Abubuwan Dake Haifar da Ciwon Daji
![]() | |
---|---|
Bayanai | |
Ƙaramin ɓangare na | Dalilan Ciwon Daji |
![](http://upload.wikimedia.org/wikipedia/commons/thumb/4/4f/The_hallmarks_of_cancer_according_to_Hanahan_and_Weinberg.webp/220px-The_hallmarks_of_cancer_according_to_Hanahan_and_Weinberg.webp.png)
![](http://upload.wikimedia.org/wikipedia/commons/thumb/5/5c/Symptoms_of_cancer_metastasis-ru.svg/220px-Symptoms_of_cancer_metastasis-ru.svg.png)
![](http://upload.wikimedia.org/wikipedia/commons/thumb/d/d6/EMpylori.jpg/220px-EMpylori.jpg)
Qiyasi ya sanya haɗarin kamuwa da cutar kansa a duniya da kashi 16.1%.[1] Cututtukan ƙwayoyin cuta sune abubuwan haɗari ga kansar mahaifa, 80% na cututtukan hanta, da 15-20% na sauran cututtukan daji.[2] Wannan rabo ya bambanta a yankuna daban-daban na duniya daga babban na 32.7% a yankin Saharar Afirka zuwa 3.3% a Australia da New Zealand.[1] Helicobacter pylori yana da alaƙa da ciwon daji na ciki, kuma Mycobacterium, wasu ƙwayoyin cuta da ƙwayoyin cuta suma suna da tasiri.
Kwayar cutar da ke iya haifar da ciwon daji ana kiranta oncovirus ko ƙwayar cuta. Wadannan sun hada da kwayar cutar papilloma na mutum, wanda ke hade da ciwon daji na mahaifa da kuma nasopharyngeal carcinoma ; Kwayar cutar Epstein-Barr, wanda ke hade da nau'in kwayar cutar Epstein-Barr da ke hade da lymphomas na lymphoproliferative ; Kaposi's sarcoma herpesvirus, wanda ke hade da sarcoma na Kaposi da lymphoma na farko ; ciwon hanta na B da hepatitis C wadanda ke hade da ciwon hanta; mutum T-cell cutar sankarar bargo-1, wanda ke hade da manya T-cell cutar sankarar bargo / lymphoma ; da kuma cutar sankarar bargo, wanda ke hade da ciwon nono (sake nazari a cikin Jarida ta Duniya na Muhalli da Kiwon Lafiyar Jama'a, marubuta = Buehring GC, Sans HM / Title: Ciwon nono ya tafi hoto ko bidiyo mai zagaya yanar gizo da sauri? Bita na ƙwayar cutar sankarar bargo a cikin haddasawa, da damar da ke da alaƙa don rigakafin kansa. Har ila yau, kamuwa da ƙwayoyin cuta na iya ƙara haɗarin ciwon daji, kamar yadda aka gani a cikin Helicobacter pylori - ciwon daji na ciki.[3] Kwayoyin cututtukan da ke da alaƙa da ciwon daji sun haɗa da Schistosoma haematobium ( squamous cell carcinoma na mafitsara ) da kuma hanta flukes, Opisthorchis viverrini da Clonorchis sinensis ( cholangiocarcinoma ).[4]
Kamuwa da cuta, ciwon daji da mace-mace a kasashen da suka ci gaba
[gyara sashe | gyara masomin]Kamuwa da cuta shine abu na hudu mafi mahimmancin haɗari ga mutuwar ciwon daji a cikin ƙasashen da suka ci gaba, yana haifar da kusan 10% na mutuwar ciwon daji (duba rigakafin ciwon daji ), zuwa bayan taba (~ 30% na ciwon daji), abinci (~ 30%) da kiba (~ 15%). Ciwon daji yana haifar da kashi 22.5% na mace-mace a Amurka,[5] ta yadda kusan kashi 2% na mace-mace a Amurka ya zama sanadin ciwon daji da cututtuka ke haifarwa. Wannan yana kwatankwacin mace-macen da mura da ciwon huhu ke haifarwa, wanda ke haifar da kashi 2.1% na mace-mace a Amurka.[5]
Muhimmancin abubuwan da ke haifar da mutuwar ciwon daji a duniya
[gyara sashe | gyara masomin]A duk duniya a cikin shekarar 2015, mafi yawan abubuwan da ke haifar da mutuwar ciwon daji sune ciwon huhu (mutuwar miliyan 1.6), ciwon hanta (mutuwar 745,000), da ciwon ciki (mutuwar 723,000).[6] Ciwon daji na huhu yana da yawa saboda abubuwan da ba sa kamuwa da su, kamar hayakin taba. Duk da haka, ciwon hanta da ciki na farko ne saboda cututtuka masu yaduwa. Ciwon daji na hanta yana faruwa ne ta hanyar kamuwa da cutar hepatitis B (HBV) da kuma cutar hanta ta C (HBC) kuma ciwon daji na ciki yana da yawa daga kwayoyin Helicobacter pylori . A duk duniya, kiyasin adadin mutanen da suka kamu da cutar HBV da/ko HCV sun kai miliyan 325.[7] Fiye da rabin al'ummar duniya suna fama da H. pylori kuma an kiyasta cewa marasa lafiya na H. pylori suna da haɗarin 1-2% na kamuwa da ciwon daji na ciki.[8]
Rashin kwanciyar hankali na kwayoyin halitta saboda cututtukan oncogenic
[gyara sashe | gyara masomin]Rashin kwanciyar hankali na al'ada ta hanyoyi daban-daban kamar lalacewar DNA da gyare-gyare na epigenetic[9] ya bayyana su ne ainihin abubuwan da ke haifar da ciwon daji na lokaci-lokaci (wanda ba na iyali ba). Duk da yake cututtuka suna da tasiri da yawa, kwayoyin cututtuka da ke kara haɗarin ciwon daji akai-akai sune tushen lalacewar DNA ko rashin zaman lafiyar kwayoyin halitta, kamar yadda aka tattauna a kasa don ƙwayoyin cuta na oncogenic da kwayoyin cutar oncogenic.[ana buƙatar hujja]
Kwayoyin cuta
[gyara sashe | gyara masomin]Kwayoyin cuta na ɗaya daga cikin mahimman abubuwan da ke haifar da ci gaban kansa a cikin ɗan adam. [2]
Kamuwa da wasu ƙwayoyin cutar hanta, musamman hepatitis B da hepatitis C, na iya haifar da kamuwa da cuta na dogon lokaci wanda ke haifar da ciwon hanta a cikin kusan 1 cikin 200 na mutanen da ke kamuwa da cutar hanta ta hepatitis B kowace shekara (ƙananan a Asiya, kaɗan a Arewacin Amurka). kuma a cikin kusan 1 cikin 45 na mutanen da ke kamuwa da cutar hanta a kowace shekara. [10] Mutanen da ke fama da ciwon hanta na kullum sun fi sau 200 suna iya kamuwa da ciwon hanta fiye da mutanen da ba su kamu da cutar ba.[10] Ciwon hanta, ko daga kamuwa da cutar hanta na yau da kullum ko amfani da barasa mai yawa ko wani dalili, yana da alaƙa da kansa tare da ci gaban ciwon hanta, kuma haɗuwa da cirrhosis da ciwon hanta na ƙwayar cuta yana ba da mafi girman hadarin ci gaban ciwon hanta. Domin ciwon hanta na ciwon hanta ya zama ruwan dare gama gari, kuma ciwon hanta yana da kisa, ciwon hanta na daya daga cikin abubuwan da ke haifar da mace-mace masu alaka da cutar kansa a duniya, musamman a gabashin Asiya da wasu sassan Afirka kudu da hamadar Sahara.[ana buƙatar hujja]
Human papillomaviruses (HPV) kuma suna haifar da ciwon daji da yawa. HPV sananne ne don haifar da warts na al'ada da gaske duk lokuta na ciwon daji na mahaifa, amma kuma yana iya kamuwa da cutar kansa da kuma haifar da ciwon daji a wasu sassa na jiki, ciki har da larynx na esophagus, rufin baki, hanci, da makogwaro, anus, vulva ., farji, da azzakari . smear Papanicolaou ("Pap" smear) gwajin cutar kansa ne da ake amfani da shi sosai don cutar kansar mahaifa. Hakanan ana samun gwajin tushen DNA don gano ƙwayar cuta.[11]
Herpesviruses rukuni ne na uku na ƙwayoyin cuta masu haifar da kansa. An danganta nau'ikan ƙwayoyin cuta guda biyu tare da ciwon daji: cutar Epstein-Barr (EBV) da cutar herpesvirus 8 (HHV-8).[12] EBV ya bayyana yana haifar da dukkanin carcinomas na nasopharyngeal marasa lafiya, Epstein-Barr kwayar cutar-tabbatacce yaduwa manyan lymphomas B-cell, ba a ƙayyade ba,[13] yaduwa da manyan lymphomas na B-cell da ke hade da kumburi na kullum,[13] Epstein-Barr kwayar cutar mucocutaneous. ulcers, [14] Lymphomatoid granulomatoses [15] kuma, a yawancin lokuta, fibrin da ke da alaƙa suna yaɗa manyan ƙwayoyin lymphoma na B-cell[16] da ƙwayoyin lymphomas NK/T na ciki .[17] Har ila yau, ya bayyana ya haifar da wasu lokuta na lymphoma, ciki har da lymphoma na Burkitt (wannan haɗin gwiwar yana da karfi musamman a Afirka) da kuma cutar Hodgkin,[12] EBV an samo shi a cikin wasu nau'o'in nau'in ciwon daji, kodayake rawar da ya taka wajen haifar da wadannan. sauran cututtukan daji ba su da kyau. KSHV / HHV-8[18] yana haifar da duk lokuta na sarcoma na Kaposi, kuma an same shi a wasu lokuta na ciwon daji da ake kira cutar Castleman .[12] Nazarin da suka shafi wasu nau'ikan ciwon daji, musamman ciwon daji na prostate, sun kasance marasa daidaituwa.[12] Duk waɗannan ƙwayoyin cuta na herpes suna yawanci ana samun su a cikin ƙwayoyin cuta na ƙwayoyin cuta na lymphoma na farko . [19] Herpesvirus kuma yana haifar da ciwon daji a cikin dabbobi, musamman cutar sankarar bargo da lymphomas.[12]
Human T cell lymphotropic virus ( HTLV-1 ) shi ne na farko mutum retrovirus gano ta Robert Gallo da abokan aiki a NIH .[19] Kwayar cutar tana haifar da cutar sankarar T-cell Adult, cutar da Takatsuki da abokan aiki a Japan suka fara bayyanawa [20] da sauran cututtukan jijiyoyin jini. Yana da alaƙa da ƙwayar cutar sankarar ƙwayar cuta ta T-cell ɗan adam, wata cuta ce ta deltaretrovirus, ƙwayar cutar sankarar bargo (BLV), wacce kwanan nan ta cika ka'idodin da ake tsammani don karɓar yiwuwar kamuwa da cutar sankarar nono, ta amfani da hanyoyin PCR masu mahimmanci don gano BLV, da samun samfuran. daga mata masu fama da ciwon nono idan aka kwatanta da samfurin kulawa na mata ba tare da tarihin ciwon nono ba. [21][22]
Merkel cell polyomavirus ita ce kwayar cutar kansar ɗan adam da aka gano kwanan nan, wacce ta keɓe daga kyallen carcinoma cell cell a cikin 2008,[23] ta ƙungiya ɗaya wacce ta gano KSHV /HHV-8 a 1994, ta amfani da sabuwar fasaha mai suna dijital transcriptome subtraction . Kimanin kashi 80 cikin 100 na cutar kansar kwayar cutar Merkel cell polyomavirus ne ke haifar da su; sauran ciwace-ciwacen suna da ilimin etiology da ba a san su ba kuma maiyuwa ne daban-daban histogenesis. Wannan shine kawai memba na wannan rukunin ƙwayoyin cuta da aka sani suna haifar da kansar ɗan adam amma sauran ƙwayoyin cuta na polyoma ana zargin su da kasancewa ƙarin ƙwayoyin cutar kansa.[ana buƙatar hujja]
HIV ba ya haifar da ciwon daji kai tsaye, amma yana da alaƙa da wasu cututtuka masu yawa, musamman sarcoma na Kaposi, lymphoma ba Hodgkin, ciwon daji na tsuliya da kuma ciwon mahaifa . Kaposi's sarcoma yana haifar da cutar herpesvirus 8 . Kwayoyin cutar kanjamau masu alaƙa da ciwon daji na dubura da sankarar mahaifa yawanci cutar papillomavirus ce ke haifar da ita. Bayan HIV ya lalata tsarin rigakafi, jiki ya daina sarrafa waɗannan ƙwayoyin cuta, kuma cututtuka suna bayyana a matsayin ciwon daji. Wasu jihohi na rashin ƙarfi na rigakafi (misali ƙarancin rigakafi na yau da kullun da rashi IgA ) suma suna da alaƙa da haɓakar haɗari.[24]
Kwayoyin cutar oncogenic na kowa
[gyara sashe | gyara masomin]A kasashen da suka ci gaba na Yamma, kwayar cutar papillomavirus (HPV), cutar hanta ta B (HBV) da kuma cutar hanta ta C (HCV) su ne kwayoyin cutar DNA na oncogenic da aka fi ci karo da su.[25]
Human papillomavirus
[gyara sashe | gyara masomin]A duk duniya, HPV yana haifar da kashi na biyu mafi girma na cututtukan daji masu alaƙa da kamuwa da cuta ko kashi 5.2% na nauyin kansar duniya. [26]
A Amurka, HPV yana haifar da mafi yawan ciwon daji na mahaifa, da kuma wasu ciwon daji na farji, vulva, azzakari, dubura, dubura, da oropharynx (ciwon daji na baya na makogwaro, ciki har da tushe na harshe da tonsils). [27] A kowace shekara a Amurka, ana samun sabbin cututtukan daji kusan 39,800 a sassan jiki inda ake samun HPV sau da yawa. HPV yana haifar da kusan 31,500 na waɗannan cututtukan daji. [27]
Kamar yadda Münger et al.[28] akwai kusan 200 HPVs. Ana iya rarraba su cikin mucosal da HPVs na fata. A cikin kowane ɗayan waɗannan ƙungiyoyin HPV, ƙwayoyin ƙwayoyin cuta guda ɗaya an sanya su babban haɗari ko ƙarancin haɗari gwargwadon kusanci ga mummunan ci gaban raunukan da suke haifarwa. Daga cikin ƙwayoyin cuta masu haɗari na HPV, HPV E6 da E7 oncoproteins suna aiki tare da p53 da retinoblastoma suppressors. Bugu da ƙari, babban haɗari na HPV E6 da E7 oncoproteins na iya haifar da rashin zaman lafiyar kwayoyin halitta a cikin ƙwayoyin sel na al'ada. Suna haifar da lahani na mitotic da aneuploidy ta hanyar shigar da rashin daidaituwa na centrosome.[ana buƙatar hujja]
Hepatitis B da Hepatitis C
[gyara sashe | gyara masomin]Hepatocarcinogenesis mai alaƙa da ƙwayar cutar hanta yana da matukar damuwa ga lafiya.[29] Ciwon daji na hanta a Amurka yana faruwa ne saboda manyan abubuwa guda uku: cutar hanta (HCV) (22%), cutar hanta B (HBV) (12%) da shan barasa (47%).[30] A cikin 2017 za a sami sabbin cututtukan daji na hanta kusan 40,710 a Amurka.[31] A duk duniya, yawan mace-macen ciwon daji na hanta ya fi yawa saboda cutar hanta (HBV) (33%), ƙasa da ƙasa saboda cutar hanta ta C (HCV) (21%), kuma har yanzu akai-akai saboda amfani da barasa (30%).[32] A duk duniya, cutar kansar hanta ita ce ta 4 mafi yawan sanadin mutuwar cutar kansa, wanda ke haifar da kashi 9% na yawan mace-macen cutar kansa (jimilar mutuwar cutar kansar hanta a shekarar 2015 ya zama 810,500), kuma yana zuwa, a cikin mita, bayan huhu, ciwon daji da ciwon ciki.[32]
Kamar yadda Takeda et al., [33] HCV da HBV suka yi nazari suna haifar da lalacewar DNA na carcinogenic da rashin zaman lafiyar kwayoyin halitta ta hanyoyi da yawa. HBV, kuma musamman HCV, yana haifar da kumburi na yau da kullun a cikin hanta, haɓaka nau'in oxygen mai amsawa (ROS). ROS yana hulɗa kai tsaye tare da DNA, yana haifar da lalacewar DNA da yawa (26 ROS da aka haifar da lalacewar DNA an kwatanta Yu et al.[34] Hakanan ya bayyana cewa kumburi na yau da kullun da kamuwa da cutar HCV ya haifar yana haifar da ƙayyadaddun ƙa'idodin cytidine deaminase (AID) da ke haifar da kunnawa a cikin hanta . AID yana haifar da maye gurbi a cikin DNA ta hanyar deamination (lalacewar DNA) na tushen cytosine, wanda ke canza cytosine zuwa uracil . Don haka, yana canza nau'in tushe na C:G zuwa madaidaicin U:G mai mutagenic. A cikin ƙarin dalilin lalacewar DNA, furotin na HCV yana ɗaure da furotin NBS1 kuma yana hana samuwar hadadden Mre11/NBS1/Rad50, ta haka yana hana haɗin DNA na enzymes gyara.[35] Sakamakon raguwar gyaran DNA na lalacewar DNA na mutagenic na iya tarawa.
Kwayoyin cuta
[gyara sashe | gyara masomin]H. pylori, kwayar cutar oncogenic na kowa
[gyara sashe | gyara masomin]Baya ga ƙwayoyin cuta, wasu nau'ikan ƙwayoyin cuta na iya haifar da wasu cututtukan daji. Mafi shahararren misali shine haɗin gwiwa tsakanin kamuwa da cuta mai tsanani na bangon ciki tare da Helicobacter pylori da ciwon daji na ciki. [36][37][38]
Kodayake bayanan sun bambanta tsakanin ƙasashe daban-daban, gabaɗaya kusan kashi 1% zuwa 3% na mutanen da ke ɗauke da Helicobacter pylori suna kamuwa da cutar kansar ciki a rayuwarsu idan aka kwatanta da 0.13% na mutanen da ba su da ciwon H. pylori .[38] [8]Saboda yawan kamuwa da cutar ta H. pylori a cikin manya masu matsakaicin shekaru (74% a kasashe masu tasowa da kashi 58% a cikin kasashen da suka ci gaba a 2002 ), da kuma yiwuwar 1% zuwa 3% masu kamuwa da cutar ciwon daji na ciki, H. pylori -induced ciwon daji na ciki shine na uku mafi girma sanadin mutuwar ciwon daji a duniya kamar na 2018.[39]
Hanyar da H. pylori ke haifar da ciwon daji na iya haɗawa da kumburi na yau da kullum, ko kuma aikin kai tsaye na wasu abubuwan da ke haifar da cutar, alal misali, CagA ya shiga cikin carcinogenesis.[40]
Kamar yadda Chang da Parsonnet suka yi bita,[41] ciwon H. pylori na yau da kullun a cikin cikin ɗan adam yana da alaƙa da kumburi na yau da kullun.[41] Wannan yana tare da sakin kwayar halitta na epithelial na nau'in oxygen mai amsawa (ROS) da nau'in nitrogen mai amsawa (RNOS), sannan taron macrophages da aka kunna a wurin ciki na kamuwa da cuta. Hakanan macrophages suna sakin ROS da RNOS. Matakan 8-oxo-2'-deoxyguanosine (8-OHdG), daya daga cikin manyan nau'o'in free radical-induced oxidative DNA lalacewa,[42] an ƙara fiye da 8-ninka a cikin DNA bayan kamuwa da cuta ta H. pylori, musamman ma. idan H. pylori yana da cagA tabbatacce. [43] Ƙaruwa a cikin 8-OHDG mai yiwuwa yana ƙara maye gurbi.[44] Bugu da ƙari, damuwa na oxidative, tare da manyan matakan 8-OHdG a cikin DNA, kuma yana rinjayar zaman lafiyar kwayoyin halitta ta hanyar canza yanayin chromatin. Irin waɗannan sauye-sauye na iya haifar da rashin daidaituwa na methylation na masu tallata ƙwayoyin cuta masu hana ƙari.[45]
Bugu da ƙari, maye gurbi da lalacewa ta kai tsaye ga DNA ta hanyar H. pylori -induced ROS, H. pylori - haifar da maye gurbi na carcinogenic da sauye-sauyen maganganun furotin suna sau da yawa sakamakon H. pylori - haifar da sauye-sauye na epigenetic .[46][47] Wadannan sauye-sauye na epigenetic sun hada da H. pylori -induced methylation na shafukan CpG a cikin masu tallata kwayoyin halitta [48] da H. pylori da aka canza yanayin bayyanar microRNAs masu yawa. [47]
Kamar yadda Santos da Ribeiro [48] H. pylori suka yi nazari akan kamuwa da cuta yana da alaƙa da raguwar haɓakar ingantattun injinan gyaran DNA, wanda ke ba da gudummawar tarin maye gurbi da rashin kwanciyar hankali na ƙwayoyin cuta da kuma ciwon daji na ciki. Musamman, kamar yadda Raza et al., [49] cututtuka na ciki na mutum tare da H. pylori ya haifar da raguwar furotin na epigenetically na sunadarai na gyaran DNA MLH1, MGMT da MRE11 . Bugu da kari, Raza et al. [49] ya nuna cewa ƙarin sunadaran gyaran DNA guda biyu, ERCC1 da PMS2 sun rage girman bayyanar furotin da epigenetically da zarar kamuwa da cutar H. pylori ya ci gaba da haifar da dyspepsia (wanda ke faruwa a cikin 20% na masu kamuwa da cuta [50] ).
Mycobacterium
[gyara sashe | gyara masomin]Tuberculosis abu ne mai haɗari ga kansar huhu .[51]
Sauran kwayoyin cuta
[gyara sashe | gyara masomin]Ɗaya daga cikin ƙididdiga na bayanan serological kwatanta kafin Chlamydia ciwon huhu kamuwa da cuta a cikin marasa lafiya tare da kuma ba tare da ciwon huhu ba ya samo sakamakon da ke nuna kafin kamuwa da cuta yana da alaƙa da ƙananan haɗari na tasowa ciwon huhu.[52][53][54]
Kwayoyin cuta
[gyara sashe | gyara masomin]Kwayoyin da ke haifar da schistosomiasis (bilharzia), musamman S. haematobium, na iya haifar da ciwon daji na mafitsara da ciwon daji a wasu wuraren.[55] Kumburi da ƙwai tsutsa ke haifarwa ya bayyana shine hanyar da ake haifar da ƙwayar ƙwayar ƙwayar cuta ta mafitsara. A Asiya, kamuwa da cuta ta S. japonicum yana da alaƙa da ciwon daji na colorectal.[55]
Distomiasis, lalacewa ta hanyar ciwon hanta na parasitic, yana hade da cholangiocarcinoma (ciwon daji na bile duct ) a Gabashin Asiya.[55]
Zazzabin cizon sauro yana da alaƙa da lymphoma na Burkitt a Afirka, musamman idan akwai tare da cutar Epstein-Barr, kodayake ba a sani ba ko yana da haɗari.[55]
Kwayoyin cuta kuma suna da mahimmancin cutar daji a cikin dabbobi . Cysticercus fasciolaris, nau'in tsutsa na nau'in tsutsa na kowa na cat, Taenia taeniaformis, yana haifar da ciwon daji a cikin berayen.[55] Spirocerca lupi yana da alaƙa da ciwon daji na esophageal a cikin karnuka, aƙalla a cikin kudancin Amurka.[55]
Wani sabon nau'i na shari'ar, wanda aka ruwaito a cikin 2015, ya ƙunshi wani mutum mai rigakafi wanda tepeworm ya sami mummunan canji, yana haifar da metastasis na tapeworm cell neoplasia a cikin jikinsa. Wannan ba ciwon daji ba ne na ƙwayoyin kansa amma na parasites. Wannan keɓantaccen shari'ar ba shi da wani tasiri mai mahimmanci kan lafiyar jama'a amma yana da ban sha'awa don kasancewa "wani sabon tsarin cuta wanda ke danganta kamuwa da cuta da kansa."[56]
Duba kuma
[gyara sashe | gyara masomin]- Barry Marshall
- Ciwon daji mai saurin yaduwa
- Harald zur Hausen
- Ka'idojin kawar da Helicobacter pylori
- J. Robin Warren
- Jerin cututtukan ɗan adam da ke da alaƙa da ƙwayoyin cuta masu kamuwa da cuta
- Jerin kwayoyin cutar oncogenic
- Francis Peyton Rous
Ci gaba da karatu
[gyara sashe | gyara masomin]- Cornwall, Claudia M. Kama ciwon daji : Neman abubuwan da ke haifar da ƙwayoyin cuta da ƙwayoyin cuta. Lanham: Rowman & Littlefield Publishers, 2013.
Manazarta
[gyara sashe | gyara masomin]- Littafi Mai Tsarki
- Pelini P (2016). "Tumor and metastases to the lung caused by the bacterium Pseudomonas". Journal Contribution. figshare. doi:10.6084/m9.figshare.3382954.v1.
Hanyoyin haɗi na waje
[gyara sashe | gyara masomin]Media related to Infectious causes of cancer at Wikimedia Commons
Manazarta
[gyara sashe | gyara masomin]- ↑ 1.0 1.1 de Martel C, Ferlay J, Franceschi S, Vignat J, Bray F, Forman D, Plummer M (June 2012). "Global burden of cancers attributable to infections in 2008: a review and synthetic analysis". The Lancet. Oncology. 13 (6): 607–15. doi:10.1016/S1470-2045(12)70137-7. PMID 22575588.
- ↑ 2.0 2.1 De Paoli P, Carbone A (October 2013). "Carcinogenic viruses and solid cancers without sufficient evidence of causal association". International Journal of Cancer. 133 (7): 1517–29. doi:10.1002/ijc.27995. PMID 23280523. S2CID 38402898.
- ↑ Pagano JS, Blaser M, Buendia MA, Damania B, Khalili K, Raab-Traub N, Roizman B (December 2004). "Infectious agents and cancer: criteria for a causal relation". Seminars in Cancer Biology. 14 (6): 453–71. doi:10.1016/j.semcancer.2004.06.009. PMID 15489139.
- ↑ Samaras V, Rafailidis PI, Mourtzoukou EG, Peppas G, Falagas ME (June 2010). "Chronic bacterial and parasitic infections and cancer: a review". Journal of Infection in Developing Countries. 4 (5): 267–81. doi:10.3855/jidc.819. PMID 20539059.
- ↑ 5.0 5.1 "The top 10 leading causes of death in the United States". 4 July 2019.
- ↑ Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, et al. (March 2015). "Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012". International Journal of Cancer. 136 (5): E359-86. doi:10.1002/ijc.29210. PMID 25220842. S2CID 6067341.
- ↑ "WHO | New hepatitis data highlight need for urgent global response". Archived from the original on April 21, 2017.
- ↑ 8.0 8.1 Kusters JG, van Vliet AH, Kuipers EJ (July 2006). "Pathogenesis of Helicobacter pylori infection". Clinical Microbiology Reviews. 19 (3): 449–90. doi:10.1128/CMR.00054-05. PMC 1539101. PMID 16847081.
- ↑ Ferguson LR, Chen H, Collins AR, Connell M, Damia G, Dasgupta S, et al. (December 2015). "Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition". Seminars in Cancer Biology. 35 Suppl: S5–S24. doi:10.1016/j.semcancer.2015.03.005. PMC 4600419. PMID 25869442.
- ↑ 10.0 10.1 Empty citation (help)
- ↑ McLachlin CM, Crum CP (2000). "Papillomaviruses and Cervical Neoplasia". In Bast RC, Kufe DW, Pollock RE, et al. (eds.). Holland-Frei Cancer Medicine (e.5 ed.). Hamilton, Ontario: B.C. Decker. ISBN 1-55009-113-1.
- ↑ 12.0 12.1 12.2 12.3 12.4 Cohen JI (2000). "Herpesviruses". In Bast RC, Kufe DW, Pollock RE, et al. (eds.). Cancer Medicine (e.5 ed.). Hamilton, Ontario: B.C. Decker. ISBN 1-55009-113-1.
- ↑ 13.0 13.1 Grimm KE, O'Malley DP (February 2019). "Aggressive B cell lymphomas in the 2017 revised WHO classification of tumors of hematopoietic and lymphoid tissues". Annals of Diagnostic Pathology. 38: 6–10. doi:10.1016/j.anndiagpath.2018.09.014. PMID 30380402.
- ↑ Ikeda T, Gion Y, Yoshino T, Sato Y (2019). "A review of EBV-positive mucocutaneous ulcers focusing on clinical and pathological aspects". Journal of Clinical and Experimental Hematopathology. 59 (2): 64–71. doi:10.3960/jslrt.18039. PMC 6661964. PMID 31257347.
- ↑ Sukswai N, Lyapichev K, Khoury JD, Medeiros LJ (January 2020). "Diffuse large B-cell lymphoma variants: an update". Pathology. 52 (1): 53–67. doi:10.1016/j.pathol.2019.08.013. PMID 31735345.
- ↑ Boyer DF, McKelvie PA, de Leval L, Edlefsen KL, Ko YH, Aberman ZA, Kovach AE, Masih A, Nishino HT, Weiss LM, Meeker AK, Nardi V, Palisoc M, Shao L, Pittaluga S, Ferry JA, Harris NL, Sohani AR (March 2017). "Fibrin-associated EBV-positive Large B-Cell Lymphoma: An Indolent Neoplasm With Features Distinct From Diffuse Large B-Cell Lymphoma Associated With Chronic Inflammation". The American Journal of Surgical Pathology. 41 (3): 299–312. doi:10.1097/PAS.0000000000000775. PMID 28195879. S2CID 3521190.
- ↑ Zanelli M, Mengoli MC, Del Sordo R, Cagini A, De Marco L, Simonetti E, Martino G, Zizzo M, Ascani S (November 2018). "Intravascular NK/T-cell lymphoma, Epstein-Barr virus positive with multiorgan involvement: a clinical dilemma". BMC Cancer. 18 (1): 1115. doi:10.1186/s12885-018-5001-6. PMC 6238309. PMID 30442097.
- ↑ Chang Y, Cesarman E, Pessin MS, Lee F, Culpepper J, Knowles DM, Moore PS (December 1994). "Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma". Science. 266 (5192): 1865–9. Bibcode:1994Sci...266.1865C. doi:10.1126/science.7997879. PMID 7997879.
- ↑ 19.0 19.1 Empty citation (help)
- ↑ Takatsuki K (March 2005). "Discovery of adult T-cell leukemia". Retrovirology. 2: 16. doi:10.1186/1742-4690-2-16. PMC 555581. PMID 15743528.
- ↑ Buehring GC, Shen HM, Jensen HM, Jin DL, Hudes M, Block G (2 September 2015). "Exposure to Bovine Leukemia Virus Is Associated with Breast Cancer: A Case-Control Study". PLOS ONE. 10 (9): e0134304. Bibcode:2015PLoSO..1034304B. doi:10.1371/journal.pone.0134304. PMC 4557937. PMID 26332838.
- ↑ Schwingel D, Andreolla AP, Erpen LM, Frandoloso R, Kreutz LC (27 February 2019). "Bovine leukemia virus DNA associated with breast cancer in women from South Brazil". Sci Rep. 9 (1): 2949. Bibcode:2019NatSR...9.2949S. doi:10.1038/s41598-019-39834-7. PMC 6393560. PMID 30814631.
- ↑ Feng H, Shuda M, Chang Y, Moore PS (February 2008). "Clonal integration of a polyomavirus in human Merkel cell carcinoma". Science. 319 (5866): 1096–100. Bibcode:2008Sci...319.1096F. doi:10.1126/science.1152586. PMC 2740911. PMID 18202256.
- ↑ Mellemkjaer L, Hammarstrom L, Andersen V, Yuen J, Heilmann C, Barington T, et al. (December 2002). "Cancer risk among patients with IgA deficiency or common variable immunodeficiency and their relatives: a combined Danish and Swedish study". Clinical and Experimental Immunology. 130 (3): 495–500. doi:10.1046/j.1365-2249.2002.02004.x. PMC 1906562. PMID 12452841.
- ↑ Anand P, Kunnumakkara AB, Kunnumakara AB, Sundaram C, Harikumar KB, Tharakan ST, et al. (September 2008). "Cancer is a preventable disease that requires major lifestyle changes". Pharmaceutical Research. 25 (9): 2097–116. doi:10.1007/s11095-008-9661-9. PMC 2515569. PMID 18626751.
- ↑ Parkin DM (June 2006). "The global health burden of infection-associated cancers in the year 2002". International Journal of Cancer. 118 (12): 3030–44. CiteSeerX 10.1.1.623.9022. doi:10.1002/ijc.21731. PMID 16404738. S2CID 10042384.
- ↑ 27.0 27.1 "Human Papillomavirus (HPV) and Cancer | CDC". 2019-08-21.
- ↑ Münger K, Baldwin A, Edwards KM, Hayakawa H, Nguyen CL, Owens M, et al. (November 2004). "Mechanisms of human papillomavirus-induced oncogenesis". Journal of Virology. 78 (21): 11451–60. doi:10.1128/JVI.78.21.11451-11460.2004. PMC 523272. PMID 15479788.
- ↑ Takeda H, Takai A, Inuzuka T, Marusawa H (January 2017). "Genetic basis of hepatitis virus-associated hepatocellular carcinoma: linkage between infection, inflammation, and tumorigenesis". Journal of Gastroenterology. 52 (1): 26–38. doi:10.1007/s00535-016-1273-2. PMID 27714455. S2CID 20772491.
- ↑ Akinyemiju T, Abera S, Ahmed M, Alam N, Alemayohu MA, Allen C, et al. (December 2017). "The Burden of Primary Liver Cancer and Underlying Etiologies From 1990 to 2015 at the Global, Regional, and National Level: Results From the Global Burden of Disease Study 2015". JAMA Oncology. 3 (12): 1683–1691. doi:10.1001/jamaoncol.2017.3055. PMC 5824275. PMID 28983565.
- ↑ "Key Statistics About Liver Cancer".
- ↑ 32.0 32.1 Wang H, Naghavi M, Allen C, Barber RM, Bhutta ZA, Carter A, et al. (GBD 2015 Mortality and Causes of Death Collaborators) (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.
- ↑ Empty citation (help)
- ↑ Yu Y, Cui Y, Niedernhofer LJ, Wang Y (December 2016). "Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage". Chemical Research in Toxicology. 29 (12): 2008–2039. doi:10.1021/acs.chemrestox.6b00265. PMC 5614522. PMID 27989142.
- ↑ Yu Y, Cui Y, Niedernhofer LJ, Wang Y (December 2016). "Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage". Chemical Research in Toxicology. 29 (12): 2008–2039. doi:10.1021/acs.chemrestox.6b00265. PMC 5614522. PMID 27989142.
- ↑ Peter S, Beglinger C (2007). "Helicobacter pylori and gastric cancer: the causal relationship". Digestion. 75 (1): 25–35. doi:10.1159/000101564. PMID 17429205. S2CID 21288653.
- ↑ Wang C, Yuan Y, Hunt RH (August 2007). "The association between Helicobacter pylori infection and early gastric cancer: a meta-analysis". The American Journal of Gastroenterology. 102 (8): 1789–98. PMID 17521398.
- ↑ 38.0 38.1 Traulsen, Jan; Zagami, Claudia; Daddi, Alice Anna; Boccellato, Francesco (2021-03-01). "Molecular modelling of the gastric barrier response, from infection to carcinogenesis". Best Practice & Research Clinical Gastroenterology (in Turanci). 50-51: 101737. doi:10.1016/j.bpg.2021.101737. ISSN 1521-6918. PMID 33975688 Check
|pmid=
value (help). S2CID 233900318 Check|s2cid=
value (help). - ↑ Ferlay J, Colombet M, Soerjomataram I, Mathers C, Parkin DM, Piñeros M, et al. (April 2019). "Estimating the global cancer incidence and mortality in 2018: GLOBOCAN sources and methods". International Journal of Cancer. 144 (8): 1941–1953. doi:10.1002/ijc.31937. PMID 30350310. S2CID 53034092.
- ↑ Hatakeyama M, Higashi H (December 2005). "Helicobacter pylori CagA: a new paradigm for bacterial carcinogenesis". Cancer Science. 96 (12): 835–43. doi:10.1111/j.1349-7006.2005.00130.x. PMID 16367902. S2CID 5721063.
- ↑ 41.0 41.1 Chang AH, Parsonnet J (October 2010). "Role of bacteria in oncogenesis". Clinical Microbiology Reviews. 23 (4): 837–57. doi:10.1128/CMR.00012-10. PMC 2952975. PMID 20930075.
- ↑ Valavanidis A, Vlachogianni T, Fiotakis C (April 2009). "8-hydroxy-2' -deoxyguanosine (8-OHdG): A critical biomarker of oxidative stress and carcinogenesis". Journal of Environmental Science and Health. Part C, Environmental Carcinogenesis & Ecotoxicology Reviews. 27 (2): 120–39. doi:10.1080/10590500902885684. PMID 19412858. S2CID 8109353.
- ↑ Raza Y, Khan A, Farooqui A, Mubarak M, Facista A, Akhtar SS, et al. (October 2014). "Oxidative DNA damage as a potential early biomarker of Helicobacter pylori associated carcinogenesis". Pathology & Oncology Research. 20 (4): 839–46. doi:10.1007/s12253-014-9762-1. PMID 24664859. S2CID 18727504.
- ↑ Yasui M, Kanemaru Y, Kamoshita N, Suzuki T, Arakawa T, Honma M (March 2014). "Tracing the fates of site-specifically introduced DNA adducts in the human genome". DNA Repair. 15: 11–20. doi:10.1016/j.dnarep.2014.01.003. PMID 24559511.
- ↑ Nishida N, Arizumi T, Takita M, Kitai S, Yada N, Hagiwara S, et al. (2013). "Reactive oxygen species induce epigenetic instability through the formation of 8-hydroxydeoxyguanosine in human hepatocarcinogenesis". Digestive Diseases. 31 (5–6): 459–66. doi:10.1159/000355245. PMID 24281021. S2CID 23484545.
- ↑ Muhammad JS, Eladl MA, Khoder G (February 2019). "Helicobacter pylori-induced DNA Methylation as an Epigenetic Modulator of Gastric Cancer: Recent Outcomes and Future Direction". Pathogens. 8 (1): 23. doi:10.3390/pathogens8010023. PMC 6471032. PMID 30781778.
- ↑ 47.0 47.1 Noto JM, Peek RM (2011). "The role of microRNAs in Helicobacter pylori pathogenesis and gastric carcinogenesis". Frontiers in Cellular and Infection Microbiology. 1: 21. doi:10.3389/fcimb.2011.00021. PMC 3417373. PMID 22919587.
- ↑ 48.0 48.1 Empty citation (help)
- ↑ 49.0 49.1 Raza Y, Ahmed A, Khan A, Chishti AA, Akhter SS, Mubarak M, et al. (February 2020). "Helicobacter pylori severely reduces expression of DNA repair proteins PMS2 and ERCC1 in gastritis and gastric cancer". DNA Repair. 89: 102836. doi:10.1016/j.dnarep.2020.102836. PMID 32143126.
- ↑ Dore MP, Pes GM, Bassotti G, Usai-Satta P (2016). "Dyspepsia: When and How to Test for Helicobacter pylori Infection". Gastroenterology Research and Practice. 2016: 8463614. doi:10.1155/2016/8463614. PMC 4864555. PMID 27239194.
- ↑ Pallis AG, Syrigos KN (December 2013). "Lung cancer in never smokers: disease characteristics and risk factors". Critical Reviews in Oncology/Hematology. 88 (3): 494–503. doi:10.1016/j.critrevonc.2013.06.011. PMID 23921082.
- ↑ Zhan P, Suo LJ, Qian Q, Shen XK, Qiu LX, Yu LK, Song Y, et al. (March 2011). "Chlamydia pneumoniae infection and lung cancer risk: a meta-analysis". European Journal of Cancer. 47 (5): 742–7. doi:10.1016/j.ejca.2010.11.003. PMID 21194924.
- ↑ Mager DL (March 2006). "Bacteria and cancer: cause, coincidence or cure? A review". Journal of Translational Medicine. 4 (1): 14. doi:10.1186/1479-5876-4-14. PMC 1479838. PMID 16566840.
- ↑ Littman AJ, Jackson LA, Vaughan TL (April 2005). "Chlamydia pneumoniae and lung cancer: epidemiologic evidence". Cancer Epidemiology, Biomarkers & Prevention. 14 (4): 773–8. doi:10.1158/1055-9965.EPI-04-0599. PMID 15824142. S2CID 6510957.
- ↑ 55.0 55.1 55.2 55.3 55.4 55.5 Mustacchi P (2000). "Parasites". In Bast RC, Kufe DW, Pollock RE, Weichselbaum RR, Holland JF, Frei E (eds.). Holland-Frei Cancer Medicine (5th ed.). Hamilton, Ontario: B.C. Decker. ISBN 1-55009-113-1.
- ↑ Muehlenbachs A, Bhatnagar J, Agudelo CA, Hidron A, Eberhard ML, Mathison BA, et al. (November 2015). "Malignant Transformation of Hymenolepis nana in a Human Host". The New England Journal of Medicine. 373 (19): 1845–52. doi:10.1056/NEJMoa1505892. PMID 26535513.
- Articles using generic infobox
- All articles with unsourced statements
- Articles with unsourced statements from March 2021
- Articles with invalid date parameter in template
- Commons category link from Wikidata
- Cutar daji
- Shafuka masu fassarorin da ba'a duba ba
- CS1: long volume value
- Pages with empty citations
- CS1 errors: S2CID
- CS1 errors: PMID
- CS1 Turanci-language sources (en)