Peripheral T cell lymphoma: Difference between revisions
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==Classification== | ==Classification== | ||
* | * | ||
: | clinical trials. | ||
: | == Classification == | ||
In 2008, WHO classified peripheral T cell lymphoma in 4 groups ( cutaneous, nodal, extra nodal and leukemic) based on their clinical manifestations . | |||
In which the majority of aggressive T-cell lymphomas have been included in the nodal, extranodal, and leukemic groups. | |||
The nodal lymphoma consists of 3 entities which include :PTCL, not otherwise specified (NOS) which is the most common subtype accounting for 25.9% of cases, <ref>{{cite journal|title=International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study: Pathology Findings and Clinical Outcomes|journal=Journal of Clinical Oncology|volume=26|issue=25|year=2008|pages=4124–4130|issn=0732-183X|doi=10.1200/JCO.2008.16.4558}}</ref> anaplastic large cell lymphoma (ALCL), and angioimmunoblastic T-cell lymphoma (AITL). | |||
Anaplastic large cell lymphoma (ALCS) has two recognized sub groups: ALK+ and ALK- lymphomas. Both subtypes are morphologially and immunophenotypically similar to each other however they are different molecularly. <ref name="SalaverriaBeà2008">{{cite journal|last1=Salaverria|first1=Itziar|last2=Beà|first2=Silvia|last3=Lopez-Guillermo|first3=Armando|last4=Lespinet|first4=Virginia|last5=Pinyol|first5=Magda|last6=Burkhardt|first6=Birgit|last7=Lamant|first7=Laurence|last8=Zettl|first8=Andreas|last9=Horsman|first9=Doug|last10=Gascoyne|first10=Randy|last11=Ott|first11=German|last12=Siebert|first12=Reiner|last13=Delsol|first13=Georges|last14=Campo|first14=Elias|title=Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas|journal=British Journal of Haematology|volume=140|issue=5|year=2008|pages=516–526|issn=0007-1048|doi=10.1111/j.1365-2141.2007.06924.x}}</ref>They have similar incidences (6.6% and 5.5% respectively) <ref>{{cite journal|title=International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study: Pathology Findings and Clinical Outcomes|journal=Journal of Clinical Oncology|volume=26|issue=25|year=2008|pages=4124–4130|issn=0732-183X|doi=10.1200/JCO.2008.16.4558}}</ref> | |||
Angioimmunoblastic T-cell lymphoma (AITL) comprises 18.5% of cases .<ref>{{cite journal|title=International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study: Pathology Findings and Clinical Outcomes|journal=Journal of Clinical Oncology|volume=26|issue=25|year=2008|pages=4124–4130|issn=0732-183X|doi=10.1200/JCO.2008.16.4558}}</ref> One of its variants ,lymphoepithelioid cell variant is consists of CD8 T cells with epithelioid cells in the background which is different than other variants. <ref name="GeissingerOdenwald2004">{{cite journal|last1=Geissinger|first1=Eva|last2=Odenwald|first2=Tobias|last3=Lee|first3=Seung-Sook|last4=Bonzheim|first4=Irina|last5=Roth|first5=Sabine|last6=Reimer|first6=Peter|last7=Wilhelm|first7=Martin|last8=M�ller-Hermelink|first8=Hans Konrad|last9=R�diger|first9=Thomas|title=Nodal peripheral T-cell lymphomas and, in particular, their lymphoepithelioid (Lennert?s) variant are often derived from CD8+ cytotoxic T-cells|journal=Virchows Archiv|volume=445|issue=4|year=2004|pages=334–343|issn=0945-6317|doi=10.1007/s00428-004-1077-2}}</ref> | |||
Less common entities have been described in extra nodal groups. Tissue tropism has been the characterized distinguishing factor. | |||
First subtype which comprises around 1.4% of PTCL cases <ref>{{cite journal|title=International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study: Pathology Findings and Clinical Outcomes|journal=Journal of Clinical Oncology|volume=26|issue=25|year=2008|pages=4124–4130|issn=0732-183X|doi=10.1200/JCO.2008.16.4558}}</ref>and almost always is reported in children and young adults <ref name="pmid10692026">{{cite journal| author=Charton-Bain MC, Brousset P, Bouabdallah R, Gaulard P, Merlio JP, Dubus P et al.| title=Variation in the histological pattern of nodal involvement by gamma/delta T-cell lymphoma. | journal=Histopathology | year= 2000 | volume= 36 | issue= 3 | pages= 233-9 | pmid=10692026 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10692026 }}</ref>is Hepatosplenic γδ T-cell lymphoma. In this tumor, immature or nonactivated γδ T cells infiltrate bone marrow sinusoides and spleen and Isochromosome 7q chromosomal abnormality is present. | |||
In second subgroup, which is hepatosplenic T-cell lymphoma has often poor prognoses with median survival of below 2 years. Patients usually present with B-symptoms and decreased cell counts. The cells express CD2, CD3 and CD7 markers and lack CD4, CD5 . while CD8 and natural killer cell markers expression are variable . | |||
The third sub-type , Enteropathy-associated T-cell lymphoma (EATL) is more common in populations with high incidence of celiac disease and accounts for 4.7% of cases of T-cell lymphoma. Pain, weight loss, and bowel perforation are the usual clinical presentations. Two morphological variants have been recognized ; pleomorphic and monomorphic. The former group is associated with celiac disease the cells usually express CD3 and CD7 and lack CD56 expression <ref name="ZettldeLeeuw2007">{{cite journal|last1=Zettl|first1=Andreas|last2=deLeeuw|first2=Ron|last3=Haralambieva|first3=Eugenia|last4=Mueller-Hermelink|first4=Hans-Konrad|title=Enteropathy-Type T-Cell Lymphoma|journal=American Journal of Clinical Pathology|volume=127|issue=5|year=2007|pages=701–706|issn=0002-9173|doi=10.1309/NW2BK1DXB0EQG55H}}</ref>. Conversely, The latter group is often not associated with the celiac disease and express CD56. Gains at chromosome 9q33-q34 has been reported in up to 70% of cases<ref name="ZettlOtt2002">{{cite journal|last1=Zettl|first1=Andreas|last2=Ott|first2=German|last3=Makulik|first3=Angela|last4=Katzenberger|first4=Tiemo|last5=Starostik|first5=Petr|last6=Eichler|first6=Thorsten|last7=Puppe|first7=Bernhard|last8=Bentz|first8=Martin|last9=Müller-Hermelink|first9=Hans Konrad|last10=Chott|first10=Andreas|title=Chromosomal Gains at 9q Characterize Enteropathy-Type T-Cell Lymphoma|journal=The American Journal of Pathology|volume=161|issue=5|year=2002|pages=1635–1645|issn=00029440|doi=10.1016/S0002-9440(10)64441-0}}</ref>. | |||
Furthermore, the intestinal T- and NK-cell lymphomas are part of the nasal-type NK-/T-cell lymphoma<ref name="AuWeisenburger2008">{{cite journal|last1=Au|first1=W.-y.|last2=Weisenburger|first2=D. D.|last3=Intragumtornchai|first3=T.|last4=Nakamura|first4=S.|last5=Kim|first5=W.-S.|last6=Sng|first6=I.|last7=Vose|first7=J.|last8=Armitage|first8=J. O.|last9=Liang|first9=R.|title=Clinical differences between nasal and extranasal natural killer/T-cell lymphoma: a study of 136 cases from the International Peripheral T-Cell Lymphoma Project|journal=Blood|volume=113|issue=17|year=2008|pages=3931–3937|issn=0006-4971|doi=10.1182/blood-2008-10-185256}}</ref> which have been reported in Asian countries and are associated with Epstein-Barr virus (EBV) infection . | |||
In addition, The mucocutaneous γδ T-cell lymphomas<ref name="ShapiraCaspi2009">{{cite journal|last1=Shapira|first1=Michael Y.|last2=Caspi|first2=Ofer|last3=Amir|first3=Gail|last4=Zlotogorski|first4=Abraham|last5=Naparstek|first5=Yaakov|title=Gastric-Mucocutaneous γδ T Cell Lymphoma: Possible Association with Epstein-Barr Virus ?|journal=Leukemia & Lymphoma|volume=35|issue=3-4|year=2009|pages=397–401|issn=1042-8194|doi=10.3109/10428199909145745}}</ref>,the nasal type NK-/T-cell lymphomas, and even ALCLs all can present as an intestinal lymphoma<ref name="KanavarosBoulland2009">{{cite journal|last1=Kanavaros|first1=P.|last2=Boulland|first2=M. L.|last3=Petit|first3=B.|last4=Arnulf|first4=B.|title=Expression of Cytotoxic Proteins in Peripheral T-Cell and Natural Killer-Cell (NK) Lymphomas: Association with Extranodal Site, NK or Tγδ Phenotype, Anaplastic Morphology and CD30 Expression|journal=Leukemia & Lymphoma|volume=38|issue=3-4|year=2009|pages=317–326|issn=1042-8194|doi=10.3109/10428190009087022}}</ref>. | |||
Panniculitis-like T-cell lymphomas constitute only 0.9% of PTCLs which is more common in males. The characteristic clinical presentation is subcutaneous nodules that can become necrotic .The cells express CD3 and CD8 and are CD4- .<ref name="Toro2003">{{cite journal|last1=Toro|first1=J. R.|title=Gamma-delta T-cell phenotype is associated with significantly decreased survival in cutaneous T-cell lymphoma|journal=Blood|volume=101|issue=9|year=2003|pages=3407–3412|issn=00064971|doi=10.1182/blood-2002-05-1597}}</ref> | |||
The last group,leukemia has 4 subtypes including adult T-cell lymphoma (ATL) associated with human T-lymphotropic virus type I (HTLV-1), T-cell chronic large granular lymphocytic (LGL) leukemia associated with neutropenia , aggressive NK-cell leukemia, and T-cell prolymphocytic leukemia. . NK-cell leukemia and ATL often have a poor outcome. | |||
Other types which have been included in WHO classifications include: hydroa vacciniforme-like lymphoma, NK-cell lymphoma and systemic EBV-positive T-cell lymphoproliferative disease of childhood. | |||
==Pathophysiology== | ==Pathophysiology== | ||
*The pathogenesis of [disease name] is characterized by [feature1], [feature2], and [feature3]. | *The pathogenesis of [disease name] is characterized by [feature1], [feature2], and [feature3]. | ||
Revision as of 16:58, 18 November 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The peripheral T-cell lymphomas (PTCLs) consists of a heterogeneous group of aggressive diseases that constitutes ~10%-15% of non Hodgkin lymphoma. The incidence has been estimated to be <1 case per 100,000 of ppl in United states. [1]The most common type is Peripheral T cell lymphoma, not otherwise specified (PTCL, NOS), followed by Anaplastic large cell lymphoma, primary systemic type (ALCL) , Angioimmunoblastic T cell lymphoma (AITL) and Extranodal NK/T cell lymphoma, nasal type (PTCLs ), which is the rarest type. Although each type presents differently and has special histological features, they all have similar treatment . In addition, all the types have been associated with poor prognosis. [2] The most common presentation is generalized lymphadenopathy with or without extra nodal manifestations. [3]
Historical Perspective
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
Classification
clinical trials.
Classification
In 2008, WHO classified peripheral T cell lymphoma in 4 groups ( cutaneous, nodal, extra nodal and leukemic) based on their clinical manifestations .
In which the majority of aggressive T-cell lymphomas have been included in the nodal, extranodal, and leukemic groups.
The nodal lymphoma consists of 3 entities which include :PTCL, not otherwise specified (NOS) which is the most common subtype accounting for 25.9% of cases, [4] anaplastic large cell lymphoma (ALCL), and angioimmunoblastic T-cell lymphoma (AITL).
Anaplastic large cell lymphoma (ALCS) has two recognized sub groups: ALK+ and ALK- lymphomas. Both subtypes are morphologially and immunophenotypically similar to each other however they are different molecularly. [5]They have similar incidences (6.6% and 5.5% respectively) [6]
Angioimmunoblastic T-cell lymphoma (AITL) comprises 18.5% of cases .[7] One of its variants ,lymphoepithelioid cell variant is consists of CD8 T cells with epithelioid cells in the background which is different than other variants. [8]
Less common entities have been described in extra nodal groups. Tissue tropism has been the characterized distinguishing factor.
First subtype which comprises around 1.4% of PTCL cases [9]and almost always is reported in children and young adults [10]is Hepatosplenic γδ T-cell lymphoma. In this tumor, immature or nonactivated γδ T cells infiltrate bone marrow sinusoides and spleen and Isochromosome 7q chromosomal abnormality is present.
In second subgroup, which is hepatosplenic T-cell lymphoma has often poor prognoses with median survival of below 2 years. Patients usually present with B-symptoms and decreased cell counts. The cells express CD2, CD3 and CD7 markers and lack CD4, CD5 . while CD8 and natural killer cell markers expression are variable .
The third sub-type , Enteropathy-associated T-cell lymphoma (EATL) is more common in populations with high incidence of celiac disease and accounts for 4.7% of cases of T-cell lymphoma. Pain, weight loss, and bowel perforation are the usual clinical presentations. Two morphological variants have been recognized ; pleomorphic and monomorphic. The former group is associated with celiac disease the cells usually express CD3 and CD7 and lack CD56 expression [11]. Conversely, The latter group is often not associated with the celiac disease and express CD56. Gains at chromosome 9q33-q34 has been reported in up to 70% of cases[12].
Furthermore, the intestinal T- and NK-cell lymphomas are part of the nasal-type NK-/T-cell lymphoma[13] which have been reported in Asian countries and are associated with Epstein-Barr virus (EBV) infection .
In addition, The mucocutaneous γδ T-cell lymphomas[14],the nasal type NK-/T-cell lymphomas, and even ALCLs all can present as an intestinal lymphoma[15].
Panniculitis-like T-cell lymphomas constitute only 0.9% of PTCLs which is more common in males. The characteristic clinical presentation is subcutaneous nodules that can become necrotic .The cells express CD3 and CD8 and are CD4- .[16]
The last group,leukemia has 4 subtypes including adult T-cell lymphoma (ATL) associated with human T-lymphotropic virus type I (HTLV-1), T-cell chronic large granular lymphocytic (LGL) leukemia associated with neutropenia , aggressive NK-cell leukemia, and T-cell prolymphocytic leukemia. . NK-cell leukemia and ATL often have a poor outcome.
Other types which have been included in WHO classifications include: hydroa vacciniforme-like lymphoma, NK-cell lymphoma and systemic EBV-positive T-cell lymphoproliferative disease of childhood.
Pathophysiology
- The pathogenesis of [disease name] is characterized by [feature1], [feature2], and [feature3].
- The [gene name] gene/Mutation in [gene name] has been associated with the development of [disease name], involving the [molecular pathway] pathway.
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Clinical Features
Differentiating [disease name] from other Diseases
- [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
- [Differential dx1]
- [Differential dx2]
- [Differential dx3]
Epidemiology and Demographics
- The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
- In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].
Age
- Patients of all age groups may develop [disease name].
- [Disease name] is more commonly observed among patients aged [age range] years old.
- [Disease name] is more commonly observed among [elderly patients/young patients/children].
Gender
- [Disease name] affects men and women equally.
- [Gender 1] are more commonly affected with [disease name] than [gender 2].
- The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.
Race
- There is no racial predilection for [disease name].
- [Disease name] usually affects individuals of the [race 1] race.
- [Race 2] individuals are less likely to develop [disease name].
Risk Factors
- Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
Natural History, Complications and Prognosis
- The majority of patients with [disease name] remain asymptomatic for [duration/years].
- Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
- If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
- Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
- Prognosis is generally [excellent/good/poor], and the [1/5/10year mortality/survival rate] of patients with [disease name] is approximately [#%].
Diagnosis
Diagnostic Criteria
- The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
- [criterion 1]
- [criterion 2]
- [criterion 3]
- [criterion 4]
Symptoms
- [Disease name] is usually asymptomatic.
- Symptoms of [disease name] may include the following:
- [symptom 1]
- [symptom 2]
- [symptom 3]
- [symptom 4]
- [symptom 5]
- [symptom 6]
Physical Examination
- Patients with [disease name] usually appear [general appearance].
- Physical examination may be remarkable for:
- [finding 1]
- [finding 2]
- [finding 3]
- [finding 4]
- [finding 5]
- [finding 6]
Laboratory Findings
- There are no specific laboratory findings associated with [disease name].
- A [positive/negative] [test name] is diagnostic of [disease name].
- An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
- Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
Imaging Findings
- There are no [imaging study] findings associated with [disease name].
- [Imaging study 1] is the imaging modality of choice for [disease name].
- On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
- [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
- There is no treatment for [disease name]; the mainstay of therapy is supportive care.
- The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
- [Medical therapy 1] acts by [mechanism of action 1].
- Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
Surgery
- Surgery is the mainstay of therapy for [disease name].
- [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
- [Surgical procedure] can only be performed for patients with [disease stage] [disease name].
Prevention
- There are no primary preventive measures available for [disease name].
- Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
- Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
References
- ↑ Morton, L. M. (2006). "Lymphoma incidence patterns by WHO subtype in the United States, 1992-2001". Blood. 107 (1): 265–276. doi:10.1182/blood-2005-06-2508. ISSN 0006-4971.
- ↑ Moskowitz, A. J.; Lunning, M. A.; Horwitz, S. M. (2014). "How I treat the peripheral T-cell lymphomas". Blood. 123 (17): 2636–2644. doi:10.1182/blood-2013-12-516245. ISSN 0006-4971.
- ↑ . doi:10.1182/blood-2010-09-310342. Check
|doi=value (help). Missing or empty|title=(help) - ↑ "International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study: Pathology Findings and Clinical Outcomes". Journal of Clinical Oncology. 26 (25): 4124–4130. 2008. doi:10.1200/JCO.2008.16.4558. ISSN 0732-183X.
- ↑ Salaverria, Itziar; Beà, Silvia; Lopez-Guillermo, Armando; Lespinet, Virginia; Pinyol, Magda; Burkhardt, Birgit; Lamant, Laurence; Zettl, Andreas; Horsman, Doug; Gascoyne, Randy; Ott, German; Siebert, Reiner; Delsol, Georges; Campo, Elias (2008). "Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas". British Journal of Haematology. 140 (5): 516–526. doi:10.1111/j.1365-2141.2007.06924.x. ISSN 0007-1048.
- ↑ "International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study: Pathology Findings and Clinical Outcomes". Journal of Clinical Oncology. 26 (25): 4124–4130. 2008. doi:10.1200/JCO.2008.16.4558. ISSN 0732-183X.
- ↑ "International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study: Pathology Findings and Clinical Outcomes". Journal of Clinical Oncology. 26 (25): 4124–4130. 2008. doi:10.1200/JCO.2008.16.4558. ISSN 0732-183X.
- ↑ Geissinger, Eva; Odenwald, Tobias; Lee, Seung-Sook; Bonzheim, Irina; Roth, Sabine; Reimer, Peter; Wilhelm, Martin; M�ller-Hermelink, Hans Konrad; R�diger, Thomas (2004). "Nodal peripheral T-cell lymphomas and, in particular, their lymphoepithelioid (Lennert?s) variant are often derived from CD8+ cytotoxic T-cells". Virchows Archiv. 445 (4): 334–343. doi:10.1007/s00428-004-1077-2. ISSN 0945-6317. replacement character in
|last8=at position 2 (help); replacement character in|last9=at position 2 (help) - ↑ "International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study: Pathology Findings and Clinical Outcomes". Journal of Clinical Oncology. 26 (25): 4124–4130. 2008. doi:10.1200/JCO.2008.16.4558. ISSN 0732-183X.
- ↑ Charton-Bain MC, Brousset P, Bouabdallah R, Gaulard P, Merlio JP, Dubus P; et al. (2000). "Variation in the histological pattern of nodal involvement by gamma/delta T-cell lymphoma". Histopathology. 36 (3): 233–9. PMID 10692026.
- ↑ Zettl, Andreas; deLeeuw, Ron; Haralambieva, Eugenia; Mueller-Hermelink, Hans-Konrad (2007). "Enteropathy-Type T-Cell Lymphoma". American Journal of Clinical Pathology. 127 (5): 701–706. doi:10.1309/NW2BK1DXB0EQG55H. ISSN 0002-9173.
- ↑ Zettl, Andreas; Ott, German; Makulik, Angela; Katzenberger, Tiemo; Starostik, Petr; Eichler, Thorsten; Puppe, Bernhard; Bentz, Martin; Müller-Hermelink, Hans Konrad; Chott, Andreas (2002). "Chromosomal Gains at 9q Characterize Enteropathy-Type T-Cell Lymphoma". The American Journal of Pathology. 161 (5): 1635–1645. doi:10.1016/S0002-9440(10)64441-0. ISSN 0002-9440.
- ↑ Au, W.-y.; Weisenburger, D. D.; Intragumtornchai, T.; Nakamura, S.; Kim, W.-S.; Sng, I.; Vose, J.; Armitage, J. O.; Liang, R. (2008). "Clinical differences between nasal and extranasal natural killer/T-cell lymphoma: a study of 136 cases from the International Peripheral T-Cell Lymphoma Project". Blood. 113 (17): 3931–3937. doi:10.1182/blood-2008-10-185256. ISSN 0006-4971.
- ↑ Shapira, Michael Y.; Caspi, Ofer; Amir, Gail; Zlotogorski, Abraham; Naparstek, Yaakov (2009). "Gastric-Mucocutaneous γδ T Cell Lymphoma: Possible Association with Epstein-Barr Virus ?". Leukemia & Lymphoma. 35 (3–4): 397–401. doi:10.3109/10428199909145745. ISSN 1042-8194.
- ↑ Toro, J. R. (2003). "Gamma-delta T-cell phenotype is associated with significantly decreased survival in cutaneous T-cell lymphoma". Blood. 101 (9): 3407–3412. doi:10.1182/blood-2002-05-1597. ISSN 0006-4971.