Wikipedia

Sankaran Bargo (Leukemia)

(an turo daga Sankaran Mahaifa (Leukemia))

Leukemia (Hakanan an rubuta cutar sankara da haruffan /l uː ˈk iː m iːə / loo-KEE -mee-ə ) ya kasance wani rukuni ne na cututtukan daji na jini wanda yawanci ke farawa a cikin`kasusuwa kuma yana haifar da adadi mai yawa na kwayoyin jini marasa al'ada. .[1] Wadannan kwayoyin jini ba su cika habaka ba kuma ana kiran su blasts ko kwayoyin cutar sankara [2] Alamu na iya hadawa da zub da jini da barna, ciwon Kashi, gajiya, zazzabi, da kara hadarin cututtuka.[3] Wadannan alamun suna faruwa ne saboda rashin kwayoyin jini na al'ada. [2] Ana ganewa su ta asalin hanyar gwaje-gwajen jini ko kwayar dake cikin kasusuwa. [2]

Sankaran Bargo
Description (en) Fassara
Iri hematologic cancer (en) Fassara, myeloproliferative disorders (en) Fassara
cuta
Specialty (en) Fassara hematology (en) Fassara
Symptoms and signs (en) Fassara bone pain (en) Fassara, Jiri, weight loss (en) Fassara, chest pain (en) Fassara, Kumburi
angina pectoris (en) Fassara
Medical treatment (en) Fassara
Magani methotrexate (en) Fassara, cytarabine (en) Fassara, vincristine (en) Fassara, pipobroman (en) Fassara, irinotecan (en) Fassara, isotretinoin (en) Fassara, doxorubicin hydrochloride (en) Fassara, (RS)-lenalidomide (en) Fassara, nilotinib (en) Fassara, dasatinib monohydrate (en) Fassara, ibrutinib (en) Fassara, ruxolitinib (en) Fassara, imatinib (en) Fassara, bosutinib (en) Fassara da rituximab (en) Fassara
Identifier (en) Fassara
ICD-10-CM C95.90, C95 da C95.9
ICD-9-CM 208, 208.9, 207.8, 208.80, 207, 208.90, 207.80 da 208.8
ICD-O: 9800, 980-994 da 980
DiseasesDB 7431
MedlinePlus 001299
eMedicine 001299
MeSH D007938
Disease Ontology ID DOID:1240

Ba a san ainihin dalilin cutar sankara ba. [4] Hadin abubuwan kwayoyin halitta da abubuwan muhalli (marasa kyau) an yi imanin hakan kuma yana taka rawa.[4] Abubuwan hadari sun hada da shan taba, ionizing radiation, wasu sinadarai (irin su benzene ), kafin chemotherapy, da Down syndrome . [4][5] Mutanen da ke da gadon cutar sankara su ma suna cikin hadari mafi girma. [5] Akwai manyan nau'ukan cutar sankara guda hudu - m lymphoblastic leukemia (ALL), m myeloid leukemia (AML), cutar sankara ta lymphocytic na yau da kullun (CLL) da cutar sankara ta myeloid (CML) - da kuma nau'ikan da ba su da yawa.[5][6] Cutar sankara da lymphomas duka suna cikin rukunin da ke shafar jini, kasusuwa, da tsarin lymphoid, wadanda aka sani da kwayoyin hematopoietic da lymphoid .[7][8]

chemotherapy, farfesan ban garen magani, da kuma dashen kasusuwa, ban da kulawa da tallafi kamar yadda ake bukata. [9] Ana iya sarrafa wasu nau'ikan cutar sankara tare da jira a hankali. [5] Nasarar jinya ya dogara da nau'in cutar sankara da shekarun mutum. Sakamako ya inganta a kasashen da suka ci gaba.[6] Yawan rayuwa na shekaru biyar shi ne 57% a Amurka.[10] A cikin yara 'yan ƙasa da 15, adadin rayuwa na shekaru biyar ya fi 60% ko ma 90%, ya danganta da nau'in cutar sankara.[11] A cikin yara masu fama da cutar sankara waɗanda ba su da kansa bayan shekaru biyar, da wuya ciwon daji ya dawo .[11]

A cikin 2015, cutar sankara ta kasance a cikin mutane miliyan 2.3 a duk duniya kuma ta haifar da mutuwar muta ne sama da 353,500.[12][13] A cikin 2012 cutar ta fara haɓakawa a cikin mutane 352,000.[6] Shi ne mafi yawan nau'in ciwon daji a cikin yara, tare da kashi uku cikin hudu na cutar sankara a cikin yara shine nau'in lymphoblastic kuma mai tsanani. Duk da haka, fiye da kashi 90 cikin 100 na duk cutar sankara ana gano su a cikin manya, tare da CLL da AML sun fi yawa a cikin manya.[5][14] Ya kuma fi faruwa a kasashen da suka ci gaba .[6]

Rabewa

gyara sashe
Manyan cutar sankarar bargo guda hudu
Nau'in salula M Na kullum
Lymphocytic cutar sankarar bargo


(ko "lymphoblastic") 		Cutar sankarar bargo ta lymphoblastic


(ALL) 		Cutar sankarar lymphocytic na yau da kullun



(CLL)
Myelogenous cutar sankarar bargo



("myeloid" ko "nonlymphocytic") 		M myelogenous cutar sankarar bargo



(AML ko myeloblastic) 		Myelogenous cutar sankarar bargo



(CML)

Gaba daya rarrabuwa

gyara sashe

A asibiti da kuma pathologically, cutar sankarar bargo ya kasu kashi da dama manyan kungiyoyin. Kashi na farko yana tsakanin sifofinsa masu tsanani da na yau da kullum :[15]

  • Cutar sankarar bargo tana da saurin habaka adadin kwayoyin jini marasa balaga. Cunkushewar da ke haifar da irin wadannan kwayoyin yana sa kasusuwan kasusuwa ya kasa samar da lafiyayyen kwayoyin jini wanda ke haifar da karancin haemoglobin da kananan platelets. Ana bukatar magani nan da nan a cikin cutar sankarar bargo mai tsanani saboda saurin ci gaba da tarawa na kwayoyin cuta masu cutarwa, wanda sai ya zube cikin jini kuma ya yada zuwa wasu gabobin jiki. Siffofin cutar sankarar bargo sune mafi yawan nau'in cutar sankarar bargo a cikin yara .
  • Ciwon sankarar bargo na yau da kullun yana da alaka da habakar dimbin yawa na manyan kwayoyin jini, amma har yanzu mara kyau. Yawanci ana daukar watanni ko shekaru don ci gaba, kwayoyin suna samar da su da yawa fiye da na al'ada, wanda ke haifar da yawancin fararen kwayoyin jini marasa kyau. Ganin cewa dole ne a yi maganin cutar sankarar bargo mai tsanani nan da nan, ana lura da nau'ikan na yau da kullun na dan lokaci kafin jiyya don tabbatar da iyakar tasirin jiyya. Ciwon sankarar bargo na yau da kullun yana faruwa a cikin tsofaffi amma yana iya faruwa a kowane rukuni na shekaru.

Bugu da Kari, an rarraba cututtuka bisa ga irin nau'in kwayar cutar ta jini. Wannan ya raba cutar sankarar bargo zuwa lymphoblastic ko lymphocytic leukemias da myeloid ko myelogenous sankarar bargo :[11]

  • A cikin kwayar cutar sankarar lymphoblastic ko lymphocytic, canjin ciwon daji yana faruwa a cikin wani nau'i na kwayar cuta wanda yakan ci gaba da haifar da lymphocytes, wadanda suke kamuwa da kwayoyin cuta. Yawancin leukemias na lymphocytic sun hada da wani nau'i na musamman na lymphocyte, cell B.
  • A cikin cutar sankarar myeloid ko myelogenous, canjin ciwon daji yana faruwa a cikin wani nau'in tantanin halitta wanda yawanci yakan haifar da jajayen kwayoyin jini, wasu nau'ikan fararen sel, da platelets .

Hada wadannan rabe-rabe guda biyu yana ba da jimillar manyan nau'ikan guda hudu. A cikin kowane dayan manyan nau'ikan, yawanci akwai kananan rukunai da yawa. A karshen, wasu nau'ikan nau'ikan da ba su da yawa ana ɗaukar su a waje da wannan tsarin rarrabawa. [15][16]

Nau'i na musamman

gyara sashe
  • Cutar sankara ta lymphoblastic (ALL) ita ce mafi yawan nau'in cutar sankarar bargo a cikin yara kanana. Har ila yau yana shafar manya, musamman masu shekaru 65 zuwa sama. Daidaitattun jinya sun hada da chemotherapy da radiotherapy . Subtypes sun hada da precursor B m lymphoblastic cutar sanka, bargo, precursor T m lymphoblastic, cutar sankara, sankarar bargon burkitt's, da sankarar bargo na biphenotypic. Yayin da mafi yawan lokuta na DUK suna faruwa ne a jikin yara, kashi 80% na mutuwar daga ALL suna faruwa shi kuma a jikin manya.[17]
  • Cutar sankarar lymphocytic na yau da kullun (CLL) galibi tana shafar manya wadanda suka haura shekaru 55. Wani lokaci yana faruwa a jikin kananan yara, amma kusan ba ya shafar yara. Kashi biyu bisa uku na mutanen da abin ya shafa maza ne. Adadin rayuwa na shekaru biyar shine 85%.[18] Ba shi da magani, amma akwai magunguna masu tasiri da yawa. daya daga cikin nau'i-nau'i shine B-cell prolymphocytic cutar sankarar bargo, cutace mai tsanani.
  • Mummunan cutar sankarar bargo (AML) ta fi faruwa a jikin manya fiye da yara, kuma yawanci a cikin maza fiye da mata. Ana bi da shi da chemotherapy. Adadin tsira na shekaru biyar shine 20%.[19] Nau'o'in AML sun haaa da cutar sankarar bargo na promyelocytic, myeloblastic cutar sankarar bargo, da kuma megakaryoblastic.
  • Cutar sankarar bargo ta myelogenous (CML) tana faruwa musamman a jikin manya; kananan yara kuma suna kamuwa da wannan cuta. Ana maganinta da imatinib (Gleevec a Amurka, Glivec a Turai) ko wasu magunguna.[20] Adadin tsira na shekaru biyar shine 90%. [21][22] daya daga cikin nau'in cutar sankarar bargo shine myelomonocytic cutar .
  • Leukemia mai gashi (HCL) wani lokaci ana ɗaukarsa a matsayin wani yanki na cutar sankarar lymphocytic na yau da kullun, amma bai dace da wannan rukunin ba. Kusan kashi 80% na mutanen da abin ya shafa manyan maza ne. Ba a sami rahoton bullar cutar a jikin yara ba. HCL ba shi da magani amma ana iya magance shi cikin sauki. Rayuwa shine 96% zuwa 100% a cikin shekaru goma.[23]
  • T-cell prolymphocytic cutar sankarar bargo (T-PLL) cuta ce mai wuyar gaske da cutar sankarar bargo da ke shafar manya; an fi samun maza fiye da mata da wannan cuta.[24] Duk da ƙarancinsa gabaɗaya, ita ce mafi yawan nau'in cutar sankarar mahaifa ta T.[25] Kusan sauran cutar sankarar bargo sun hada da kwayoyin B. Yana da wuyar magani, kuma ana auna matsakaicin rayuwa a cikin watanni.
  • Large granular lymphocytic cutar sankarar bargo na iya kunsar ko dai T-cell ko NK Kwayoyin ; kamar leukemia cell mai gashi, wanda ya kunshi kwayoyin B kawai, cutar sankarar bargo ce da ba kasafai ake gane ta da wuri ba (ba mai tsanani ba).[26]
  • T-cell cutar sankarar bargo yana haifar da cutar ta T-lymphotropic virus (HTLV), kwayar cuta mai kamu da HIV . Kamar HIV, HTLV yana cutar da kwayoyin CD4+ T kuma suna yin kwafi a cikinsu; duk da haka, ba kamar HIV ba, ba ya halaka su. Madadin haka, HTLV yana “dauwama” kwayoyin T-cell masu kamuwa da cuta, yana ba su ikon yaduwa ta hanyar da ba ta dace ba. Nau'in kwayar cutar lymphotropic T-cell na mutum I da II (HTLV-I/II) suna da yawa a wasu yankuna na duniya.[ana buƙatar hujja]
  • Clonal eosinophilia (wanda ake kira clonal hypereosinophilia ) rukuni ne na rikice-rikice na jini wanda ke nuna habakar eosinophils a cikin kasusuwa, jini. Suna iya zama pre-cancer ko ciwon daji . Clonal eosinophilia ya kunshi "clone" na eosinophils, watau, rukuni na eosinophils iri daya wadanda duk suka girma daga kwayar halittar kakanni iri daya.[27] Wadannan rikice-rikice na iya canzawa zuwa cutar sankarar jini na eosinophilic na yau da kullun ko kuma ana iya danganta su da nau'ikan myeloid neoplasms, lymphoid neoplasms, myelofibrosis, ko ciwon myelodysplastic .[28][29][30]

Pre-leukemia

gyara sashe
  • Cutar sankarar mahaifa ta wucin gadi, wacce kuma ake kira cutar sankarar bargo ta wucin gadi, ta hada da habakar kwayar cuta na megakaryoblasts marasa cutar kansa. Cutar ta iyakance ga mutanen da ke da Down syndrome ko canje-canje na kwayoyin halitta kamar na Down syndrome, yana tasowa a cikin jariri a lokacin daukar ciki ko jim kadan bayan haihuwa, kuma yana warwarewa a cikin watanni 3 ko, a cikin ~ 10% na lokuta, yana ci gaba zuwa megakaryoblastic cutar sankarar bargo . Ciwon sankarar mahaifa na wucin gadi shine yanayin pre-leukemia.[31][32][33]

Alamomi

gyara sashe
 
Alamomi na yau da kullun na cutar sankarar bargo na yau da kullun ko matsananciyar cutar sankarar bargo [34]

Alamun da aka fi sani a yara sune saukakan kullawar fata, Zazzabi, da kuma barar saifa ko hanta .[34]

Lalacewa ga kasusuwa, ta hanyar maye gurbin kwayoyin halitta na al'ada tare da adadi mafi girma na kwayoyin jini marasa girma, yana haifar da rashin jinin jiki, wanda ke da mahimmanci a cikin tsarin jini. Wannan yana nufin mutanen da ke fama da cutar sankarar bargo na iya samun saukin zubar da jinin da yawa, ko rage zub da jini na pinprick ( petechiae ).[35]

Farin kwayoyin jini, wadanda ke da alaƙa wajen yakar kwayoyin cuta, ana iya danne su ko rashin aiki su. Wannan na iya sa garkuwar jikin mutum ta kasa yakar kamuwa da cuta mai sauki ko kuma ta fara kai hari ga sauran kwayoyin jikin. Domin cutar sankarar bargo tana hana tsarin garkuwar jiki yin aiki akai-akai, wasu suna fuskantar kamuwa da cuta akai-akai, kama daga tonsils masu kamuwa da cuta, raunuka a baki, ko gudawa zuwa ciwon huhu ko cututtuka masu hadari .

A ƙarshe, rashi na jan jini yana haifar da anemia, wanda zai iya haifar da dyspnea da pallor .[ana buƙatar hujja]

Wasu mutane suna fuskantar wasu alamomi, kamar zazzabi, sanyi, gumi na dare, rauni a cikin gabobi, jin gajiya da sauran alamu na gama gari. Wasu mutane suna fama da tashin zuciya ko jin cikawa saboda girman hanta ; wannan zai iya haifar da asarar nauyi ba tare da gangan ba . Fashewar da cutar ta shafa na iya haɗuwa tare kuma su kumbura a cikin hanta ko a cikin ƙwayoyin lymph suna haifar da ciwo kuma suna haifar da tashin zuciya.

Idan kwayoyin cutar sankarar bargo sun mamaye tsarin kulawa na tsakiya, to, alamun cututtuka (musamman ciwon kai ) na iya faruwa. Alamun cututtukan da ba a sani ba kamar migraines, seizures, ko coma na iya faruwa a sakamakon matsa lamba na kwakwalwa. Dukkan alamun da ke da alaƙa da cutar sankarar bargo ana iya danganta su zuwa wasu cututtuka. Saboda haka, cutar sankarar bargo a koyaushe ana gano ta ta hanyar gwaje-gwajen likita .

Kalmar cutar sankarar bargo, wacce ke nufin 'fararen jini', ta samo asali ne daga sifa mai yawan adadin farin jinin da ke nunawa ga mafi yawan masu fama da cutar kafin a yi musu magani. Yawan adadin fararen sel na jini yana bayyana lokacin da aka duba samfurin jini a karkashin na'urar hangen nesa, tare da karin fararen kwayoyin jini akai-akai ba su girma ko rashin aiki. Yawan adadin kwayoyin sel kuma na iya tsoma baki tare da matakin sauran sel, yana haifar da rashin daidaituwa mai cutarwa a cikin adadin jini.[ana buƙatar hujja]

Wasu mutanen da aka gano suna da cutar sankarar bargo ba su da adadin fararen jinin da ake iya gani yayin kirgawar jini na yau da kullun. Wannan yanayin da ba a san shi ba ana kiransa cutar sankarau . Har ila yau kasusuwa na dauke da kwayoyin farin jini masu cutar kansa wadanda ke kawo cikas ga samar da kwayoyin jini na yau da kullun, amma suna zama a cikin bargo maimakon shiga cikin jini, inda za a iya ganin su a gwajin jini. Ga mai fama da cutar sankarau, adadin farin jinin da ke cikin jini na iya zama al'ada ko ƙasa. Aleukemia na iya faruwa a cikin kowane ɗayan manyan nau'ikan cutar sankarar bargo guda huɗu, kuma yana da yawa a cikin cutar sankarar fata mai gashi . [36]

Duba kuma

gyara sashe
  • M erythroid cutar sankarar bargo
  • Magungunan Antileukemic, magungunan da ake amfani da su don kashe kwayoyin cutar sankarar bargo
  • Gajiya mai alaka da cutar daji
  • Cututtukan jini, babban nau'in cututtukan da ke da alaka da jini, gami da cutar sankarar bargo
  • Multiple myeloma

Manazarta

gyara sashe
  1. ↑ "Leukemia". NCI. 1 January 1980. Archived from the original on 27 May 2014. Retrieved 13 June 2014. Cancer that starts in blood-forming tissue, such as the bone marrow, and causes large numbers of abnormal blood cells
  2. ↑ 2.0 2.1 2.2 Empty citation (help)
  3. ↑ "What You Need To Know About™ Leukemia". National Cancer Institute. 23 December 2013. Archived from the original on 6 July 2014. Retrieved 18 June 2014.
  4. ↑ 4.0 4.1 4.2 Hutter, JJ (Jun 2010). "Childhood leukemia". Pediatrics in Review. 31 (6): 234–41. doi:10.1542/pir.31-6-234. PMID 20516235.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 Empty citation (help)
  6. ↑ 6.0 6.1 6.2 6.3 World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 5.13. ISBN 978-9283204299.
  7. ↑ Vardiman, JW; Thiele, J; Arber, DA; Brunning, RD; Borowitz, MJ; Porwit, A; Harris, NL; Le Beau, MM; Hellström-Lindberg, E; Tefferi, A; Bloomfield, CD (30 July 2009). "The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes". Blood. 114 (5): 937–51. doi:10.1182/blood-2009-03-209262. PMID 19357394. S2CID 3101472.
  8. ↑ Cătoi, Alecsandru Ioan Baba, Cornel (2007). Comparative oncology. Bucharest: The Publishing House of the Romanian Academy. p. Chapter 17. ISBN 978-973-27-1457-7. Archived from the original on 10 September 2017.
  9. ↑ Cordo V, Meijerink J (January 2021). "T-cell Acute Lymphoblastic Leukemia: A Roadmap to Targeted Therapies". Blood Cancer Discovery. 2 (1): 19–31. doi:10.1158/2643-3230.BCD-20-0093. ISSN 2643-3230. PMC 8447273 Check |pmc= value (help). PMID 34661151 Check |pmid= value (help).
  10. ↑ "SEER Stat Fact Sheets: Leukemia". National Cancer Institute. 2011. Archived from the original on 16 July 2016.
  11. ↑ 11.0 11.1 11.2 American Cancer Society (2 March 2014). "Survival rates for childhood leukemia". Archived from the original on 14 July 2014.
  12. ↑ GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. (8 October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
  13. ↑ GBD 2015 Mortality and Causes of Death, Collaborators. (8 October 2016). "Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1459–1544. doi:10.1016/s0140-6736(16)31012-1. PMC 5388903. PMID 27733281.
  14. ↑ "Chronic Lymphocytic Leukemia (CLL) - Hematology and Oncology". MSD Manual Professional Edition (in Turanci). Retrieved 2020-02-01.
  15. ↑ 15.0 15.1 "Questions and Answers About Leukemia" (PDF). Center for Disease Control and Prevention. Archived (PDF) from the original on July 30, 2021. Retrieved August 8, 2021.
  16. ↑ "Leukemia - Symptoms and causes". Mayo Clinic (in Turanci). Retrieved 2021-08-08.
  17. ↑ "Key Statistics for Acute Lymphocytic Leukemia (ALL)". American Cancer Society. 8 January 2019. Retrieved 9 December 2019.
  18. ↑ Finding Cancer Statistics » Cancer Stat Fact Sheets »Chronic Lymphocytic Leukemia Archived 16 ga Afirilu, 2008 at the Wayback Machine National Cancer Institute.
  19. ↑ "Survival: Acute Myeloid Leukaemia". Cancer Research UK. 10 July 2019. Retrieved 2 December 2019.
  20. ↑ "Novartis Oncology". Archived from the original on 5 November 2013.
  21. ↑ Patients with Chronic Myelogenous Leukemia Continue to Do Well on Imatinib at 5-Year Follow-Up Archived 15 Mayu 2013 at the Wayback Machine Medscape Medical News 2006.
  22. ↑ Updated Results of Tyrosine Kinase Inhibitors in CML Archived 29 Disamba 2007 at the Wayback Machine ASCO 2006 Conference Summaries.
  23. ↑ Else, M., Ruchlemer, R., Osuji, N. (2005). "Long remissions in hairy cell leukemia with purine analogs: a report of 219 patients with a median follow-up of 12.5 years". Cancer. 104 (11): 2442–8. doi:10.1002/cncr.21447. PMID 16245328. S2CID 43282431.CS1 maint: multiple names: authors list (link)
  24. ↑ Elaine Sarkin Jaffe, Nancy Lee Harris, World Health Organization, International Agency for Research on Cancer, Harald Stein, J. W. Vardiman (2001). Pathology and genetics of tumours of haematopoietic and lymphoid tissues. World Health Organization Classification of Tumors. 3. Lyon: IARC Press. ISBN 978-92-832-2411-2.CS1 maint: multiple names: authors list (link)
  25. ↑ Valbuena JR, Herling M, Admirand JH, Padula A, Jones D, Medeiros LJ (March 2005). "T-cell prolymphocytic leukemia involving extramedullary sites". American Journal of Clinical Pathology. 123 (3): 456–64. doi:10.1309/93P4-2RNG-5XBG-3KBE. PMID 15716243. Archived from the original on 15 May 2013.
  26. ↑ Elaine Sarkin Jaffe, Nancy Lee Harris, World Health Organization, International Agency for Research on Cancer, Harald Stein, J. W. Vardiman (2001). Pathology and genetics of tumours of haematopoietic and lymphoid tissues. World Health Organization Classification of Tumors. 3. Lyon: IARC Press. ISBN 978-92-832-2411-2.CS1 maint: multiple names: authors list (link)
  27. ↑ Reiter A, Gotlib J (2017). "Myeloid neoplasms with eosinophilia". Blood. 129 (6): 704–714. doi:10.1182/blood-2016-10-695973. PMID 28028030.
  28. ↑ Gotlib J (2015). "World Health Organization-defined eosinophilic disorders: 2015 update on diagnosis, risk stratification, and management". American Journal of Hematology. 90 (11): 1077–89. doi:10.1002/ajh.24196. PMID 26486351. S2CID 42668440.
  29. ↑ Arber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM, Bloomfield CD, Cazzola M, Vardiman JW (2016). "The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia". Blood. 127 (20): 2391–405. doi:10.1182/blood-2016-03-643544. PMID 27069254. S2CID 18338178.
  30. ↑ Reiter A, Gotlib J (2017). "Myeloid neoplasms with eosinophilia". Blood. 129 (6): 704–714. doi:10.1182/blood-2016-10-695973. PMID 28028030.
  31. ↑ Bhatnagar N, Nizery L, Tunstall O, Vyas P, Roberts I (October 2016). "Transient Abnormal Myelopoiesis and AML in Down Syndrome: an Update". Current Hematologic Malignancy Reports. 11 (5): 333–41. doi:10.1007/s11899-016-0338-x. PMC 5031718. PMID 27510823.
  32. ↑ Crispino JD, Horwitz MS (April 2017). "GATA factor mutations in hematologic disease". Blood. 129 (15): 2103–2110. doi:10.1182/blood-2016-09-687889. PMC 5391620. PMID 28179280.
  33. ↑ Seewald L, Taub JW, Maloney KW, McCabe ER (September 2012). "Acute leukemias in children with Down syndrome". Molecular Genetics and Metabolism. 107 (1–2): 25–30. doi:10.1016/j.ymgme.2012.07.011. PMID 22867885.
  34. ↑ 34.0 34.1 Reference list is found at image description page in Wikimedia Commons
  35. ↑ Jyothi, K. T. N.; Subrahmanyam, P. S. R.; Sravanthi, A. Ch. (July 2017). "Application of Differential Equations in Medical Science". Research Journal of Science and Technology. 9 (3): 425–426. doi:10.5958/2349-2988.2017.00074.2.
  36. ↑ American Cancer Society (2010). "How is Leukemia Diagnosed?". Detailed Guide: Leukemia – Adult Chronic. American Cancer Society. Archived from the original on 5 April 2010. Retrieved 4 May 2010.
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