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Related Concept Videos

Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

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Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

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Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
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Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

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Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
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PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Related Experiment Video

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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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Essential thrombocythaemia progression to the fibrotic phase is associated with a decrease in JAK2 and PDL1 levels.

Krzysztof Lewandowski1, Zuzanna Kanduła2, Michał Gniot2

  • 1Department of Hematology and Bone Marrow Transplantation, Poznan University of Medical Sciences, Poznan, Poland. lewandowski@ump.edu.pl.

Annals of Hematology
|October 20, 2022
PubMed
Summary

Myeloproliferative neoplasms (MPNs) involve JAK-STAT signaling, leading to immune escape. This study found lower JAK2 and PD-L1 mRNA levels in post-ET-myelofibrosis compared to essential thrombocythaemia, correlating with fibrosis.

Keywords:
Driver defectsEssential thrombocythaemiaJAK2V617F allele burdenJAK2V617F expressionNon-driver defects, InflammationPDL1 expressionPost-essential thrombocythaemia myelofibrosisTotal JAK2 expression

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A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Myeloproliferative neoplasms (MPNs) are characterized by molecular changes and aberrant JAK-STAT signaling, contributing to disease progression and immune evasion.
  • Continuous JAK-STAT activation upregulates programmed death-1 receptor ligand (PD-L1), promoting immune escape in MPN cells.

Purpose of the Study:

  • To investigate the levels of PD-L1 and JAK2 mRNA during the progression of essential thrombocythaemia (ET) to post-ET-myelofibrosis (post-ET-MF).
  • To explore the relationship between these molecular markers, specific mutations (JAK2V617F, CALR, MPL), and disease phase.

Main Methods:

  • Quantitative analysis of PD-L1 and JAK2 mRNA levels in 162 ET patients, including 30 with post-ET-MF.
  • Genotyping for JAK2V617F, CALR, and MPL mutations; assessment of copy-number alterations.
  • Correlation analysis of mRNA levels with mutation status, variant allele frequency (VAF), and bone marrow fibrosis grade.

Main Results:

  • PD-L1 mRNA levels were significantly higher in JAK2V617F-positive patients compared to other genotypes.
  • Total JAK2 and PD-L1 mRNA levels were lower in post-ET-MF patients than in ET patients, inversely correlating with bone marrow fibrosis grade.
  • A weak correlation was observed between PD-L1 mRNA levels and JAK2V617F VAF.

Conclusions:

  • The observed decrease in JAK2 and PD-L1 mRNA levels during ET progression to post-ET-MF may indicate reduced proliferative potential of the JAK2V617F clone and diminished PD-L1-mediated immunosuppression.
  • Bone marrow fibrosis grade is a key factor influencing JAK2 and PD-L1 mRNA levels in MPN progression.