David Baloyan
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
David Baloyan has a total of 51 co-authors. Here are the top co-authors by number of shared publications:
- Matthias Ernst
Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia
17 shared publications - Moritz F. Eissmann
Cancer and Inflammation Laboratory, Olivia Newton John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Melbourne, VIC 3083, Australia
16 shared publications - Tracy L. Putoczki
The Walter and Eliza Hall Institute of Medical Research
15 shared publications - Ashwini L. Chand
Olivia Newton-John Cancer Research Institute and School of Cancer Medicine, La Trobe University, Heidelberg, Australia
12 shared publications - Ashleigh R. Poh
The Jreissati Pancreatic Centre at Epworth, Richmond, Australia
11 shared publications - Clifford A. Lowell
Department of Laboratory Medicine, UCSF, San Francisco, United States of America
11 shared publications
Latest Publications
- 17 September 2024
- Published by American Association for the Advancement of Science (AAAS) in Science Signaling
- Vol. 17 (854) , eabq4888
DCLK1 induces a pro-tumorigenic phenotype to drive gastric cancer progression
Doublecortin-like kinase 1 (DCLK1) is a proposed driver of gastric cancer (GC) that phosphorylates serine and threonine residues. Here, we showed that the kinase activity of DCLK1 orchestrated cancer cell–intrinsic and–extrinsic processes that led to pro-invasive and pro-metastatic reprogramming of GC cells. Inhibition of the kinase activity of DCLK1 reduced the growth of subcutaneous xenograft tumors formed from MKN1 human gastric carcinoma cells in mice and decreased the abundance of the stromal markers α-Sma, vimentin, and collagen. Similar effects were seen in mice with xenograft tumors formed from MKN1 cells expressing a kinase-inactive DCLK1 mutant (MKN1 D511N ). MKN1 D511N cells also had reduced in vitro migratory potential and stemness compared with control cells. Mice orthotopically grafted with MKN1 cells overexpressing DCLK1 (MKN1 DCLK1 ) showed increased invasiveness and had a greater incidence of lung metastases compared with those grafted with control MKN1 cells. Mechanistically, we showed that the chemokine CXCL12 acted downstream of DCLK1 in cultured MKN1 cells and in mice subcutaneously implanted with gastric tumors formed by MKN1 DCLK1 cells. Moreover, inhibition of the kinase activity of DCLK1 or the expression of DCLK1 D511N reversed the pro-tumorigenic and pro-metastatic phenotype. Together, this study establishes DCLK1 as a broadly acting and potentially targetable promoter of GC.
- 17 September 2024
- Published by American Association for the Advancement of Science (AAAS) in Science Signaling
- Vol. 17 (854) , eabq4888
DCLK1 induces a pro-tumorigenic phenotype to drive gastric cancer progression
Doublecortin-like kinase 1 (DCLK1) is a proposed driver of gastric cancer (GC) that phosphorylates serine and threonine residues. Here, we showed that the kinase activity of DCLK1 orchestrated cancer cell–intrinsic and–extrinsic processes that led to pro-invasive and pro-metastatic reprogramming of GC cells. Inhibition of the kinase activity of DCLK1 reduced the growth of subcutaneous xenograft tumors formed from MKN1 human gastric carcinoma cells in mice and decreased the abundance of the stromal markers α-Sma, vimentin, and collagen. Similar effects were seen in mice with xenograft tumors formed from MKN1 cells expressing a kinase-inactive DCLK1 mutant (MKN1 D511N ). MKN1 D511N cells also had reduced in vitro migratory potential and stemness compared with control cells. Mice orthotopically grafted with MKN1 cells overexpressing DCLK1 (MKN1 DCLK1 ) showed increased invasiveness and had a greater incidence of lung metastases compared with those grafted with control MKN1 cells. Mechanistically, we showed that the chemokine CXCL12 acted downstream of DCLK1 in cultured MKN1 cells and in mice subcutaneously implanted with gastric tumors formed by MKN1 DCLK1 cells. Moreover, inhibition of the kinase activity of DCLK1 or the expression of DCLK1 D511N reversed the pro-tumorigenic and pro-metastatic phenotype. Together, this study establishes DCLK1 as a broadly acting and potentially targetable promoter of GC.
- Open Access
- 4 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 2 from Inhibition of the SRC Kinase HCK Impairs STAT3-Dependent Gastric Tumor Growth in Mice
Increased HCK activity in BMDMs supports tumor cell invasion in vitro.
- 4 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 2 from Inhibition of the SRC Kinase HCK Impairs STAT3-Dependent Gastric Tumor Growth in Mice
Increased HCK activity in BMDMs supports tumor cell invasion in vitro.
- Open Access
- 4 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from Inhibition of the SRC Kinase HCK Impairs STAT3-Dependent Gastric Tumor Growth in Mice
Increased expression of genes associated with alternative macrophage polarization confers a poorer overall survival in human intestinal-type gastric cancer patients.
- 4 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from Inhibition of the SRC Kinase HCK Impairs STAT3-Dependent Gastric Tumor Growth in Mice
Increased expression of genes associated with alternative macrophage polarization confers a poorer overall survival in human intestinal-type gastric cancer patients.