Date: 9 November 2023 (Thursday)

Time: 5:00 pm – 6:00 pm

Venue: Cheung Kung Hai Lecture Theatre 2, G/F, William M.W. Mong Block, 21 Sassoon Road

5:00 p.m.

Presenter: Yang XIANG (PhD candidate)
Primary Supervisor: Dr. Rio SUGIMURA
Presentation Title: To eat or to die – How macrophages decide their minds to cancers
Abstract: Macrophages are a key regulator in tissue homeostasis, inflammation, and pathologies. Macrophages take various actions to protect hosts from pathogens. In the tumor microenvironment, macrophages comprise the predominant cell type and are often reprogrammed to support cancer cells. However, the fundamental question of how macrophages decide their reaction to cancer cells remains unresolved. In other words, what macrophages will do when first encounter cancer cells? In this collaborative work, we aim to map the reaction of macrophages to their first encounter with cancer cells and determine key regulators in their reactions on tumors-on-chips. We separated macrophages based on their interaction mode with cancer cells. We will employ single-cell Smart-seq2 for full-length reading of transcripts to define rare splicing variants and transcription factors (TF). Our ultimate goal is to employ such factors and deliver them in the tumor to promote cancer killing by macrophages.

5:30 p.m.

Presenter: Haocheng YANG (PhD candidate)
Primary Supervisor: Dr. Jason WONG
Presentation Title: Investigating XPD Somatic Hotspot Mutations in Muscle-Invasive Bladder Cancer
Abstract: Muscle-invasive bladder cancer (MIBC) is a prevalent cancer with limited therapeutic progress that results in a high number of deaths each year. Notably, somatic hotspot mutations in the XPD gene, a critical helicase involved in transcription factor IIH and nucleotide excision repair, have been observed in approximately 10 % of MIBC cases. These mutations have been associated with COSMIC signature 5 (SBS5), potentially impairing XPD's role in maintaining genome integrity within MIBC. Through analysis of multiple cohorts, XPD is identified as a cancer driver gene in MIBC. To further elucidate the functional consequences of XPD mutations, we have generated in vitro models expressing both wild-type XPD and missense mutations identified in MIBC. Our ongoing investigations aim to further characterize the functional consequences of XPD mutations, focusing on cell responses to DNA damage agents, cell cycle, CTCF binding, and transcriptional regulation etc. Understanding of these effects will provide insights into MIBC pathogenesis and the origins of SBS5 signatures, potentially informing preventive and therapeutic strategies for this disease.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Jerry Siu at 3917 6912.