T-cell prolymphocytic leukemia
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Synonyms and keywords: T-cell chronic lymphocytic leukemia; “Knobby” type of T-cell leukemia; T-prolymphocytic leukemia/T-cell lymphocytic leukemia- Kiel; T-PLL
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2]
Synonyms and keywords: T-cell chronic lymphocytic leukemia; “Knobby” type of T-cell leukemia; T-prolymphocytic leukemia/T-cell lymphocytic leukemia- Kiel; T-PLL
Overview
T-cell-prolymphocytic leukemia (also known as T-PLL) is a rare, mature T-cell leukemia with aggressive behavior and predilection for blood, bone marrow, lymph nodes, liver, spleen, and skin. T-cell prolymphocytic leukemia was first described by Catovsky in 1973. There is no classification system for T-cell prolymphocytic leukemia. The inversion of chromosome 14 (14q11) has been associated with the development of T-cell prolymphocytic leukemia. T-cell prolymphocytic leukemia is very rare, and it represents 2% of all small lymphocytic leukemias in adults. T-cell prolymphocytic leukemia is more commonly observed among young adult patients aged between 30 to 40 years old. Males are slightly more affected with are more commonly affected with T-cell prolymphocytic leukemia than females. Laboratory findings consistent with the diagnosis of T-cell prolymphocytic leukemia, include high lymphocyte count (> 100 x 109/L), anemia, thrombocytopenia, and negative HTLV-1 serology. There are no specific imaging findings associated with T-cell prolymphocytic leukemia. Prognosis is generally poor, and the median survival time of patients with T-cell prolymphocytic leukemia is approximately 7 months. The mainstay of therapy for T-cell prolymphocytic leukemia is alemtuzumab (anti-CD52). However, T-cell prolymphocytic leukemia is often resistant to therapy. Autologous and allogeneic stem cell transplants is the mainstay of therapy for patients who achieve remission.
Historical Perspective
T-cell prolymphocytic leukemia was first described 40 years ago and was classified in 1994.
Classification
T-cell prolymphocytic leukemia is classified into three variants based on its morphology.
Pathophysiology
T-PLL has the immunophenotype of a mature (post-thymic) T-lymphocyte, and the neoplastic cells are typically positive for pan-T antigens. Clonal TCR gene rearrangements for the γ and δ chains are typically found. It arises from mature (post-thymic) T-cell, which are normally involved in in cell-mediated immunity. On microscopic histopathological analysis, T-cell prolymphocytic leukemia has characteristic findings. In the peripheral blood, T-PLL consists of medium-sized lymphocytes with single nucleoli and basophilic cytoplasm with occasional blebs or projections. Different variants of T-cell lymphocytic leukemias can be differentiated based on the microscopic and gross finding.
Causes
T-cell prolymphocytic leukemia is caused by gene mutations and chromosomal abnormalities. Details of which are described below.
Differentiating Xyz from Other Diseases
T-cell prolymphocytic leukemia presents with Lymphadenopathy, hepatomegaly, and fever which are also presenting symptoms of a number of other conditions.
Epidemiology and Demographics
T-cell prolymphocytic leukemia is a rare condition. Its incidence increases with age, with ataxia telangiectasia, the median age at diagnosis is 30 years.
Risk Factors
There are no identified risk factors of T-cell prolymphocytic leukemia.
Screening
Screening for T-cell prolymphocytic leukemia is not done.
Natural History, Complications, and Prognosis
T-cell prolymphocytic leukemia is diagnosed after its symptoms appear. Failure to treat can result in multiple organ failure.
Diagnosis
There is no established diagnostic criteria.
History and Symptoms
T-cell prolymphocytic leukemia presents with fever, weight loss and night sweats.
Treatment
T-cell prolymphocytic leukemia responds better when combinations of chemotherapy drugs are used. Monoclonal antibodies are a type of biological therapy that has been effective in treating certain types of leukemias. Splenectomy and external beam radiation therapy to the spleen may be used in some people with prolymphocytic leukemia.
Primary Prevention
There are no established measures for the primary prevention of T-cell prolymphocytic leukemia.
Secondary Prevention
There are no established measures for the secondary prevention of T-cell prolymphocytic leukemia.
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Overview
T-cell prolymphocytic leukemia was first described 40 years ago and was classified in 1994.
Historical Perspective
- 40 years ago, in 1973, Catovsky first described four cases of T-cell prolymphocytic leukemia.[1][2]
- In 1994, Harris a pathologist from Boston and his colleagues made an effort to classify T-cell prolymphocytic leukemia.[3]
References
- ↑ Catovsky D, Galetto J, Okos A, Galton DA, Wiltshaw E, Stathopoulos G (August 1973). “Prolymphocytic leukaemia of B and T cell type”. Lancet. 2 (7823): 232–4. PMID 4124423.
- ↑ Sud A, Dearden C (April 2017). “T-cell Prolymphocytic Leukemia”. Hematol. Oncol. Clin. North Am. 31 (2): 273–283. doi:10.1016/j.hoc.2016.11.010. PMID 28340878.
- ↑ Harris NL, Jaffe ES, Stein H, Banks PM, Chan JK, Cleary ML, Delsol G, De Wolf-Peeters C, Falini B, Gatter KC (September 1994). “A revised European-American classification of lymphoid neoplasms: a proposal from the International Lymphoma Study Group”. Blood. 84 (5): 1361–92. PMID 8068936.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Overview
T-cell prolymphocytic leukemia is classified into three variants based on its morphology.
Classification
T-cell prolymphocytic leukemia classification is based on its morphology. [1][2][3][4]
| Morphological Variant | Percentage of total number |
|---|---|
| Typical T-cell prolymphocytic leukemia | 75 percent |
| Small cell variant | 20 percent |
| Cerebriform (Sézary cell-like) variant | 5 percent |
References
- ↑ Graham RL, Cooper B, Krause JR (2013). “T-cell prolymphocytic leukemia”. Proc (Bayl Univ Med Cent). 26 (1): 19–21. PMC 3523759. PMID 23382603.
- ↑ Swerdlow SH, Campo E, Pileri SA, Harris NL, Stein H, Siebert R, Advani R, Ghielmini M, Salles GA, Zelenetz AD, Jaffe ES (May 2016). “The 2016 revision of the World Health Organization classification of lymphoid neoplasms”. Blood. 127 (20): 2375–90. doi:10.1182/blood-2016-01-643569. PMC 4874220. PMID 26980727.
- ↑ Matutes E, Brito-Babapulle V, Swansbury J, Ellis J, Morilla R, Dearden C, Sempere A, Catovsky D (December 1991). “Clinical and laboratory features of 78 cases of T-prolymphocytic leukemia”. Blood. 78 (12): 3269–74. PMID 1742486.
- ↑ Foucar K (April 2007). “Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome”. Am. J. Clin. Pathol. 127 (4): 496–510. doi:10.1309/KWJYBCCGTB90B6AE. PMID 17369126.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Overview
T-PLL has the immunophenotype of a mature (post-thymic) T-lymphocyte, and the neoplastic cells are typically positive for pan-T antigens. Clonal TCR gene rearrangements for the γ and δ chains are typically found.It arises from mature (post-thymic) T-cell, which are normally involved in in cell-mediated immunity. On microscopic histopathological analysis, T-cell prolymphocytic leukemia has characteristic findings. In the peripheral blood, T-PLL consists of medium-sized lymphocytes with single nucleoli and basophilic cytoplasm with occasional blebs or projections. Different variants of T-cell lymphocytic leukemias can be differentiated based on the microscopic and gross finding.
Pathophysiology
It is postulated that the originating cell line for this disease is a mature (post-thymic) T-cell. Due to the systemic nature of this disease, leukemic cells can be found in peripheral blood, lymph nodes, bone marrow, spleen, liver, skin.
Molecular Findings
Immunophenotype
T-PLL has the immunophenotype of a mature (post-thymic) T-lymphocyte, and the neoplastic cells are typically positive for pan-T antigens CD2, CD3, and CD7 and negative for TdT and CD1a. The immunophenotype CD4+/CD8– is present in 60% of cases, the CD4+/CD8+ immunophenotype is present in 25%, and the CD4-/CD8+ immunophenotype is present in 15% of cases.
Genetic Findings
Clonal TCR gene rearrangements for the γ and δ chains are typically found. The most frequent chromosomal abnormality is the inversion of chromosome 14, specifcally inv 14(q11;q32). This is found in 80% of cases, while 10% of cases show a reciprocal translocation of chromosome 14 (t(14;14)(q11;q32)). [1]
[2] Also, abnormalities of chromosome 8 are seen approximately 75% of patients, including idic (8p11), t(8;8)(p11-12;q12), and trisomy 8. [3]
- T-cell prolymphocytic leukemia is a uncommon T- cell malignancy.
- It arises from mature (post-thymic) T-cell, which are normally involved in in cell-mediated immunity.[4]
- It is a relatively aggressive malignancy, characterized by marked lymphocytosis and involving peripheral blood, liver, spleen and bone marrow.[5]
- Factors playing role in the pathogenesis of these cells are:[6][7][8][9]
- Mutations in chromosome 14
- Mutations in chromosome 8
- Mutations in tumor suppressor gene 11q23, at the ataxia telangiectasia mutated (ATM) locus
- Inversion of chromosome 14 (14q11)
- TCR gene rearrangements for the γ and δ chains
| Factors Involved in the Pathophysiology of T-cell Pro-Lymphocytic Leukemia | |||||||||||||||||||||||||||||||||||
| Genetic Factors | Association with different Immunophenotypes | ||||||||||||||||||||||||||||||||||
Different types of genetic abnormalities are as follows, mostly involve chromosme 14:[6][10][11][12][13]
Chromosome 8 defects:[11] | T-cell prolymphocytic leukemia cells express different markers including:
Pan-T cell markers such as: | ||||||||||||||||||||||||||||||||||
Microscopic Pathology
- On gross pathology, characteristic findings of T-cell prolymphocytic leukemia has no remarkable finding.
- On microscopic histopathological analysis, characteristic findings of T-cell prolymphocytic leukemia include:[18]
Marrow involvement is typically diffuse with morphology similar to what is observed in peripheral blood. In the spleen, the leukemic cell infiltrate both the red pulp and white pulp, and lymph node involvement is typically diffuse through the paracortex. Skin infiltrates are seen in 20% of patients, and the infiltrates are usually dense and confined to the dermis and around the skin appendages.
In the peripheral blood, T-PLL consists of medium-sized lymphocytes with single nucleoli and basophilic cytoplasm with occasional blebs or projections. The nuclei are usually round to oval in shape, with occasional patients having cells with a more irregular nuclear outline that is similar to the cerebriform nuclear shape seen in Sézary syndrome.[19] A small cell variant comprises 20% of all T-PLL cases, and the Sézary cell-like (cerebriform) variant is seen in 5% of cases.[19]
- On microscopic histopathological analysis, characteristic findings of T-cell prolymphocytic leukemia include:[18]
- The immunophenotype CD4+/CD8– (present in 60% of cases)
- The immunophenotype CD4+/CD8+ (present in 25%)
- The immunophenotype CD4-/CD8+ (15% of cases) Different variants of T-cell Lymphocytic leukemias can be differentiated based on microscopic and gross finding.[20][21]
| Morphological Variant | Microscopic Findings |
|---|---|
| Typical T-cell
prolymphocytic leukemia |
|
| Small cell variant |
|
| Cerebriform
(Sézary cell-like) variant |
References
- ↑ Brito-Babapulle V, Catovsky D (1991). “Inversions and tandem translocations involving chromosome 14q11 and 14q32 in T-prolymphocytic leukemia and T-cell leukemias in patients with ataxia telangiectasia”. Cancer Genet. Cytogenet. 55 (1): 1–9. PMID 1913594.
- ↑ Maljaei SH, Brito-Babapulle V, Hiorns LR, Catovsky D (1998). “Abnormalities of chromosomes 8, 11, 14, and X in T-prolymphocytic leukemia studied by fluorescence in situ hybridization”. Cancer Genet. Cytogenet. 103 (2): 110–6. PMID 9614908.
- ↑ Sorour A, Brito-Babapulle V, Smedley D, Yuille M, Catovsky D (2000). “Unusual breakpoint distribution of 8p abnormalities in T-prolymphocytic leukemia: a study with YACS mapping to 8p11-p12”. Cancer Genet. Cytogenet. 121 (2): 128–32. PMID 11063795.
- ↑ Sud A, Dearden C (April 2017). “T-cell Prolymphocytic Leukemia”. Hematol. Oncol. Clin. North Am. 31 (2): 273–283. doi:10.1016/j.hoc.2016.11.010. PMID 28340878.
- ↑ Jaffe E.S., Harris N.L., Stein H., Vardiman J.W. (eds): World Health Organization Classification of Tumors. Pathology and Genetics of Tumours of Haemopoietic and Lymphoid Tissues. IARC Press: Lyon 2001
- ↑ 6.0 6.1 6.2 Brito-Babapulle V, Catovsky D (August 1991). “Inversions and tandem translocations involving chromosome 14q11 and 14q32 in T-prolymphocytic leukemia and T-cell leukemias in patients with ataxia telangiectasia”. Cancer Genet. Cytogenet. 55 (1): 1–9. PMID 1913594.
- ↑ 7.0 7.1 Hetet G, Dastot H, Baens M, Brizard A, Sigaux F, Grandchamp B, Stern MH (2000). “Recurrent molecular deletion of the 12p13 region, centromeric to ETV6/TEL, in T-cell prolymphocytic leukemia”. Hematol. J. 1 (1): 42–7. doi:10.1038/sj/thj/6200008. PMID 11920168.
- ↑ 8.0 8.1 Brito-Babapulle V, Hamoudi R, Matutes E, Watson S, Kaczmarek P, Maljaie H, Catovsky D (July 2000). “p53 allele deletion and protein accumulation occurs in the absence of p53 gene mutation in T-prolymphocytic leukaemia and Sezary syndrome”. Br. J. Haematol. 110 (1): 180–7. PMID 10930996.
- ↑ 9.0 9.1 Costa D, Queralt R, Aymerich M, Carrió A, Rozman M, Vallespí T, Colomer D, Nomdedeu B, Montserrat E, Campo E (November 2003). “High levels of chromosomal imbalances in typical and small-cell variants of T-cell prolymphocytic leukemia”. Cancer Genet. Cytogenet. 147 (1): 36–43. PMID 14580769.
- ↑ Maljaei SH, Brito-Babapulle V, Hiorns LR, Catovsky D (June 1998). “Abnormalities of chromosomes 8, 11, 14, and X in T-prolymphocytic leukemia studied by fluorescence in situ hybridization”. Cancer Genet. Cytogenet. 103 (2): 110–6. PMID 9614908.
- ↑ 11.0 11.1 Pekarsky Y, Hallas C, Isobe M, Russo G, Croce CM (March 1999). “Abnormalities at 14q32.1 in T cell malignancies involve two oncogenes”. Proc. Natl. Acad. Sci. U.S.A. 96 (6): 2949–51. PMC 15875. PMID 10077617.
- ↑ Stern MH, Soulier J, Rosenzwajg M, Nakahara K, Canki-Klain N, Aurias A, Sigaux F, Kirsch IR (September 1993). “MTCP-1: a novel gene on the human chromosome Xq28 translocated to the T cell receptor alpha/delta locus in mature T cell proliferations”. Oncogene. 8 (9): 2475–83. PMID 8361760.
- ↑ Hu Z, Medeiros LJ, Fang L, Sun Y, Tang Z, Tang G, Sun T, Quesada AE, Hu S, Wang SA, Pei L, Lu X (May 2017). “Prognostic significance of cytogenetic abnormalities in T-cell prolymphocytic leukemia”. Am. J. Hematol. 92 (5): 441–447. doi:10.1002/ajh.24679. PMID 28194886.
- ↑ Bergmann AK, Schneppenheim S, Seifert M, Betts MJ, Haake A, Lopez C, Maria Murga Penas E, Vater I, Jayne S, Dyer MJ, Schrappe M, Dührsen U, Ammerpohl O, Russell RB, Küppers R, Dürig J, Siebert R (April 2014). “Recurrent mutation of JAK3 in T-cell prolymphocytic leukemia”. Genes Chromosomes Cancer. 53 (4): 309–16. doi:10.1002/gcc.22141. PMID 24446122.
- ↑ Kiel MJ, Velusamy T, Rolland D, Sahasrabuddhe AA, Chung F, Bailey NG, Schrader A, Li B, Li JZ, Ozel AB, Betz BL, Miranda RN, Medeiros LJ, Zhao L, Herling M, Lim MS, Elenitoba-Johnson KS (August 2014). “Integrated genomic sequencing reveals mutational landscape of T-cell prolymphocytic leukemia”. Blood. 124 (9): 1460–72. doi:10.1182/blood-2014-03-559542. PMC 4148768. PMID 24825865.
- ↑ Stilgenbauer S, Schaffner C, Litterst A, Liebisch P, Gilad S, Bar-Shira A, James MR, Lichter P, Döhner H (October 1997). “Biallelic mutations in the ATM gene in T-prolymphocytic leukemia”. Nat. Med. 3 (10): 1155–9. PMID 9334731.
- ↑ Vorechovský I, Luo L, Dyer MJ, Catovsky D, Amlot PL, Yaxley JC, Foroni L, Hammarström L, Webster AD, Yuille MA (September 1997). “Clustering of missense mutations in the ataxia-telangiectasia gene in a sporadic T-cell leukaemia”. Nat. Genet. 17 (1): 96–9. doi:10.1038/ng0997-96. PMID 9288106.
- ↑ 18.0 18.1 Graham RL, Cooper B, Krause JR (2013). “T-cell prolymphocytic leukemia”. Proc (Bayl Univ Med Cent). 26 (1): 19–21. PMC 3523759. PMID 23382603.
- ↑ 19.0 19.1 Matutes E, Garcia Talavera J, O’Brien M, Catovsky D (1986). “The morphological spectrum of T-prolymphocytic leukaemia”. Br. J. Haematol. 64 (1): 111–24. PMID 3489482.
- ↑ Matutes E, Brito-Babapulle V, Swansbury J, Ellis J, Morilla R, Dearden C, Sempere A, Catovsky D (December 1991). “Clinical and laboratory features of 78 cases of T-prolymphocytic leukemia”. Blood. 78 (12): 3269–74. PMID 1742486.
- ↑ Ravandi F, O’Brien S (December 2005). “Chronic lymphoid leukemias other than chronic lymphocytic leukemia: diagnosis and treatment”. Mayo Clin. Proc. 80 (12): 1660–74. doi:10.4065/80.12.1660. PMID 16342661.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Overview
T-cell prolymphocytic leukemia is caused by gene mutations and chromosomal abnormalities. Details of which are described below.
Causes
Common causes of T-cell prolymphocytic leukemia, include genetic factors and chromosomal abnormalities:[1]
References
Differentiating T-cell prolymphocytic leukemia historical perspective from other Diseases
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Overview
T-cell prolymphocytic leukemia presents with Lymphadenopathy, hepatomegaly, and fever which are also presenting symptoms of a number of other conditions.
T-cell prolymphocytic leukemia differential diagnosis
- T-cell prolymphocytic leukemia must be differentiated from other diseases that cause lymphadenopathy, hepatomegaly, and fever, such as:[1]
References
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Overview
T-cell prolymphocytic leukemia is a rare condition. Its incidence increases with age, and with ataxia telangiectasia. The median age at diagnosis is 30 years.
Epidemiology and Demographics
- T-cell prolymphocytic leukemia is very rare, and it represents 2% of all small lymphocytic leukemias in adults.
- The incidence of T-cell prolymphocytic leukemia increases with age; the median age at diagnosis is 65 years.[1]
- Patients with ataxia telangiectasia and T-cell prolymphocytic leukemia are young adults; the median age at diagnosis is 30 years.
- Males are slightly more affected with T-cell prolymphocytic leukemia than females.
- There is no racial predilection for T-cell prolymphocytic leukemia.
- T-PLL is a rare leukemia, primarily affecting adults over the age of 30. It represents 2% of all small lymphocytic leukemias in adults.[2]
References
- ↑ Graham RL, Cooper B, Krause JR (2013). “T-cell prolymphocytic leukemia”. Proc (Bayl Univ Med Cent). 26 (1): 19–21. PMC 3523759. PMID 23382603.
- ↑ Matutes E, Brito-Babapulle V, Swansbury J; et al. (1991). “Clinical and laboratory features of 78 cases of T-prolymphocytic leukemia”. Blood. 78 (12): 3269–74. PMID 1742486.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Overview
There are no identified risk factors of T-cell prolymphocytic leukemia.
Risk Factors
There are no risk factors associated with the development of T-cell prolymphocytic leukemia.[1]
References
Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2]
Overview
Screening for T-cell prolymphocytic leukemia is not done.
Screening
There is insufficient evidence to recommend routine screening for T-cell prolymphocytic leukemia.
References
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2], Maria Fernanda Villarreal, M.D. [3]
Overview
T-cell prolymphocytic leukemia is diagnosed after its symptoms appear. Failure to treat can result in multiple organ failure.
Natural History, Complications and Prognosis
- The majority of patients with T-cell prolymphocytic leukemia are symptomatic at the time of diagnosis.
- Early clinical features include fever, fatigue, and lymphadenopathy.
- If left untreated, patients with T-cell prolymphocytic leukemia may progress to develop multiple organ failure.
- Common complications of T-cell prolymphocytic leukemia, include:[1]
- Prognosis is generally poor, and the median survival time of patients with T-cell prolymphocytic leukemia is approximately one to two years.[1]
- Patients with CD45RO+/CD45RA- immunophenotype tend to have a more indolent course.
- It seems following factors are associated with worse prognosis:
- Increased expression of TCL1
- Increased activity of the serine-threonine kinase AKT
References
T-cell prolymphocytic leukemia Diagnosis
T-cell prolymphocytic leukemia Diagnosis
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