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Prof. Zelig Eshhar

Pools of donor immune cells could reduce the cost and expand the...


Portrazza is approved to by the US FDA to treat lung cancer

Mutations shed light on cancer

In children, lack of a protein causes a dangerous disease. Why do cancer cells suppress the same protein?

 Metastatic melanoma cells. Image: NIH

Scientists can now begin to make sense of the way a deadly cancer develops

PYK2 (red) and the cell-surface receptor (green) that triggers the cellular transition to a pro-metastatic state are found in the same membrane compartment (yellow) from which the transition signal is transmitted

A signal stuck in the “on” position may hasten metastasis in certain breast cancers

A partially unfolded protein (yellow) is broken down by a “scissor”-proteasome (blue and red)

Understanding how a pair of molecular “scissors” are kept in check may help treat disease

Immortalized cells, left, pretreated with a drug that blocks the ERK signal, and right, without the pretreatment. Top cells are untreated, while the bottom ones are stimulated

Weizmann Institute scientists identify a potential drug molecule that stops cancer cells, but not healthy ones, from getting their “mail”

Prof. Lea Eisenbach

Combining two innovative treatments might help keep cancer from spreading

(l-r) bottom: Tamar Gross, Prof. Lea Eisenbach, Dr. Esther Tzehoval and Zoya Alteber; middle row: David Bassan and Adi Sharbi-Yunger; top row: Lior Roitman, Mareike Grees and Adam Solomon

New strategies might help the immune system outwit cancer cells

NPM1 interacts with DNA polymerase eta and regulates polymerase eta-promoted TLS. Assay of polymerase eta and NPM1 in unirradiated (l) and ultraviolet irradiated cells ((c) after one hour, (r) after 18 hours). Blue: DNA in the nucleus; green: polymerase eta–NPM1 interaction

A mechanism for keeping DNA repair mistakes to a minimum might advance the development of cancer drugs