CAJ | 학술논문

目的探讨人乳头瘤病毒16(HPV16)和Epstein-Barr病毒(EBV)在不同病理类型乳腺癌及乳腺良性病变中的表达。方法采用PCR方法对2013年6月至2014年6月本院收治的90例不同病理类型的乳腺癌(40例浸润性导管癌、30例浸润性小叶癌,20例原位癌)、20例乳腺纤维瘤以及10例乳腺正常组织标本HPV16的E6基因位点和EBV的内部重复序列BamHIW区域进行扩增,并采用免疫组织化学方法对上述标本进行HPV16和EBV潜在膜蛋白( LMP-1)染色,以判断标本是否有HPV16及EBV感染,计算病毒检出率。比较不同病理类型乳腺癌的病毒检出率及比较PCR、免疫组织化学两种方法对乳腺组织标本病毒感染的检出率有无差异采用χ2检验。不同病理类型的乳腺癌标本中HPV16及EBV阳性细胞率的比较选用方差分析以及Bonferroni两两比较。结果 PCR结果显示：HPV16病毒检出率在乳腺癌标本为44.44%(40/90),乳腺纤维瘤标本为5%(1/20),正常乳腺组织为0；EBV的病毒检出率在乳腺癌标本中为43.33%(39/90),乳腺纤维瘤标本及正常乳腺组织均为0。在不同病理类型乳腺癌中,HPV16和 EBV 的病毒检出率差异均无统计学意义(χ2=1.238,P=0.539；χ2=1.867,P=0.393)。免疫组织化学结果显示：HPV16病毒检出率在乳腺癌标本为42.22%(38/90),乳腺纤维瘤标本为5%(1/20),正常乳腺组织为0；EBV病毒检出率在乳腺癌标本为42.22%(38/90),乳腺纤维瘤标本及正常乳腺组织均为0。有HPV16病毒感染的乳腺癌组织标本中,HPV16阳性细胞率在浸润性导管癌为(29.78±0.38)%,浸润性小叶癌为(28.31±0.53)%,原位癌为(51.83±0.65)%,3组比较差异有统计学意义(F=537.779,P=0.000)；有 EBV 病毒感染的乳腺癌组织标本中,EBV 阳性细胞率分别为(29.73±0.51)%、(28.14±0.65)%及(51.11±0.68)%,3组比较差异有统计学意义(F=427.771,P=0.000)；原位癌标本中,HPV16和EBV的阳性细胞率均显著高于其他两种病理类型的乳腺癌( P均=0.000)。两种方法对乳腺癌标本 HPV16及 EBV 的检出率差异不具有统计学意义(χ2=0.090, P=0.764；χ2=0.023,P=0.880)。结论 HPV16和EBV两种病毒的感染与乳腺癌的发生可能有一定的关系,其感染程度可能与乳腺癌的病理类型有关。目的探討人乳頭瘤病毒16(HPV16)和Epstein-Barr病毒(EBV)在不同病理類型乳腺癌及乳腺良性病變中的錶達。方法採用PCR方法對2013年6月至2014年6月本院收治的90例不同病理類型的乳腺癌(40例浸潤性導管癌、30例浸潤性小葉癌,20例原位癌)、20例乳腺纖維瘤以及10例乳腺正常組織標本HPV16的E6基因位點和EBV的內部重複序列BamHIW區域進行擴增,併採用免疫組織化學方法對上述標本進行HPV16和EBV潛在膜蛋白( LMP-1)染色,以判斷標本是否有HPV16及EBV感染,計算病毒檢齣率。比較不同病理類型乳腺癌的病毒檢齣率及比較PCR、免疫組織化學兩種方法對乳腺組織標本病毒感染的檢齣率有無差異採用χ2檢驗。不同病理類型的乳腺癌標本中HPV16及EBV暘性細胞率的比較選用方差分析以及Bonferroni兩兩比較。結果 PCR結果顯示：HPV16病毒檢齣率在乳腺癌標本為44.44%(40/90),乳腺纖維瘤標本為5%(1/20),正常乳腺組織為0；EBV的病毒檢齣率在乳腺癌標本中為43.33%(39/90),乳腺纖維瘤標本及正常乳腺組織均為0。在不同病理類型乳腺癌中,HPV16和 EBV 的病毒檢齣率差異均無統計學意義(χ2=1.238,P=0.539；χ2=1.867,P=0.393)。免疫組織化學結果顯示：HPV16病毒檢齣率在乳腺癌標本為42.22%(38/90),乳腺纖維瘤標本為5%(1/20),正常乳腺組織為0；EBV病毒檢齣率在乳腺癌標本為42.22%(38/90),乳腺纖維瘤標本及正常乳腺組織均為0。有HPV16病毒感染的乳腺癌組織標本中,HPV16暘性細胞率在浸潤性導管癌為(29.78±0.38)%,浸潤性小葉癌為(28.31±0.53)%,原位癌為(51.83±0.65)%,3組比較差異有統計學意義(F=537.779,P=0.000)；有 EBV 病毒感染的乳腺癌組織標本中,EBV 暘性細胞率分彆為(29.73±0.51)%、(28.14±0.65)%及(51.11±0.68)%,3組比較差異有統計學意義(F=427.771,P=0.000)；原位癌標本中,HPV16和EBV的暘性細胞率均顯著高于其他兩種病理類型的乳腺癌( P均=0.000)。兩種方法對乳腺癌標本 HPV16及 EBV 的檢齣率差異不具有統計學意義(χ2=0.090, P=0.764；χ2=0.023,P=0.880)。結論 HPV16和EBV兩種病毒的感染與乳腺癌的髮生可能有一定的關繫,其感染程度可能與乳腺癌的病理類型有關。
목적탐토인유두류병독16(HPV16)화Epstein-Barr병독(EBV)재불동병리류형유선암급유선량성병변중적표체。방법채용PCR방법대2013년6월지2014년6월본원수치적90례불동병리류형적유선암(40례침윤성도관암、30례침윤성소협암,20례원위암)、20례유선섬유류이급10례유선정상조직표본HPV16적E6기인위점화EBV적내부중복서렬BamHIW구역진행확증,병채용면역조직화학방법대상술표본진행HPV16화EBV잠재막단백( LMP-1)염색,이판단표본시부유HPV16급EBV감염,계산병독검출솔。비교불동병리류형유선암적병독검출솔급비교PCR、면역조직화학량충방법대유선조직표본병독감염적검출솔유무차이채용χ2검험。불동병리류형적유선암표본중HPV16급EBV양성세포솔적비교선용방차분석이급Bonferroni량량비교。결과 PCR결과현시：HPV16병독검출솔재유선암표본위44.44%(40/90),유선섬유류표본위5%(1/20),정상유선조직위0；EBV적병독검출솔재유선암표본중위43.33%(39/90),유선섬유류표본급정상유선조직균위0。재불동병리류형유선암중,HPV16화 EBV 적병독검출솔차이균무통계학의의(χ2=1.238,P=0.539；χ2=1.867,P=0.393)。면역조직화학결과현시：HPV16병독검출솔재유선암표본위42.22%(38/90),유선섬유류표본위5%(1/20),정상유선조직위0；EBV병독검출솔재유선암표본위42.22%(38/90),유선섬유류표본급정상유선조직균위0。유HPV16병독감염적유선암조직표본중,HPV16양성세포솔재침윤성도관암위(29.78±0.38)%,침윤성소협암위(28.31±0.53)%,원위암위(51.83±0.65)%,3조비교차이유통계학의의(F=537.779,P=0.000)；유 EBV 병독감염적유선암조직표본중,EBV 양성세포솔분별위(29.73±0.51)%、(28.14±0.65)%급(51.11±0.68)%,3조비교차이유통계학의의(F=427.771,P=0.000)；원위암표본중,HPV16화EBV적양성세포솔균현저고우기타량충병리류형적유선암( P균=0.000)。량충방법대유선암표본 HPV16급 EBV 적검출솔차이불구유통계학의의(χ2=0.090, P=0.764；χ2=0.023,P=0.880)。결론 HPV16화EBV량충병독적감염여유선암적발생가능유일정적관계,기감염정도가능여유선암적병리류형유관。
Objective To explore the expression of human papilloma virus 16 (HPV16) and Epstein-Barr virus( EBV) in different pathological types of breast cancer and breast benign lesions. Methods We analyzed the samples from 90 cases of different pathological types of breast cancer ( including 40 cases of invasive ductal carcinoma, 30 invasive lobular carcinoma and 20 carcinoma in situ), 20 cases of mammary fibroma and 10 cases of normal breast tissues. All specimens were collected from the patients treated in our hospital from June 2013 to June 2014. PCR was performed to amplify E6 gene site of HPV16 and the repeated sequence BamHIW of EBV. The expressions of HPV16 and latent membrane protein 1 (LMP-1) of EBV were detected by immunohistochemical staining to determine whether existed HPV16 or EBV infections, and the positive rate was calculated accordingly. The detection rate of virus between different pathological types of breast cancer and the detection rate of virus between PCR detection and immunohistochemistry was compared by χ2 test;the proportion of HPV16 positive cells and the proportion of EBV positive cells among different pathological types of breast cancer was compared by analysis of variance and Bonferroni pairwise comparison. Results PCR showed that HPV16 detection rate was 44. 44% (40/90) in breast cancer, 5% (1/20) in mammary fibroma and 0 in normal breast tissues; EBV detection rate was 43. 33% ( 39/90 ) in breast cancer, 0 in mammary fibroma and normal breast tissues; there were no statistically significant difference in the detection rate of HPV16 and EBV between different pathological types of breast cancer (χ2= 1. 238, P=0. 539; χ2= 1. 867, P=0. 393). Immunohistochemistry showed that HPV16 detection rate was 42. 22% (38/90) in breast cancer, 5% (1/20) in mammary fibroma and 0 in normal breast tissues; EBV detection rate was 42. 22%(38/90) in breast cancer, 0 in mammary fibroma and normal breast tissues. The proportion of HPV16 positive cells was (29. 78±0. 38)% in invasive ductal carcinoma, (28. 31±0. 53)% in invasive lobular carcinoma, (51. 83± 0. 65)% in carcinoma in situ, suggesting a significant difference (F=537. 779, P=0. 000). The proportion of EBV positive cells was (29. 73±0. 51)%, (28. 14±0. 65)% and (51. 11±0. 68)% respectively, which was significantly different (F=427. 771, P=0. 000);the sample of carcinoma in situ showed the higher proportion of HPV16 and EBV positive cells, compared with other two pathological types(all P=0. 000). The detection rates of HPV16 or EBV by PCR and immunohistochemistry in breast cancer specimens were not significantly different (χ2=0. 090, P=0. 764; χ2=0. 023, P=0. 880). Conclusion The infection of HPV16 and EBV may be related to the occurrence of breast cancer, and the infection degree is probably related to the pathological types of breast cancer.