Familial adult T‐cell leukemia/lymphoma

Ratner, Lee; Heyden, Nancy Vander; Paine, Elizabeth; Frei‐Lahr, Debra; Brown, Randy A.; Petruska, Paul J.; Reddy, Satyanarayan; Lairmore, Michael Dale

doi:10.1002/ajh.2830340312

Cited by 11 publications

(5 citation statements)

References 18 publications

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“…Reports from non-endemic countries ( n = 17) described HTLV-1-associated diseases in migrants from endemic regions or in specific ethnic groups (Denic et al, 1988, 1990; Ratner and Poiesz, 1988; Mowbray et al, 1989; Dixon et al, 1990; Nightingale and Desselberger, 1990; Nomura et al, 1990; Ratner et al, 1990; Salazar-Grueso et al, 1990; Major et al, 1993; Matutes et al, 1995; Hu et al, 1998; Prates et al, 2000; Biglione et al, 2003; Mahé et al, 2004; Dosik and Wilson, 2009; Díaz Torres et al, 2010). Table 2 summarizes the countries where family aggregation of HTLV-1-associated diseases has been reported.…”

Section: Resultsmentioning

confidence: 99%

Family Aggregation of Human T-Lymphotropic Virus 1-Associated Diseases: A Systematic Review

Álvarez¹,

Gotuzzo

Vandamme

et al. 2016

Front. Microbiol.

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Human T-lymphotropic virus 1 (HTLV-1) is a retrovirus that produces a persistent infection. Two transmission routes (from mother to child and via sexual intercourse) favor familial clustering of HTLV-1. It is yet unknown why most HTLV-1 carriers remain asymptomatic while about 10% of them develop complications. HTLV-1 associated diseases were originally described as sporadic entities, but familial presentations have been reported. To explore what is known about family aggregation of HTLV-1-associated diseases we undertook a systematic review. We aimed at answering whether, when, and where family aggregation of HTLV-1-associated diseases was reported, which relatives were affected and which hypotheses were proposed to explain aggregation. We searched MEDLINE, abstract books of HTLV conferences and reference lists of selected papers. Search terms used referred to HTLV-1 infection, and HTLV-1-associated diseases, and family studies. HTLV-1-associated diseases considered are adult T-cell leukemia/lymphoma (ATLL), HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), HTLV-1-associated uveitis, and infective dermatitis. Seventy-four records reported HTLV-1-associated diseases in more than one member of the same family and were included. Most reports came from HTLV-1-endemic countries, mainly Japan (n = 30) and Brazil (n = 10). These reports described a total of 270 families in which more than one relative had HTLV-1-associated diseases. In most families, different family members suffered from the same disease (n = 223). The diseases most frequently reported were ATLL (115 families) and HAM/TSP (102 families). Most families (n = 144) included two to four affected individuals. The proportion of ATLL patients with family history of ATLL ranged from 2 to 26%. The proportion of HAM/TSP patients with family history of HAM/TSP ranged from 1 to 48%. The predominant cluster types for ATLL were clusters of siblings and parent-child pairs and for HAM/TSP, an affected parent with one or more affected children. The evidence in the literature, although weak, does suggest that HTLV-1-associated diseases sometimes cluster in families. Whether familial transmission of HTLV-1 is the only determining factor, or whether other factors are also involved, needs further research.

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Section: Resultsmentioning

confidence: 99%

Family Aggregation of Human T-Lymphotropic Virus 1-Associated Diseases: A Systematic Review

Álvarez¹,

Gotuzzo

Vandamme

et al. 2016

Front. Microbiol.

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“…A father -daughter pair with ATL was subsequently reported from the United States [51], but again no genetic studies were performed. Two siblings with HTLV I positivity and ATL were recorded [52] and in another family of 4 HTLV I+brothers, 2 developed ATL [53]. In the largest family reported to date 6 of 7 siblings developed ATL [54].…”

Section: Adult T-cell Leukemia (Atl) and T-acute Lymphocytic Leukemiamentioning

confidence: 95%

Familial Leukemias

Wiernik

2015

Curr. Treat. Options in Oncol.

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Familial leukemia has been described for more than 50 years but only recently have modern genetic techniques allowed for the investigation of the genome. Genome-wide association studies have identified a number of genetic sites that appear to relate to susceptibility to leukemia in certain families and occasionally to susceptibility to a specific leukemia in general. Many questions remain, including susceptibility to what? An oncogenic virus? An environmental chemical? Mutation of another gene induced by a heritable mutation-promoting gene?.Clinically important facts have been learned. Chronic lymphocytic leukemia (CLL) is by far the most common familial leukemia. Patients with CLL have approximately a 10% chance of a first-degree relative developing CLL, and even a greater chance of one developing monoclonal B-cell lymphocytosis which may be an asymptomatic forme fruste of the neoplasm. Furthermore, there may be an increased incidence of breast cancer in familial CLL pedigrees which raises the question of a common etiology for neoplasms in general, or at least a previously unrecognized relationship among them.

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“…This study revealed 4 major risk factors for the development of ATLL in HTLV-1 carriers using a multivariate analysis, i.e., high HTLV-1 proviral loads (in other words, an increase in HTLV-1 infected cells) in the PB, advanced age (over 40 years of age), the existence of a family history of ATLL, and detecting HTLV-1 antibody positivity during treatment for other diseases . Familial ATLL cases were reported by several researchers (Miyamoto et al, 1985;Ratner et al, 1990;Wilks et al, 1993). Surprisingly, we experienced a family with accumulated familial ATLL, in which six of seven siblings (excluding one who died during World War II) developed acute type ATLL between 1978 and 1989 (Nomura et al, 2006).…”

Section: Epidemiology Etiology and Leukemogenesismentioning

confidence: 97%