Role of Septin 6 in the lymphoid lineage and hematopoiesis

2016 ◽  
Vol 44 (9) ◽  
pp. S98
Author(s):  
Katharina Senger ◽  
Maria Carolina Florian ◽  
Hartmut Geiger
Keyword(s):  
2020 ◽  
Vol 21 (10) ◽  
Author(s):  
Paulina Żelechowska ◽  
Ewa Brzezińska‐Błaszczyk ◽  
Aleksandra Kusowska ◽  
Elżbieta Kozłowska

2019 ◽  
Author(s):  
Judith Schütte ◽  
Aniththa Thivakaran ◽  
Yahya Al-Matary ◽  
Pradeep Kumar Patnana ◽  
Daria Frank ◽  
...  

AbstractGfi1 (Growth factor independence 1) is a transcription factor that influences the stem cell capacity of hematopoietic stem cells (HSCs) as well as their differentiation into the myeloid and lymphoid lineage. Loss of Gfi1 impedes the repopulation capacity of HSCs and leads to a block in granulocyte generation causing severe neutropenia and monocytosis. Competitive transplantation assays showed that Gfi1-deficient cells were not able to reconstitute myeloid and lymphoid hematopoiesis in competition with Gfi1-wildtype (GFI1-36S) cells. Low Gfi1 levels (GFI1-knockdown = GFI1-KD) in blasts of myelodysplastic neoplasms, acute and chronic myeloid leukemia patients are associated with poor patient survival. To understand how reduced levels or loss of Gfi1 contribute to hematopoiesis, we analyzed the effect of GFI1-KD and Gfi1-KO on HSCs and more mature cell types in mice. GFI1-KD and Gfi1-KO led to strong decrease in HSC numbers, while the numbers of early progenitors (Lin− Sca1+cKit+ cells) were slightly increased. Competitive transplantation assays showed that GFI1-KD and Gfi1-KO HSCs can still engraft and expand, but they cannot contribute to myeloid and lymphoid differentiation.


1995 ◽  
Vol 217 (2) ◽  
pp. 395-403 ◽  
Author(s):  
Takao Sakai ◽  
Masatsugu Ohta ◽  
Hisaaki Kawakatsu ◽  
Yusuke Furukawa ◽  
Masaki Saito

Author(s):  
Archana P. Thankamony ◽  
Ayalur Raghu Subbalakshmi ◽  
Mohit Kumar Jolly ◽  
Radhika Nair

Lineage plasticity, the switching of cells from one lineage to another has been recognized to be a cardinal property essential for embryonic development, tissue repair and homeostasis. However, such a highly regulated process goes awry when cancer cells exploit this inherent ability to their advantage, resulting in tumorigenesis, relapse, metastasis and therapy resistance. In this review, we summarize our current understanding on the role of lineage plasticity in tumor progression and therapeutic resistance in multiple cancers. Lineage plasticity can be triggered by treatment itself and is reported across various solid as well as liquid tumors. Here we focus on the importance of lineage switching in tumor progression and therapeutic resistance of solid tumors such as the prostate, lung, hepatocellular and colorectal carcinoma and the myeloid and lymphoid lineage switch observed in leukemias. Besides this, we also discuss the role of Epithelial-Mesenchymal Transition (EMT) in facilitating the lineage switch in biphasic cancers such as aggressive carcinosarcomas. We also discuss the mechanisms involved, current therapeutic approaches and challenges that lie ahead in taming the scourge of lineage plasticity in cancer.


Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3602
Author(s):  
Archana P. Thankamony ◽  
Ayalur Raghu Subbalakshmi ◽  
Mohit Kumar Jolly ◽  
Radhika Nair

Lineage plasticity, the switching of cells from one lineage to another, has been recognized as a cardinal property essential for embryonic development, tissue repair and homeostasis. However, such a highly regulated process goes awry when cancer cells exploit this inherent ability to their advantage, resulting in tumorigenesis, relapse, metastasis and therapy resistance. In this review, we summarize our current understanding on the role of lineage plasticity in tumor progression and therapeutic resistance in multiple cancers. Lineage plasticity can be triggered by treatment itself and is reported across various solid as well as liquid tumors. Here, we focus on the importance of lineage switching in tumor progression and therapeutic resistance of solid tumors such as the prostate, lung, hepatocellular and colorectal carcinoma and the myeloid and lymphoid lineage switch observed in leukemias. Besides this, we also discuss the role of epithelial-mesenchymal transition (EMT) in facilitating the lineage switch in biphasic cancers such as aggressive carcinosarcomas. We also discuss the mechanisms involved, current therapeutic approaches and challenges that lie ahead in taming the scourge of lineage plasticity in cancer.


Cell Cycle ◽  
2011 ◽  
Vol 10 (2) ◽  
pp. 191-190 ◽  
Author(s):  
Lan V. Pham ◽  
Richard J. Ford
Keyword(s):  

JAMA ◽  
1966 ◽  
Vol 195 (12) ◽  
pp. 1005-1009 ◽  
Author(s):  
D. J. Fernbach
Keyword(s):  

JAMA ◽  
1966 ◽  
Vol 195 (3) ◽  
pp. 167-172 ◽  
Author(s):  
T. E. Van Metre

2018 ◽  
Vol 41 ◽  
Author(s):  
Winnifred R. Louis ◽  
Craig McGarty ◽  
Emma F. Thomas ◽  
Catherine E. Amiot ◽  
Fathali M. Moghaddam

AbstractWhitehouse adapts insights from evolutionary anthropology to interpret extreme self-sacrifice through the concept of identity fusion. The model neglects the role of normative systems in shaping behaviors, especially in relation to violent extremism. In peaceful groups, increasing fusion will actually decrease extremism. Groups collectively appraise threats and opportunities, actively debate action options, and rarely choose violence toward self or others.


2018 ◽  
Vol 41 ◽  
Author(s):  
Kevin Arceneaux

AbstractIntuitions guide decision-making, and looking to the evolutionary history of humans illuminates why some behavioral responses are more intuitive than others. Yet a place remains for cognitive processes to second-guess intuitive responses – that is, to be reflective – and individual differences abound in automatic, intuitive processing as well.


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