Georgios Vlachogiannis
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
Georgios Vlachogiannis has a total of 322 co-authors. Here are the top co-authors by number of shared publications:
- Nicola Valeri
Centre for Evolution and Cancer, The Institute of Cancer Research, London, United Kingdom
109 shared publications - Andrea Sottoriva
Computational Biology Research Centre, Human Technopole, Milan, Italy
85 shared publications - Inmaculada Spiteri
Centre for Evolution and Cancer, The Institute of Cancer Research, London, United Kingdom
82 shared publications - Javier Fernandez-Mateos
Centre for Evolution and Cancer, The Institute of Cancer Research, London, United Kingdom
76 shared publications - George D. Cresswell
Centre for Evolution and Cancer, The Institute of Cancer Research, London, United Kingdom
75 shared publications - Chela James
Human Technopole, Milan, Italy
73 shared publications
Latest Publications
- Open Access
- 24 August 2026
- Published by Springer Nature in Nature Communications
- Vol. 17 (1) , 10091
The anion channel GPR89 is a tumor-specific dependency in breast cancer
How cancers regulate endoplasmic reticulum (ER) pH and minimize ER stress remains unclear. Here we show that in breast cancer, these processes are governed by the anion channel GPR89. While normally localized to the Golgi, we find GPR89 is also present in the ER of tumor cells, where it collaborates with vacuolar H⁺ ATPase to regulate pH, and reduces ER stress via IRE1α-HSP47-XBP1s, ATF6 and ATP2A2 pathways. This ER localization of GPR89 drives a tumor-specific dependency, rendering breast cancer cells, but not normal tissues, dependent on this anion channel. Structural modeling and mutagenesis identify five key amino acids essential for GPR89’s ER pH regulatory function and tumor cell survival. Consistent with its cancer-specific functions, GPR89 cooperates with Myc to accelerate mammary tumorigenesis. These findings uncover how breast cancers adapt to oncogenic stress by co-opting Golgi mechanisms of pH regulation to support ER homeostasis and survival.
- 24 August 2026
- Published by Springer Nature in Nature Communications
- Vol. 17 (1) , 10091
Open AccessThe anion channel GPR89 is a tumor-specific dependency in breast cancer
How cancers regulate endoplasmic reticulum (ER) pH and minimize ER stress remains unclear. Here we show that in breast cancer, these processes are governed by the anion channel GPR89. While normally localized to the Golgi, we find GPR89 is also present in the ER of tumor cells, where it collaborates with vacuolar H⁺ ATPase to regulate pH, and reduces ER stress via IRE1α-HSP47-XBP1s, ATF6 and ATP2A2 pathways. This ER localization of GPR89 drives a tumor-specific dependency, rendering breast cancer cells, but not normal tissues, dependent on this anion channel. Structural modeling and mutagenesis identify five key amino acids essential for GPR89’s ER pH regulatory function and tumor cell survival. Consistent with its cancer-specific functions, GPR89 cooperates with Myc to accelerate mammary tumorigenesis. These findings uncover how breast cancers adapt to oncogenic stress by co-opting Golgi mechanisms of pH regulation to support ER homeostasis and survival.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per genomic bin copy number calls (gains=3, diploid=2, loss=1) for data presented in Figure 1.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per genomic bin copy number calls (gains=3, diploid=2, loss=1) for data presented in Figure 1.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 5 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per segment raw sWGS copy number data for patients presented in Figure 2.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 5 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per segment raw sWGS copy number data for patients presented in Figure 2.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 8 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per genomic bin copy number calls for single-cell data presented in Figure 3.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 8 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per genomic bin copy number calls for single-cell data presented in Figure 3.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 9 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Cohort information per sample for the longitudinal metastasis cohort (Figure 4), including description of organ, timepoint sampled, tumour stage at diagnosis, whether the sample is treatment naïve, if the sample was treated in the prior interval, the number of days and months elapsing since the first timepoint, in addition to per sample genomic metrics such as PGA, number of segments, patient ploidy, per sample GD classification and overall patient GD classification.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 9 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Cohort information per sample for the longitudinal metastasis cohort (Figure 4), including description of organ, timepoint sampled, tumour stage at diagnosis, whether the sample is treatment naïve, if the sample was treated in the prior interval, the number of days and months elapsing since the first timepoint, in addition to per sample genomic metrics such as PGA, number of segments, patient ploidy, per sample GD classification and overall patient GD classification.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Note on Modelling 1 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Supplementary note where we describe the gland mathematical modelling and simulations
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Note on Modelling 1 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Supplementary note where we describe the gland mathematical modelling and simulations
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 3 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Clinical information for CRC cohort presented in Figure 1.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 3 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Clinical information for CRC cohort presented in Figure 1.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 10 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per sample, per segment, raw copy number data (log2 ratios) and integer calls for the longitudinal metastasis cohort presented in Figure 4.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 10 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per sample, per segment, raw copy number data (log2 ratios) and integer calls for the longitudinal metastasis cohort presented in Figure 4.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 4 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per patient clinical information for the CRC cases presented in Figure 2.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 4 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Per patient clinical information for the CRC cases presented in Figure 2.
- Open Access
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Pairwise comparison metrics for data presented in Figure 1.
- 9 February 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer
Pairwise comparison metrics for data presented in Figure 1.