本文選題：浸潤性微乳頭狀癌 + 結(jié)直腸腺癌��； 參考：《浙江大學(xué)》2017年碩士論文

【摘要】：背景:浸潤性微乳頭狀癌被認為是具有明顯侵襲性行為的罕見腫瘤。然而,胃腸道腺癌中伴浸潤性微乳頭狀分化腺癌的病理學(xué)特征的研究報道則較為少見,特別是在結(jié)直腸腺癌中。這種罕見的組織學(xué)類型經(jīng)常侵襲淋巴血管,顯示侵襲性的生物學(xué)行為,導(dǎo)致預(yù)后不良。最近的研究顯示類似于乳腺的浸潤性微乳頭狀癌已經(jīng)被報道發(fā)生在各種器官,包括膀胱、輸尿管、肺和腮腺。還有報道顯示在結(jié)直腸腺癌中同樣發(fā)現(xiàn)浸潤性微乳頭狀分化。以往對結(jié)直腸癌中伴浸潤性微乳頭狀分化的腺癌的認識尚受到限制,對該類型腺癌的臨床意義尚不十分清楚。以前的原發(fā)性浸潤性微乳頭狀分化胃腸癌的研究顯示E-鈣粘蛋白(E-Cadherin)表達下調(diào),和存在于其他器官一樣,意味著伴浸潤性微乳頭狀分化在結(jié)直腸腺癌中的存在是一個不良的預(yù)后因素。材料和方法:1.回顧性分析2007年1月至2009年12月期間浙江大學(xué)附屬第二醫(yī)院治療的134例行手術(shù)治療的結(jié)直腸癌病例,其中存在伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組53例,與同一時期行手術(shù)治療的無微乳頭狀分化的對照組腺癌81例,對比分析兩組腺癌的臨床病理學(xué)特征。2.通過免疫組化方法研究分析EMA、CD10、E-Cadherin在伴浸潤性微乳頭狀分化結(jié)直腸腺癌和無微乳頭狀分化普通結(jié)直腸腺癌中的表達差異。3.采用SPSS16軟件進行統(tǒng)計學(xué)分析。結(jié)果:1.實驗組53例(39.5%)組織學(xué)顯示伴浸潤性微乳頭狀分化;對照組58例(43.3%)為無微乳頭分化普通中-高分化腺癌及23例(17.2%)為無微乳頭分化普通低分化腺癌。中位年齡為伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組和對照組分別為62.1±11.2歲和60.4±12.1歲(P=0.37)。在性別分布,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組中男性32(60.4%)例;對照組中男性49(60.5%)例(P=0.565)。在腫瘤部位,伴浸潤性微乳頭狀分化組在結(jié)腸有36(67.9%)例,直腸有17(32.1%)例;對照組中結(jié)腸48(59.3%)例,直腸33(40.7%)例(P=0.203),差異均無顯著統(tǒng)計學(xué)意義。2.組織病理學(xué)表現(xiàn)相比。伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組和對照組在腫瘤大體類型上,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組多見為潰瘍型,占58.5%;而對照組多見為隆起型,占70.4%,差異具有明顯統(tǒng)計學(xué)意義(P0.001)。在原發(fā)腫瘤的大小上發(fā)現(xiàn),腫瘤的長徑在伴浸潤性微乳頭分化的結(jié)直腸腺癌組明顯小于對照組(P0.001)。在腫瘤浸潤的深度,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組浸潤至粘膜下層0(0%)例,肌層及漿膜下層12(22.6%)例,穿透漿膜層41(77.4%)例;對照組浸潤至粘膜下層4(4.9%)例,肌層及漿膜下層33(40.7%)例,穿透漿膜層44(54.3%)例(P=0.015)。3.本研究發(fā)現(xiàn),在腫瘤組織的侵襲程度上,淋巴侵犯、血管侵犯和神經(jīng)侵犯在兩組之間均有明顯統(tǒng)計學(xué)差異,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組的血管侵犯程度明顯高于對照組(13.2%和2.5%);神經(jīng)侵犯程度也明顯高于對照組(18.9%和3.7%);伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組中有66%存在淋巴結(jié)轉(zhuǎn)移,高于對照組的49.4%。其中淋巴結(jié)陽性數(shù)量上兩組之間差異具有顯著統(tǒng)計學(xué)差異,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組的3.8±1.7個和對照組的2.4±1.1個(P0.001)。此外,手術(shù)中發(fā)現(xiàn)伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組有12(22.6%)例發(fā)現(xiàn)有遠處轉(zhuǎn)移,而對照組為4(4.9%)例有遠處轉(zhuǎn)移(P0.001)。但是在淋巴結(jié)檢出數(shù)目上差異無統(tǒng)計學(xué)意義,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組為13.5±4.9個,對照組為14.4±5.6個(P=0.897)。術(shù)后腫瘤病理分級,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組15(28.3%)例為Ⅰ～Ⅱ期,38(71.7%)例為Ⅲ-Ⅳ期;而對照組中分別為 38(46.9%)例和 43(53.1%)例(P=0.023)。4.在免疫組化結(jié)果中,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組的微乳頭癌細胞簇EMA抗體"內(nèi)向外"陽性模式有48(90.6%)例,陰性有5(9.4%)例;與無微乳頭分化的對照組相比,在各個分類之間差異均有意義(P=0.001)。伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組的微乳頭癌細胞簇CD10抗體"內(nèi)向外"陽性模式8(15.1%)例,陽性17(32.1%)例,陰性28(52.8%)例;與無微乳頭分化的對照組相比,在各個分類之間差異均有意義(P=0.001)。E-cadherin抗體在伴浸潤性微乳頭狀分化組癌細胞簇34(64.2%)例陽性,19(35.9%)例微乳頭癌細胞簇細胞與細胞接觸面弱陽性及間質(zhì)側(cè)膜陰性;在無微乳頭狀分化組所有病例81(100%)例均陽性,在各個分類之間差異均有意義(P0.001)。5.在生存時間上,兩組具有顯著統(tǒng)計學(xué)差異,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組明顯低于對照組(31.9±16.5月和37.8±14.7月,P=0.032)。此外,研究還發(fā)現(xiàn)伴浸潤性微乳頭狀分化結(jié)直腸腺癌患者的3年無病生存率是40.5%,而同時期對照組的3年無病生存率為72.6%(P=0.02)。此外,如圖3.4所示,伴浸潤性微乳頭狀分化的結(jié)直腸腺癌的患者3年總生存率為59.3%,而對照組為80.6%(P=0.07)。6.單變量分析結(jié)果顯示以下因素是患者生存的重要指標參數(shù):浸潤性微乳頭狀分化(P=0.001),腫瘤浸潤深度(P=0.015),腫瘤類型(P0.001),血管侵犯(P=0.020),神經(jīng)侵犯(P=0.004),淋巴結(jié)轉(zhuǎn)移(P=0.042),手術(shù)時遠處轉(zhuǎn)移(P0.001),腫瘤分期(P=0.023)。為進一步評估這8個因素的意義,進行多變量分析。多因素分析與Cox比例風(fēng)險模型顯示是否伴有浸潤性微乳頭狀分化(OR:4.28,95%置信區(qū)間(CI)1.493～12.320,P0.01)和淋巴結(jié)轉(zhuǎn)移[OR:6.29,95%置信區(qū)間(CI):1.749～22.686,P0.01)是無病生存的獨立預(yù)后因素,而腫瘤侵犯程度不是無病存活的獨立預(yù)后因素。結(jié)論:1.伴浸潤性微乳頭狀分化的結(jié)直腸腺癌與普通腺癌患者在性別、年齡、腫瘤部位上無明顯差異。2.伴浸潤性微乳頭狀分化的結(jié)直腸腺癌組患者顯示為明顯的血管侵犯,神經(jīng)侵犯,淋巴結(jié)轉(zhuǎn)移傾向,預(yù)后較普通結(jié)直腸腺癌組更差。3.CD10在部分伴浸潤性微乳頭狀分化結(jié)直腸腺癌病例中表達形式如同EMA一樣為"內(nèi)向外"陽性模式。
[Abstract]:Background: invasive micropapillary carcinoma is considered to be a rare tumor with obvious invasive behavior. However, the pathological features of the invasive micropapillary differentiated adenocarcinoma in the gastrointestinal adenocarcinoma are rarely reported, especially in the colorectal adenocarcinoma. This rare histologic type often invades the lymphatic vessels and shows invasiveness. Biological behavior, resulting in poor prognosis. Recent studies have shown that invasive micropapillary carcinoma similar to the breast has been reported in various organs, including the bladder, ureter, lung, and parotid gland. Also, invasive micropapillary differentiation is also found in colorectal adenocarcinoma. The recognition of adenocarcinoma of the differentiated adenocarcinoma is still limited. The clinical significance of this type of adenocarcinoma is not yet very clear. Previous studies of primary invasive micropapillary differentiated gastric cancer showed that the expression of E- cadherin (E-Cadherin) was downregulated, as in other organs, implying invasive micropapillary differentiation in colorectal adenocarcinoma. Existence is a bad prognostic factor. Materials and methods: 1. retrospective analysis of 134 cases of colorectal cancer treated by surgical treatment in the Second Affiliated Hospital of Zhejiang University from January 2007 to December 2009, including 53 cases of colorectal adenocarcinoma with invasive micropapillary differentiation, and non micropapillae treated with surgical treatment at the same time. A comparative analysis of 81 cases of adenocarcinoma in the control group. Comparative analysis of the clinicopathological features of the two groups of adenocarcinoma.2., the differential expression of EMA, CD10, and E-Cadherin in the adenocarcinoma with invasive micropapillary differentiated colorectal adenocarcinoma and non micropapillary differentiation of common colorectal adenocarcinoma was analyzed by SPSS16 software. 1. in the experimental group, 53 cases (39.5%) showed invasive micropapillary differentiation, and 58 cases in the control group (43.3%) were common medium high differentiated adenocarcinoma with no micropapillary differentiation and 23 cases (17.2%) as common low differentiated adenocarcinoma with no micropapillary differentiation. The median age of colorectal adenocarcinoma with invasive micropapilloma and the control group were 62.1 + 11.2 and 6, respectively. 0.4 + 12.1 years (P=0.37). In the sex distribution, 32 (60.4%) in the colorectal adenocarcinoma group with invasive micropapillary differentiation, 49 (60.5%) in the control group (P=0.565). In the tumor site, there were 36 (67.9%) in the colon with invasive micropapillary differentiation, 17 (32.1%) in the colon, 48 (59.3%) in the colon and rectal 33 (P=0) cases in the control group (P=0 .203), there was no significant difference in statistical significance of the.2. histopathological findings. The colorectal adenocarcinoma with invasive micropapillary differentiation and the control group were mostly ulcerated in the colorectal adenocarcinoma group with invasive micropapillary differentiation, accounting for 58.5%, while those in the group were mostly protuberant type, accounting for 70.4%, and the difference had obvious unification. Study significance (P0.001). The size of the primary tumor was found to be significantly smaller in the colorectal adenocarcinoma group with invasive micropapillary differentiation (P0.001). The depth of the tumor infiltration, with invasive micropapillary differentiation of the colorectal adenocarcinoma group infiltrated to 0 (0%) cases of the submucosa, and 12 (22.6%) cases of the muscularis and subserous layer. The serous layer 41 (77.4%) cases; the control group infiltrated to the submucosa 4 (4.9%) cases, myometrium and subserous layer 33 (40.7%) cases, penetrating serous layer 44 (54.3%) cases (P=0.015).3. study found that in the invasion degree of tumor tissue, lymphatic invasion, vascular invasion and nerve invasion were statistically significant differences between two groups, with invasive micropapillary differentiation. The degree of vascular invasion in the colorectal adenocarcinoma group was significantly higher than that in the control group (13.2% and 2.5%), and the degree of nerve invasion was significantly higher than that of the control group (18.9% and 3.7%), and 66% of the colorectal adenocarcinoma with invasive micropapillary differentiation had lymph node metastasis, which was higher than the 49.4%. in the control group, and the difference between the two groups was significant. The statistical difference was 3.8 + 1.7 in the colorectal adenocarcinoma group with invasive micropapillary differentiation and 2.4 + 1.1 in the control group (P0.001). In addition, 12 (22.6%) cases of colorectal adenocarcinoma with invasive micropapillary differentiation were found to have distant metastasis, while 4 (4.9%) in the control group had distant metastasis (P0.001), but in lymph node examination. There was no statistically significant difference in number, 13.5 + 4.9 in the colorectal adenocarcinoma group with invasive micropapillary differentiation, 14.4 in the control group (P=0.897), and 15 (28.3%) in the colorectal adenocarcinoma group with invasive micropapillary differentiation in 15 (28.3%) and 38 (71.7%) in stage III to IV; and 38 (46.) in the control group. 9%) 9% cases and 43 (53.1%) cases (P=0.023).4. in the results of immunohistochemical staining, 48 (90.6%) and 5 (9.4%) cases of micropapillary carcinoma cell cluster EMA antibody in the colorectal adenocarcinoma group with invasive micropapillary differentiation, and 5 (9.4%) negative. Compared with the control group without micropapillary differentiation, there were significant differences between the various classifications (P=0.001). 8 (15.1%) cases of CD10 antibody "introvert" positive pattern in the colorectal adenocarcinoma group with moist micropapillary differentiation, positive 17 (32.1%) and negative 28 (52.8%). Compared with the control group without micropapillary differentiation, there were significant differences in various classifications (P=0.001).E-cadherin antibody in the invasive micropapillary differentiation group. 34 (64.2%) positive, 19 (35.9%) cases of micropapillary carcinoma cell cluster cells and cell contact surface weak positive and interstitial lateral membrane negative, all cases 81 (100%) cases in the non micropapillary differentiation group were positive, the difference between the various categories was significant (P0.001).5. in the survival time, two groups with significant statistical difference, accompanied by invasive micropapilla. The differentiated colorectal adenocarcinoma group was significantly lower than the control group (31.9 + 16.5 months and 37.8 + 14.7 months, P=0.032). In addition, the 3 year disease free survival rate of patients with invasive micropapillary differentiated colorectal adenocarcinoma was 40.5%, while the 3 year disease-free survival rate in the same period control group was 72.6% (P=0.02). In addition, as shown in Figure 3.4, accompanied by infiltrating micropapilla nipples. The total 3 year survival rate of the patients with colorectal adenocarcinoma was 59.3%, while the control group was 80.6% (P=0.07).6. univariate analysis. The following factors were important parameters for the survival of the patients: invasive micropapillary differentiation (P=0.001), tumor infiltration depth (P=0.015), tumor type (P0.001), vascular invasion (P=0.020), and nerve invasion (P=0.004). Lymph node metastasis (P=0.042), distant metastasis (P0.001), and tumor staging (P=0.023). Multivariable analysis was performed to further assess the significance of these 8 factors. Multifactor analysis and Cox proportional hazard model showed whether with invasive micropapillary differentiation (OR:4.28,95% confidence interval (CI) 1.493 to 12.320, P0.01) and lymph node metastasis [OR:6.29 95% confidence interval (CI): 1.749 to 22.686, P0.01) is an independent prognostic factor for disease free survival, and the degree of tumor invasion is not an independent prognostic factor for disease-free survival. Conclusion: there is no significant difference in gender, age, and tumor location between 1. patients with invasive micropapillary differentiation and common adenocarcinoma in.2. with invasive micropapillary differentiation. The patients with colorectal adenocarcinoma showed obvious vascular invasion, nerve invasion, lymph node metastasis, and worse prognosis than common colorectal adenocarcinoma. The expression of.3.CD10 in some cases with invasive micropapillary differentiated colorectal adenocarcinoma was as "introverted" positive pattern as EMA.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R735.34

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