Guidelines on the investigation and management of thrombophilia. The British Committee for Standards in Haematology.

doi:10.1136/jcp.43.9.703

Cited by 58 publications

(2 citation statements)

References 37 publications

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“…Death receptors DR4 and DR5 were detected on the surface of both U266 and BTZ‐resistant PS‐R cells after CPT/BTZ treatment. Compared to controls, DR4 endocytosis was markedly increased in cells exposed to both agents, whereas only modest effects on DR5 in both U266 and PS‐R cells, in contrast to findings in solid tumor 29 and myeloma cells 30 exposed to BTZ and TRAIL in which DR5 was implicated in cell death. Our findings implicate endocytosis of DR4, but not DR5, in CPT/BTZ‐mediated apoptosis in MM cells.…”

Section: Discussioncontrasting

confidence: 59%

Mechanisms underlying synergism between circularized tumor necrosis factor‐related apoptosis inducing ligand and bortezomib in bortezomib‐sensitive or ‐resistant myeloma cells

Leng

et al. 2022

Hematological Oncology

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Mechanisms underlying interactions between a novel, clinically relevant circularized tumor necrosis factor-related apoptosis inducing ligand (TRAIL) agonist, circularly permuted TRAIL (CPT) have been examined in multiple myeloma (MM) cells sensitive or resistant to bortezomib (BTZ). Various MM cell lines for example, U266, including those resistant to bortezomib-resistant U266 cells were exposed to low nanomolar concentrations of bortezomib � CPT and apoptosis monitored. Circularly permuted TRAIL and bortezomib synergistically induced apoptosis in both BTZ-naïve and -resistant cells. The regimen up-regulated DR4 receptor internalization in MM cells, known to modulate both NF-κB and extrinsic apoptotic pathways. CPT/BTZ disrupted the non-canonical NF-κB pathway, reflected by tumor necrosis factor (TNF) receptor associated factors 3 (TRAF3) up-regulation, NF-κB inducing kinase down-regulation, diminished p52 and p50 processing, and B-cell lymphoma-extra large (BCL-XL) down-regulation, but failed to inactivate the canonical NF-κB pathway, reflected by unchanged or increased expression of phospho-p65. The regimen also sharply increased extrinsic apoptotic pathway activation. Cells exhibiting TRAF3 knock-down, dominant-negative Fas-associated protein with death domain, knock-down of caspase-8, BCL-2/BCL-XL, or exposure to a caspase-9 inhibitor displayed markedly reduced CPT/BTZ sensitivity. Concordant results were observed in bortezomib-resistant cells. The regimen was also active in the presence of stromal cells and was relatively sparing toward normal CD34 + hematopoietic cells. Finally, ex vivo results revealed synergism in primary MM primary cells, including those BTZ, and the CPT/BTZ regimen significantly

show abstract

Section: Discussioncontrasting

confidence: 59%

Mechanisms underlying synergism between circularized tumor necrosis factor‐related apoptosis inducing ligand and bortezomib in bortezomib‐sensitive or ‐resistant myeloma cells

Leng

et al. 2022

Hematological Oncology

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“…In heterozygous AT III deficiency, about 50% of asymptomatic family members develop the first thrombotic event before age of 25 years [13]. Thrombosis is uncommon in infancy and childhood, but the incidence rises sharply between 15 and 30 years of age [2] [14].…”

Section: Discussionmentioning

confidence: 99%

Multiple Major Thrombo-Embolic Events, including Stroke, in a Patient with Combined Congenital Anti-Thrombin III Deficiency and MTHFR Homozygous Mutation

Zaid¹,

Abbas²,

Shaker³

et al. 2017

WJCD

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We report a case of a young male patient suffering from congenital AntiThrombin III (AT III) deficiency, presented with four major thrombotic events. These events were acute coronary syndrome (Non-ST elevation myocardial infarction), cerebral infarction, peripheral acute upper limb (UL) ischemia and bilateral extensive deep venous thrombosis. The latter two developed despite that the patient was receiving full anticoagulation therapy. His International normalized ratio (INR) was 2.5. Eventually, the patient developed pulmonary embolism and died. He had a prominent family history of thrombotic events. Screening for AT III deficiency in young patients with thrombotic event (thrombophilia) is essential especially those having family history of the latter. This is justified as thrombotic events may occur in up to 80% of these patients. Our patient with 4 major thrombotic events ending in fatality in less than 1 month deserves the nomenclature.

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The Parturient with Co‐Existing Disease

Groves¹,

Avidan²

2002

Anaesthesia for Obstetrics and Gynaecology

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Guidelines on the investigation and management of thrombophilia. The British Committee for Standards in Haematology.

Cited by 58 publications

References 37 publications

Mechanisms underlying synergism between circularized tumor necrosis factor‐related apoptosis inducing ligand and bortezomib in bortezomib‐sensitive or ‐resistant myeloma cells

Mechanisms underlying synergism between circularized tumor necrosis factor‐related apoptosis inducing ligand and bortezomib in bortezomib‐sensitive or ‐resistant myeloma cells

Multiple Major Thrombo-Embolic Events, including Stroke, in a Patient with Combined Congenital Anti-Thrombin III Deficiency and MTHFR Homozygous Mutation

The Parturient with Co‐Existing Disease

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