Characteristics, outcomes, prognostic factors and treatment of patients with T-cell prolymphocytic leukemia (T-PLL)

Jain, Preetesh; Aoki, Etsuko; Keating, Michael J.; Wierda, William G.; O’Brien, Susan; González, Graciela Nogueras; Ferrajoli, Alessandra; Jain, Nitin; Thompson, Philip A.; Jabbour, Elias; Kanagal‐Shamanna, Rashmi; Pierce, Sherry; Alousi, Amin M.; Hosing, Chitra; Khouri, Issa F.; Estrov, Zeev; Cortes, Jorge; Kantarjian, Hagop M.; Ravandi, Farhad; Kadia, Tapan M.

doi:10.1093/annonc/mdx163

Cited by 51 publications

(57 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…T‐cell PLL is an usually aggressive disease presenting with high mortality rate . The patient described in this report had an unusual presentation with no symptoms with unexpected discovery of a T‐prolymphocytic clone.…”

Section: Discussionmentioning

confidence: 78%

Clinically silent indolent T‐cell leukemia

Janot

Feriel

Borie

et al. 2018

Clinical Case Reports

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 78%

Clinically silent indolent T‐cell leukemia

Janot

Feriel

Borie

et al. 2018

Clinical Case Reports

View full text Add to dashboard Cite

show abstract

“…4 The only curative approach for T-PLL remains allogeneic hematopoietic stem cell transplantation (HSCT), but even in this setting, the benefit of HSCT is based on a few retrospective series 5 and is not confirmed in all studies. 6 In a recent prospective observational study from the European Society for Blood and Marrow Transplantation that enrolled 54 patients blood® 3 OCTOBER 2019 | VOLUME 134, NUMBER 14 1113 (62% in complete remission) who received a transplant between 2007 and 2012, the 4-year progression-free survival was 30%, confirming that HSCT may result in long-term disease control in a limited proportion of patients, 7 likely because of a graft-versus-leukemia effect. 8 Novel treatment strategies for T-PLL are urgently needed; candidate agents in clinical development for T-PLL include anti-BCL2 (alone 9 or in combination with ibrutinib [NCT03873493]), JAK/STAT pathway inhibitors (eg, combined tofacitinib and ruxolitinib, 10 or itacitinib [NCT03989466]), and anti-histone deacetylase (eg, romidepsin [NCT02512497]).…”

Section: T-pll Was Recognized By the 2016 Worldmentioning

confidence: 96%

T-PLL: harmonizing criteria for research

Risitano¹

2019

Blood

View full text Add to dashboard Cite

show abstract

“…β2m is expressed in almost all nucleated cells . Elevated β2m levels suggest the presence of disease because high β2m expression levels in tissue, serum or urine can be used as a significant prognostic marker for various cancers such as haematological tumours, gallbladder cancer, cervical cancer, ovarian cancer, prostate cancer and others . β2m is non‐covalently bound to the α‐chain of MHC class I molecules on the surface of tumour cells.…”

Section: Role Of the Mhc Class I‐lilrb1 Interaction In Cancermentioning

confidence: 99%

The MHC class I‐LILRB1 signalling axis as a promising target in cancer therapy

et al. 2019

View full text Add to dashboard Cite

Immune checkpoint inhibitors are among the newest, cutting-edge methods for the treatment of cancer. Currently, they primarily influence T cell adaptive immunotherapy targeting the PD-1/PD-L1 and CTLA-4/B7 signalling pathways. These inhibitors fight cancer by reactivating the patient's own adaptive immune system, with good results in many cancers. With the discovery of the "Don't Eat Me" molecule, CD47, antibody-based drugs that target the macrophage-related innate immunosuppressive signalling pathway, CD47-SIRPα, have been developed and have achieved stunning results in the laboratory and the clinic, but there remain unexplained instances of tumour immune escape. While investigating the immunological tolerance of cancer to anti-CD47 antibodies, a second "Don't Eat Me" molecule on tumour cells, beta 2 microglobulin (β2m), a component of MHC class I, was described. Some tumour cells reduce their surface expression of MHC class I to escape T cell recognition.However, other tumour cells highly express β2m complexed with the MHC class I heavy chain to send a "Don't Eat Me" signal by binding to leucocyte immunoglobulin-like receptor family B, member 1 (LILRB1) on macrophages, leading to a loss of immune surveillance. Investigating the mechanisms underlying this immunosuppressive MHC class I-LILRB1 signalling axis in tumour-associated macrophages will be useful in developing therapies to restore macrophage function and control MHC class I signalling in patient tumours. The goal is to promote adaptive immunity while suppressing the innate immune response to tumours. This work will identify new therapeutic targets for the development of pharmaceutical-based tumour immunotherapy.

show abstract

Characteristics, outcomes, prognostic factors and treatment of patients with T-cell prolymphocytic leukemia (T-PLL)

Abstract: Outcomes in T-PLL remain poor. Multicenter collaborative effort is required to conduct prospective studies.

Cited by 51 publications

References 40 publications

Clinically silent indolent T‐cell leukemia

Clinically silent indolent T‐cell leukemia

T-PLL: harmonizing criteria for research

The MHC class I‐LILRB1 signalling axis as a promising target in cancer therapy

Contact Info

Product

Resources

About