of the PI3K/AKT/mTOR Cascade - This pathway is a master regulator of cell growth, survival, and metabolism; its hyperactivation-often due to mutations in PIK3CA or loss of the PTEN tumor suppressor-drives aggressive proliferation. The session will cover strategies for inhibiting specific nodes within this cascade, including targeting mTOR with rapalogs and developing next-generation PI3K inhibitors.

Dysregulation of the RAS/MAPK/ERK Pathway - As one of the most frequently mutated pathways in human cancer, the constitutive activation of RAS and its downstream signaling through MAPK and ERK results in unchecked cellular growth signals. Speakers will review recent breakthroughs in directly targeting the previously ‘undruggable’ RAS protein, particularly KRAS G12C, and the use of upstream and downstream inhibitors to block pathway signaling effectively.

A crucial focus is placed on the mechanisms that allow cancer cells to multiply indefinitely, starting with Cell Cycle Checkpoint Bypass and CDKs. Cancer cells circumvent the critical restrictions of the cell cycle (G1/S and G2/M) often through the overexpression of D-type cyclins and the resulting hyperactivation of Cyclin-Dependent Kinases (CDKs). The session will highlight the clinical success of CDK4/6 inhibitors in hormone-receptor positive breast cancer and explore new pan-CDK inhibitors.

This ties directly into Mechanisms of Apoptosis Evasion (BCL-2 Family), where cancer cells gain immortality by neutralizing pro-death signals, often by overexpressing anti-apoptotic proteins like BCL-2. We will examine the clinical use of BH3 mimetics to restore programmed cell death.

The discussion will also address how tumors fuel their rapid growth through Metabolic Reprogramming (The Warburg Effect). This phenomenon describes cancer cells' preference for aerobic glycolysis over oxidative phosphorylation, and experts will explore novel targets within glucose metabolism that are unique to the tumor cell.

Finally, the session tackles the major clinical challenge of acquired resistance by examining Signal Transduction Cross-talk and Bypass Resistance, where tumors activate alternative pathways to bypass the primary drug block. This knowledge guides the design of rational Targeting Kinases and Allosteric Inhibitors, moving beyond simple active-site inhibitors to use allosteric modulators that offer greater specificity and fewer off-target effects, promising more durable responses.

4th International Conference on Cancer and Breast Cancer Treatment

Track: Molecular Pathways and Signaling

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