503:
633:
580:(CBC) is performed to test for T-ALL by measuring the different types and maturity of cells in the patient's blood, allowing the doctor to determine whether leukemic cells are present. Additionally, blood tests showing high levels of white blood cells or low levels of red blood cells may also indicate T-ALL. Further testing could also help determine whether T-ALL has affected other organs, such as the kidneys, and identify the genetic alterations associated with the disease.
506:
505:
507:
504:
43:
697:(CSF). Even if leukemic cells are not found in the CSF at the time of diagnosis, it is highly likely that they will spread there over time. Thus, prophylactic intrathecal chemotherapy, a treatment to lower the risk of leukemia spreading to the spinal cord and brain by directly administering chemotherapy to the CSF, is crucial.
338:
T-ALL is neither contagious nor inherited. Its two main risk factors are age and sex. While most cases of leukemia increase with age, T-ALL is an exception, peaking in children aged 2 to 5 years. T-ALL is most prevalent in the adult population, but among paediatric cases, it has a median onset at age
562:
When doctors suspect that a patient may be suffering from T-cell acute lymphoblastic leukemia (T-ALL) after a careful examination of their medical history, signs, and symptoms, they will conduct various tests, procedures, and scans to diagnose T-ALL. Some symptoms and aspects of medical history may
680:
and medication to prevent or treat side effects associated with low white blood cell counts resulting from intensive chemotherapy regimens. The treatment typically occurs in three stages: induction, consolidation, and maintenance. The entire treatment process usually spans approximately two years,
705:
Compared to B-ALL, T-ALL patients present more high-risk features, including a tendency for earlier relapse, CNS involvement, and resistance to chemotherapy. In response, prophylactic intrathecal chemotherapy is further enhanced with CNS radiation therapy. For high-risk T-ALL patients, allogeneic
782:
In childhood, T-cell acute lymphoblastic leukemia (T-ALL) patients can expect a 5-year event-free survival (EFS) rate of 70% and an overall survival (OS) rate of 80%. Among the approximately 25% of children who relapse, survival rates drop to 30-50%, with patients generally showing a much poorer
761:
for 4 to 6 weeks, followed by intensive combination therapy for 6–8 months, and finally 18–30 months of low-intensity anti-metabolite-based therapy. It is crucial to differentiate treatment approaches between youth and adults. Studies have shown that administering either a traditional paediatric
404:
In T-ALL patients, TCRs encoded by TRA, TRD, and TRG at chromosome bands 14q11 and 7q34 become malignant. The build-up of malignant T-cells in T-ALL consists of clones with identical TCR gene arrangements originating from a single cell. The gene rearrangements resulting from the malignant cell
667:
are investigated to define T-ALL. Then, stages of thymic development are determined by identifying specific expressions in chromosomal abnormalities. This classification system identifies T-ALL cases as being either high or low risk. Patients then receive appropriate treatment based on their
339:
9 and is most prominent in adolescents. The disease also exhibits a marked male predominance, with males having a three-fold increased risk of developing T-ALL compared to females. The reasons for T-ALL's higher rate of occurrence in older children and males are currently unclear.
388:
Karyotyping has shown that TRD and TRB undergo recombination most commonly, whereas TRA is seldom involved, and TRG is rarely rearranged. These rearrangements affect the normal process of TCR formation and can lead to the failure of cellular machinery to correctly repair
508:
433:
changes, and environmental factors. However, because there are fewer cases of T-ALL compared to other subtypes of leukemia, the exact cause of T-ALL remains unclear. T-ALL is neither contagious nor inherited, but specific genetic mutations, commonly including
864:
and NOTCH1 may also be activated at higher frequencies than usual. Thus, the multistep prognosis of T-ALL has been said to intensify and rapidly progress due to the accumulation of effects resulting from the dysregulation of multiple signalling pathways.
1006:
D’Angiò, Mariella; Valsecchi, Maria G.; Testi, Anna M.; Conter, Valentino; Nunes, Vittorio; Parasole, Rosanna; Colombini, Antonella; Santoro, Nicola; Varotto, Stefania; Caniglia, Maurizio; Silvestri, Daniela (January 2015).
1410:
D’Angiò, Mariella; Valsecchi, Maria G.; Testi, Anna M.; Conter, Valentino; Nunes, Vittorio; Parasole, Rosanna; Colombini, Antonella; Santoro, Nicola; Varotto, Stefania; Caniglia, Maurizio; Silvestri, Daniela (2015-01-16).
189:
production, whereas T-lymphocytes destroy bacteria or cells infected with viruses. Approximately 20% of ALL patients suffer from T-ALL, which is more prevalent in the adult population compared to children, with
849:
location may sometimes generate subtle exchanges in DNA material at loci involved in oncogenic rearrangements of T-ALL. This causes cryptic translocation, thereby deleting the putative tumour suppressor gene
710:
has shown highly successful and promising results. However, it also increases the risk of relapse, which reduces its curative potential. Patients undergoing transplantation must be continuously monitored for
596:
are typically done simultaneously to help determine and confirm the type and severity of T-ALL. Additional biopsies, such as skin and lymph node biopsies, may also be needed to check for the spread of T-ALL.
1182:
397:. All 30 genes known to illegitimately recombine with TCR genes primarily function to regulate epigenetics through roles such as signal transducers, transcription factors (tumour suppressors or
248:
Patients with T-ALL may not always exhibit all the signs and symptoms listed below. Individuals with other medical conditions that are not leukemia may also experience similar symptoms.
318:. The symptoms can appear acutely or develop progressively over time. The most common clinical feature among patients is the proliferation of malignant clones, which suppresses normal
405:
juxtapose both TCR genes and other critical genes that code for transcription factors. This leads to the dysregulation of partner gene transcription, serving as the main cause of
409:– a multi-step process of induction, development, and progression of leukemic diseases. Approximately 20% of all leukemia demonstrate simultaneous rearrangement of these genes.
1468:
Quist-Paulsen, P.; Toft, N.; Heyman, M.; Abrahamsson, J.; Griškevičius, L.; Hallböök, H.; Jónsson, Ó G.; Palk, K.; Vaitkeviciene, G.; Vettenranta, K.; Åsberg, A. (2020-02-20).
774:, high survival and low death rates were observed in patients receiving the first treatment. In contrast, the latter approach resulted in a high toxic death rate among adults.
363:(SNP) arrays. The most common structural abnormality is the rearrangement of the T-cell receptor (TCR) gene. 95% of T-cell TCRs consist of an alpha and beta chain (encoded by
201:
is particularly prominent among adolescents. The disease stems from cytogenic and molecular abnormalities, resulting in the disruption of developmental pathways controlling
663:
is not used for T-ALL because it has already spread throughout the body at the time of diagnosis. However, T-ALL has its own system of classification. First, patterns of
563:
not be specific enough to diagnose T-ALL, so further testing may be required. Doctors may consider several factors but will not necessarily conduct all possible tests.
794:
related to clonal evolution that drive resistance, which serve as the basis for T-ALL relapse. Over 20% of patients with relapsed T-ALL show mutations in the
50:
T-lymphoblastic cells of acute leukemia in the bone marrow. In some cases, the cytoplasm is concentrated at one pole of the cell, forming "hand mirror cells".
1413:"Clinical features and outcome of SIL/TAL1-positive T-cell acute lymphoblastic leukemia in children and adolescents: a 10-year experience of the AIEOP group"
1009:"Clinical features and outcome of SIL/TAL1-positive T-cell acute lymphoblastic leukemia in children and adolescents: a 10-year experience of the AIEOP group"
78:
Most prevalent in the adult population with incidences diminishing with age. Amongst pediatric population, median onset of age 9. Marked male predominance
803:
460:
421:
leads to the development of T-cell acute lymphoblastic leukemia (T-ALL) and lead to the loss of function in white blood cells. Different subtypes of
1206:
70:
Recurrent infections, unusual or common bleeding and bruising, extreme tiredness, unexplained fever, unexplained weight gain, swollen lymph nodes
216:
Distinct from adult T-cell leukemia, in which T-cell lymphotropic virus Type I causes malignant maturation of T-cells, T-ALL is a precursor for
1103:
1386:
771:
707:
762:
regimen or intensive block-based chemotherapy yields significantly different responses. While both treatments include high-dose
539:, a chemical classified as carcinogenic to humans, is associated with an increased risk of T-ALL and other forms of leukemia.
975:
617:, can help confirm the diagnosis. These scans also provide information on the impact of T-ALL on other organs of the body.
648:
helps identify chromosomal abnormalities in patients. This can help diagnose the specific leukemia subtype by identifying
1589:
784:
356:
1237:
629:
allows doctors to determine whether the treatments will be effective. This procedure also reveals the spread of T-ALL.
1359:
20:
455:
Some patients may have familial histories with leukemia predispositions, increasing the risk of developing T-ALL.
1264:
729:
is frequently present in T-ALL patients, where SIL/TAL1 fusion leads to inappropriate TAL1 expression, promoting
351:
has shown structural chromosomal rearrangements in 50-75% of T-ALL patients, primarily involving inversions and
478:
Patients with immature thymocytes in the thymus may develop T-ALL. Additionally, hereditary conditions such as
360:
24:
1470:"T-cell acute lymphoblastic leukemia in patients 1–45 years treated with the pediatric NOPHO ALL2008 protocol"
1594:
1360:"Human T-cell leukemia virus type 1 | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program"
554:
that affects white blood cells (T-cells), which may later develop into T-ALL and other subtypes of leukemia.
390:
147:
132:
910:
1151:
614:
547:
487:
352:
712:
528:
emission from nuclear reactor accidents is also believed to increase the risk of developing T-ALL.
483:
456:
191:
826:
676:
Currently, standard treatment for T-cell acute lymphoblastic leukemia (T-ALL) involves long-term
625:
To ensure effective treatments for T-cells that have invaded the central nervous system (CNS), a
589:
154:
accumulate in the bone marrow, crowding out normal white blood cells and also accumulate in the
521:
221:
1291:"Exposure to benzene at work and the risk of leukemia: a systematic review and meta-analysis"
1069:
323:
303:
1302:
577:
394:
8:
1289:
Khalade, Abdul; Jaakkola, Maritta S.; Pukkala, Eero; Jaakkola, Jouni J. K. (2010-06-28).
694:
1306:
1560:
1505:
1445:
1412:
1333:
1290:
1041:
1008:
742:
65:
787:
analysis is critical, as mentioned previously, to evaluate the efficacy of treatment.
1552:
1544:
1509:
1497:
1489:
1450:
1432:
1338:
1320:
1133:
1125:
1046:
1028:
217:
96:
Blood test, bone marrow aspiration, biopsy, CT, MRI, lumbar puncture, genetic testing
91:
55:
1564:
1469:
1536:
1481:
1440:
1424:
1328:
1310:
1115:
1036:
1020:
943:
466:
307:
257:
225:
206:
151:
197:
Among T-ALL cases in the pediatric population, the median onset is age 9, and the
1428:
1120:
1024:
720:
690:
664:
645:
626:
491:
302:
and genetic alterations in immature thymocytes, T-ALL is a highly aggressive and
355:. Diagnostic yield can be substantially increased through other methods such as
746:
730:
660:
406:
319:
233:
1524:
1485:
814:
Although over 100 gene mutations have been identified in T-ALL patients, only
689:
T-ALL can spread to the brain and spinal cord, which can be diagnosed through
632:
1583:
1548:
1493:
1436:
1324:
1129:
1032:
842:
causing the tumour-suppressing gene to lose its functions, leading to T-ALL.
758:
723:(TCR) genes to evaluate for fusion transcripts such as SIL-TAL1. Mutation of
479:
373:, respectively), while only 5% consist of gamma and delta chains (encoded by
1556:
1501:
1454:
1342:
1315:
1137:
1050:
767:
763:
754:
677:
315:
278:
237:
236:
involvement of multiple organs, including the lymph nodes, as a result of
750:
430:
299:
210:
143:
104:
Long-term chemotherapy, CNS radiation therapy, stem cell transplantation
1540:
551:
520:
may have an increased risk of developing T-ALL. CDKN2A is an inherited
380:
374:
364:
311:
267:
220:. Its clinical presentation most commonly includes infiltration of the
163:
136:
588:
Bone marrow consists of a combination of solid and liquid components.
1525:"The genetics and mechanisms of T cell acute lymphoblastic leukaemia"
1207:"What is the Difference Between B-cell Lymphoma and T-cell Lymphoma?"
944:"Acute lymphoblastic leukemia (ALL): Symptoms, causes, and treatment"
733:. Early intervention during the early stages of relapse is critical.
517:
348:
253:
202:
109:
1387:"Acute lymphocytic leukemia - Diagnosis and treatment - Mayo Clinic"
846:
791:
649:
426:
422:
398:
327:
186:
182:
139:
1467:
830:
815:
806:
gene has also been found to confer chemo resistance in children.
795:
693:
assessment. Lumbar puncture helps identify leukemic cells in the
610:
536:
435:
306:. Patients often present with extensive bone marrow involvement,
270:) or the middle of the chest, potentially causing facial swelling
198:
741:
Young T-ALL patients have shown significant improvement through
851:
819:
593:
516:
Individuals who have had previous chemotherapy and exposure to
471:
439:
425:
share similarities in their causes, which are a combination of
229:
174:
170:
159:
1288:
605:
Since a swollen spleen and lymph nodes are symptoms of T-ALL,
42:
855:
837:
799:
783:
prognosis. Monitoring for minimal residual disease (MRD) via
606:
525:
274:
178:
155:
1409:
1104:"How I treat T-cell acute lymphoblastic leukemia in adults"
1005:
860:
725:
716:
442:, may be passed along, increasing susceptibility to T-ALL.
122:
7% at ages 1-10, 14% at ages 10-15, and 29% at ages 15-18
469:, thereby increasing the risk of T-ALL. Mutations in the
418:
1238:"T-Cell Acute Lymphoblastic Leukemia - My Cancer Genome"
475:
gene are also associated with the development of T-ALL.
359:(FISH) and various molecular technologies, for example,
976:"Typical Treatment of Acute Lymphocytic Leukemia (ALL)"
745:. This involves initial induction therapy, including a
494:
are associated with a higher risk of developing T-ALL.
114:
5-Year Event Free
Survival: 70%, Overall Survival: 80%
790:
Recent genomic studies have identified a selection of
459:
is an inherited condition that leads to mutations in
1295:
Environmental Health: A Global Access
Science Source
825:
In over 50% of paediatric T-ALL cases, mutations in
583:
1102:Litzow, Mark R.; Ferrando, Adolfo A. (2015-08-13).
681:with the maintenance phase lasting the longest.
401:), cell cycle regulators, or ribosomal proteins.
1581:
1265:"Leukemia - Chronic T-Cell Lymphocytic - Stages"
1070:"T-lineage acute lymphoblastic leukemia (T-ALL)"
911:"Pediatric T-Cell Acute Lymphoblastic Leukemia"
829:have been identified. These mutations activate
283:Unexplained weight loss and/or loss of appetite
1523:Belver, Laura; Ferrando, Adolfo (2016-08-30).
1522:
1101:
169:The two most common cells involved in ALL are
266:Extreme tiredness and swellings in the neck (
322:, resulting in a deficiency of functioning
263:Unusual and/or common bleeding and bruising
209:development, and alterations in control of
129:T-cell acute lymphoblastic leukemia (T-ALL)
524:associated with the development of T-ALL.
293:
41:
1444:
1332:
1314:
1119:
1040:
177:. B-lymphocytes protect the body against
631:
600:
501:
772:hematopoietic stem cell transplantation
708:hematopoietic stem cell transplantation
1582:
1232:
1230:
1228:
1183:"T-cell Acute Lymphoblastic Leukaemia"
150:(ALL) is a condition wherein immature
1381:
1379:
1354:
1352:
1259:
1257:
905:
903:
901:
899:
897:
737:Multimodal Therapy for Young Patients
497:
450:
243:
224:(CNS) and often is associated with a
1177:
1175:
1173:
1171:
1152:"Acute Lymphoblastic Leukemia (ALL)"
1097:
1095:
1093:
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1089:
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1001:
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995:
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938:
936:
934:
932:
930:
895:
893:
891:
889:
887:
885:
883:
881:
879:
877:
531:
16:Type of acute lymphoblastic leukemia
1403:
1225:
36:T-cell acute lymphoblastic leukemia
13:
1376:
1349:
1254:
685:Central Nervous System Involvement
620:
445:
14:
1606:
1168:
1086:
1057:
992:
961:
927:
874:
822:mutations are considered common.
584:Bone marrow aspiration and biopsy
357:fluorescent in situ hybridization
21:T-lymphoblastic leukemia/lymphoma
417:Like most cancers, mutations in
1516:
1461:
1282:
809:
640:
342:
333:
135:characterized by an aggressive
1199:
1144:
609:and ultrasound scans, such as
571:
566:
361:single nucleotide polymorphism
25:Adult T-cell leukemia/lymphoma
1:
868:
1429:10.3324/haematol.2014.112151
1211:Dana-Farber Cancer Institute
1121:10.1182/blood-2014-10-551895
1025:10.3324/haematol.2014.112151
777:
671:
557:
412:
148:Acute lymphoblastic leukemia
133:acute lymphoblastic leukemia
7:
393:gene (RAG) protein-induced
10:
1611:
1590:Acute lymphocytic leukemia
655:
548:Human T-lymphotropic virus
542:
512:Human T-Lymphotropic Virus
18:
1486:10.1038/s41375-019-0598-2
1364:rarediseases.info.nih.gov
1074:atlasgeneticsoncology.org
915:atlasgeneticsoncology.org
636:Lumbar Puncture Positions
118:
108:
100:
90:
82:
74:
64:
54:
49:
40:
35:
948:www.medicalnewstoday.com
713:minimal residual disease
484:neurofibromatosis type 1
391:recombination-activating
289:Unexplained skin itching
256:due to a lack of normal
19:Not to be confused with
314:, CNS involvement, and
294:Clinical manifestations
194:diminishing with age.
1316:10.1186/1476-069X-9-31
1242:www.mycancergenome.org
637:
590:Bone marrow aspiration
513:
467:tumour suppressor gene
324:peripheral blood cells
222:central nervous system
1529:Nature Reviews Cancer
827:epigenetic regulators
701:Comparison with B-ALL
635:
601:X-rays and ultrasound
511:
488:ataxia telangiectasia
228:originating from the
60:Haematology, oncology
1595:Lymphocytic leukemia
798:5’-nucleotidase II (
578:Complete blood count
552:retroviral infection
522:polymorphism variant
457:Li–Fraumeni syndrome
395:double-strand breaks
304:heterogenous disease
213:and proliferation.
1541:10.1038/nrc.2016.63
1307:2010EnvHe...9...31K
858:). Simultaneously,
715:(MRD), usually via
695:cerebrospinal fluid
286:Swollen lymph nodes
1391:www.mayoclinic.org
802:) gene, while the
743:multimodal therapy
638:
514:
498:Radiation exposure
451:Genetic conditions
244:Signs and symptoms
950:. 14 October 2019
650:genetic mutations
532:Chemical exposure
509:
385:, respectively).
298:Originating from
277:, chills, and/or
258:white blood cells
238:hyperleukocytosis
218:lymphoid neoplasm
207:tumour suppressor
152:white blood cells
126:
125:
92:Diagnostic method
86:Currently unknown
30:Medical condition
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1356:
1347:
1346:
1336:
1318:
1286:
1280:
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1276:
1261:
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1249:
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1234:
1223:
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1197:
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1194:
1193:
1179:
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1142:
1141:
1123:
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1084:
1083:
1081:
1080:
1066:
1055:
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1003:
990:
989:
987:
986:
972:
959:
958:
956:
955:
940:
925:
924:
922:
921:
907:
792:genetic variants
668:classification.
510:
308:mediastinal mass
226:mediastinal mass
45:
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32:
1610:
1609:
1605:
1604:
1603:
1601:
1600:
1599:
1580:
1579:
1578:
1569:
1567:
1521:
1517:
1466:
1462:
1408:
1404:
1395:
1393:
1385:
1384:
1377:
1368:
1366:
1358:
1357:
1350:
1287:
1283:
1274:
1272:
1263:
1262:
1255:
1246:
1244:
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1235:
1226:
1216:
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1200:
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1169:
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1100:
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1068:
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1004:
993:
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953:
951:
942:
941:
928:
919:
917:
909:
908:
875:
871:
812:
780:
770:and allogeneic
721:T-cell receptor
691:lumbar puncture
674:
665:gene expression
658:
646:Genetic testing
643:
627:lumbar puncture
623:
621:Lumbar puncture
603:
586:
574:
569:
560:
545:
534:
502:
500:
492:Noonan syndrome
453:
448:
446:Causes of T-ALL
415:
345:
336:
326:, particularly
296:
246:
31:
28:
17:
12:
11:
5:
1608:
1598:
1597:
1592:
1577:
1576:
1535:(8): 494–507.
1515:
1480:(2): 347–357.
1460:
1423:(1): e10–e13.
1402:
1375:
1348:
1281:
1253:
1224:
1198:
1187:Leukaemia Care
1167:
1156:www.stjude.org
1143:
1114:(7): 833–841.
1085:
1056:
1019:(1): e10–e13.
991:
980:www.cancer.org
960:
926:
872:
870:
867:
811:
808:
779:
776:
755:L-asparaginase
747:glucocorticoid
731:leukemogenesis
673:
670:
661:Normal staging
657:
654:
642:
639:
622:
619:
602:
599:
585:
582:
573:
570:
568:
565:
559:
556:
550:(HTLV-1) is a
544:
541:
533:
530:
499:
496:
452:
449:
447:
444:
414:
411:
407:leukemogenesis
353:translocations
344:
341:
335:
332:
320:haematopoiesis
295:
292:
291:
290:
287:
284:
281:
271:
264:
261:
245:
242:
234:extramedullary
192:incidence rate
124:
123:
120:
116:
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112:
106:
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102:
98:
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94:
88:
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84:
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51:
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1499:
1495:
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1487:
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1479:
1475:
1471:
1464:
1456:
1452:
1447:
1442:
1438:
1434:
1430:
1426:
1422:
1418:
1417:Haematologica
1414:
1406:
1392:
1388:
1382:
1380:
1365:
1361:
1355:
1353:
1344:
1340:
1335:
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1326:
1322:
1317:
1312:
1308:
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1300:
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1292:
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1243:
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1229:
1213:. 18 Jun 2019
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334:Risk factors
328:thrombocytes
316:splenomegaly
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279:night sweats
273:Unexplained
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751:vincristine
572:Blood tests
567:Assessments
349:karyotyping
268:lymph nodes
211:cell growth
164:lymph nodes
144:bone marrow
75:Usual onset
1584:Categories
1570:2020-04-05
1396:2020-04-07
1369:2020-04-07
1275:2020-04-07
1269:Cancer.Net
1247:2020-04-07
1192:2020-04-07
1161:2020-04-07
1079:2020-04-07
985:2020-04-07
954:2020-04-07
920:2020-04-07
869:References
431:epigenetic
312:adenopathy
300:epigenetic
254:infections
252:Recurrent
1549:1474-1768
1510:204459614
1494:1476-5551
1437:0390-6078
1325:1476-069X
1301:(1): 31.
1130:0006-4971
1033:0390-6078
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757:, and an
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413:Pathology
399:oncogenes
203:thymocyte
137:malignant
119:Frequency
110:Prognosis
101:Treatment
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1565:28636912
1557:27451956
1502:31611626
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427:genetics
423:leukemia
187:antibody
185:through
183:bacteria
140:neoplasm
66:Symptoms
1446:4281327
1334:2903550
1303:Bibcode
1042:4281327
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656:Staging
543:Viruses
537:Benzene
199:disease
179:viruses
142:of the
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832:NOTCH1
820:CDKN2A
816:NOTCH1
607:X-rays
490:, and
472:SPRED1
440:CDKN2A
436:NOTCH1
347:Basic
275:fevers
230:thymus
162:, and
160:spleen
83:Causes
1561:S2CID
1506:S2CID
1217:7 Apr
1108:Blood
856:INK4A
838:FBXW7
804:TFDP3
800:NT5C2
526:SR-90
156:liver
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1339:PMID
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1219:2020
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861:TLX1
835:and
818:and
785:qPCR
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717:qPCR
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462:TP53
438:and
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1482:doi
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419:DNA
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