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Thursday, November 13, 2025

Tissue and Cancer Stem Cells from the Lens of 3D Imaging

| CARSON FAMILY AUDITORIUM (CRC)
Seminars, Stem Cell Biology Seminars
Jacco Van Rheenan, Ph.D., group leader, Hubrecht Institute; professor in intravital microscopy, University Medical Center Utrecht; senior group leader, Netherlands Cancer Institute and the Oncode Institute

Surfing the Cell Surface: A Deep Dive into the ‘Superficial’

| CARSON FAMILY AUDITORIUM (CRC)
Seminars, Neuroscience Seminar Series
Li Jiefu, Ph.D., group leader, Janelia Research Campus, Howard Hughes Medical Institute

A Step Toward Deciphering Type 2 Innate Immune Sensing

| BELFER RESEARCH BUILDING, SECOND FLOOR, WCM, 413 E. 69TH ST.
Tri-Institutional Events (at MSK & WCM), Immunology Program
Mo Xu, Ph.D., assistant investigator, National Institute of Biological Sciences, Beijing

Tri-Institutional Calendars

The close proximity among the three institutions which comprise the Tri-I has led to a culture that encourages interinstitutional interactions and shared resources, including access to lectures and seminars from internationally renowned scientists and clinicians:

Upcoming Events

Self-Organization and Symmetry Breaking in Human Embryo and Models

| CARSON FAMILY AUDITORIUM (CRC)

Rare Sugar Probes to Identify Glycan Binding Proteins

| 116 ROCKEFELLER RESEARCH LABORATORIES, MSKCC, 430 E. 67TH ST.

Title TBA

| CARSON FAMILY AUDITORIUM (CRC)

News

Why understanding stem cells lies as the root of treating diseases from psoriasis to cancer

Elaine Fuchs has spent decades uncovering why our bodies are so good at regenerating skin—and how we might harness that understanding to combat illness, hair loss, and possibly the aging process itself.

New model demonstrates how a dynamic mechanism regulates traffic through the nuclear pore complex

A new study reveals that nuclear pore complexes—tiny gateways in a cell’s nuclear membrane—are governed by dynamic action.

Scientists can finally answer an old question about cellular aging

Replicative aging of human cells, the result of telomere shortening, is slower at physiological oxygen than at atmospheric oxygen, a difference now shown to be due to low oxygen impairing the ATM kinase response to withered telomeres.