组织扩张术在即刻乳房再造中的应用

目的改进即刻乳房再造的手术方法,将软组织扩张术应用于即刻乳房再造术中,避免再造乳房术后出现"补丁样"外观,并保留乳房再造的最佳条件。方法在乳腺癌切除后即刻于胸大肌后间隙置入圆形扩张器,并于术后8~12周注水扩张至理想体积。Ⅱ期再造手术采用硅凝胶乳房假体、背阔肌肌皮瓣+硅凝胶乳房假体、背阔肌肌皮瓣及DIEP皮瓣置换扩张器完成乳房再造。结果 2009年6月至2011年6月,采用该技术进行扩张法即刻乳房再造36例,平均完成乳房再造时间3.5个月。术后无假体外露、皮瓣坏死等并发症出现,也无原手术切口的延长或新手术切口增加。术后随访6~12个月,患者对手术效果满意率达97.2%。结论采用组织扩张法进行即刻乳房再造,可以保留最佳的乳房再造条件,避免了术后放疗对乳房假体的影响,可以避免由于采用皮瓣修补胸部皮肤缺损而出现的"补丁样"外观,是理想的即刻乳房再造方法之一。     

组织扩张器在乳腺癌术后乳房重建中的应用现状

乳腺癌的治疗已经从传统的根治术发展到了现今的保乳及乳房重建治疗。假体置入在乳腺癌即刻乳房重建中得到广泛应用,但部分患者术后需行放射治疗,增加了假体包膜挛缩的发生率,同时二期乳房再造患者形成胸壁瘢痕组织,影响假体置入乳房再造效果。软组织扩张器的应用很好地解决了上述问题,作者就软组织扩张器在乳腺癌术后乳房重建中的应用现状进行综述。     

对侧胸廓内动脉穿支皮瓣修复巨大胸壁缺损或即刻乳房重建

目的探讨单侧乳腺癌改良根治术同时行对侧胸廓内动脉穿支皮瓣修复巨大胸壁缺损或即刻乳房重建的可行性及临床价值。方法回顾分析2013年7月至2016年5月安徽医科大学第一附属医院收治8例内乳区巨大乳腺癌患者的临床资料,其中7例患者行新辅助化疗。8例患者均在单侧乳腺癌改良根治术同时行对侧胸廓内动脉穿支皮瓣修复巨大胸壁缺损(1例)或即刻乳房重建(7例),且8例患者均同时行对侧乳房缩乳上提术,其中3例患者同时联合假体乳房重建术,4例患者同时行双侧乳头乳晕重建术。术后予以综合治疗。统计患者手术时间及住院时间,观察皮瓣成活情况及术后并发症,并调查患者对手术效果的满意度。结果平均手术时间为3.0 h(2.3~4.8 h)。平均住院时间为8.9 d(7.0~14.0 d)。进行了4~33个月的随访,中位随访23个月。术后8例皮瓣均未见坏死。1例皮瓣淤血,1例出现皮下积液,经过抽液后痊愈。患者供体区域未见明显并发症,对侧乳腺未见原发乳腺癌及远处转移。所有患者均对修复或者重建效果满意。结论对侧胸廓内动脉穿支皮瓣适用于特定人群的胸壁缺损修复或乳房重建,患者恢复快及供皮瓣区并发症低为其优点,尤其适用于内乳区巨大乳腺癌患者。     

保留乳头的乳腺癌改良根治术后Ⅰ期假体植入乳房重建术

目的探讨保留乳头的乳腺癌改良根治术Ⅰ期假体植入乳房重建的可行性。方法早期乳腺癌极少侵犯皮肤、乳头的特点,保留乳头行皮下切除 腋窝淋巴清扫,Ⅰ期假体植入乳房重建。结果对15例早期乳腺癌患者,行上述手术治疗,术后外观良好,双侧乳房对称。1例出现乳头坏死。术后随访10~41个月,所有病例均无局部复发或远处转移。结论对于早期乳腺癌,行保留乳头的乳腺癌改良根治术、Ⅰ期假体植入乳房重建,具有操作方便、效果明显,是安全可行的手术方法。     

乳腺切除术后即刻乳房再造术式的选择

乳腺切除术后即刻乳房再造与二期再造相比在术后效果、患者心理、住院时间以及所需费用等方面均具有明显优势.为乳腺癌术后患者选择一个合适的即刻乳房再造方式十分必要.本文对TRAM皮瓣、双蒂TRAM皮瓣、DIEP皮瓣、背阔肌肌皮瓣、扩张器/假体置入以及背阔肌肌皮瓣联合假体置入等各种即刻乳房再造术式的适应证与禁忌症进行综述.并从肿瘤学角度针对各种乳腺癌根治术如改良根治术、保留乳头、乳晕的乳腺切除术，以及保留皮肤的乳腺切除术、保乳手术后即刻乳房再造等术式的选择策略进行讨论.     

保留乳房天然结构的乳腺癌改良根治术后即刻乳房成形术的临床应用

目的探讨保留乳房天然结构的乳腺癌改良根治术后即刻自体组织乳房成形术在临床中的运用价值。方法乳腺癌患者12例,其中DCIS 6例,浸润性导管癌3例,小管癌1例,髓样癌1例,黏液癌1例;保留乳房皮肤的乳腺癌改良根治术9例,保留乳头乳晕复合体的乳腺癌改良根治术3例。全组均保留或重建乳房下皱襞,切除乳腺组织和腋窝淋巴结,应用下腹部横行腹直肌肌皮瓣或背阔肌肌皮瓣即刻乳房成形。结果横行腹直肌肌皮瓣乳房成形术3例,背阔肌肌皮瓣乳房成形术9例,术后皮瓣均存活,皮瓣血管通畅,成形乳房外观良好。结论对早期乳腺癌患者行保留乳房天然结构的乳腺癌改良根治术后即刻自体组织乳房成形,切口隐蔽,成形乳房形态效果良好,可以获得较好的美容效果。     

乳腺癌根治术后乳房重建方法及进展

近年来 ,对于乳腺癌的治疗不仅致力于提高乳腺癌患者的生存率 ,而且要重视手术治疗后的整复效果。对于早期乳腺癌患者 ,可采取保乳手术 ;对于肿瘤较大而需切除乳腺者 ,另 1种常用的治疗手段是根治性手术后做乳房重建 ,包括假体的植入及应用自身组织重建乳房。 2 0 0 0年 9月 ,美国国立医学研究所(ＮＩＨ )报道了对 135 0 0名接受假体植入的妇女进行的平均长达 12 .9年的随访结果 :假体植入不会增加妇女患乳腺癌的可能性。假体植入是乳腺癌根治术后乳房重建的 1种方式 ,这一发现无疑会坚定肿瘤外科医生开展乳腺癌根治术后乳房重建的信心。我…     

乳腺癌术后乳房重建术式的选择

目的探讨如何选择乳腺癌手术后乳房重建的手术方法及效果分析。方法根据患者乳腺癌手术的具体方法及个体差异，选择转移下腹部横行腹直肌肌皮瓣、背阔肌肌皮瓣、腹壁下动脉穿支游离皮瓣或联合假体乳房重建158例。结果转移下腹部横行腹直肌肌皮瓣乳房重建93例，其中即刻乳房重建65例（满意率为95．38％），延期乳房重建28例（满意率为92．86％）。背阔肌肌皮瓣或联合假体乳房重建59例，满意率为96．61％。腹壁下动脉穿支游离皮瓣乳房重建3例，满意率为100％。假体植入乳房重建3例，满意率为100％。结论乳腺癌手术后选择适当乳房重建的手术方法十分重要；根据个体差异选择不同乳房重建术式，使重建的乳房更加逼真，达到令人满意的效果。     

应用腹壁下动脉穿支皮瓣即刻乳房重建

目的总结乳腺癌切除同时应用腹壁下动脉穿支（DIEP）皮瓣行即刻乳房重建的手术经验,探讨DIEP皮瓣即刻乳房重建的适应证及优点。方法2003年4月-2009年6月,中国医学科学院肿瘤医院乳腺中心接受乳腺癌切除术患者21例（根治术6例,改良根治术15例）,术前应用多排螺旋CT（MDCT）血管造影及多普勒血流仪探明穿支位置,乳腺癌切除的同时,解剖腹壁下动脉穿支,形成腹壁下动脉穿支蒂皮瓣,与患侧胸背血管吻合,进行即刻乳房重建。结果术后随访6个月至6年。21例患者中,20例皮瓣全部存活,1例出现皮瓣远端1／3脂肪液化;胸部受区出现1例血肿;无腹壁膨隆、腹壁疝、切口脂肪液化等供区并发症;再造乳房外形满意,形态自然。结论乳腺癌切除同时,采用DIEP皮瓣进行即刻乳房重建,可以使患者免受乳房缺失的痛苦,同时具有受区组织条件好、皮瓣组织量丰富、供区损伤小及并发症少的优点,是一种理想的即刻乳房重建方法。     

乳腺癌改良根治术同期假体植入重建乳房

目的探讨乳腺癌行改良根治术后，同期硅胶假体植入重建乳房的可行性。方法2005年6月至2006年9月，对20例Ⅰ、Ⅱ期乳腺癌患者行保留皮肤的乳腺癌改良根治术后，同期于胸大、小肌间植入硅胶假体重建乳房，并根据冰冻切片检查结果决定是否保留乳头乳晕复合体。结果20例患者客观评价效果优良和尚好者达95％，主观评价效果优良和尚好者达100％。其中有6例保留乳头乳晕复合体。术后随访3～18个月，所有病例均无局部复发和远处转移，无明显术后并发症。结论保留皮肤的乳腺癌改良根治术后用硅胶假体行一期乳房重建，能达到满意的乳房美容效果，是治疗早期乳腺癌安全可行的方法。     

Mutations in normal breast tissue and breast tumours

The accumulation of mutations is a feature of all normal cells. The probability of any individual gene in any cell acquiring a mutation is, however, low. Cancer is therefore a rare disease in comparison with the number of susceptible cells. Mutations in normal tissue are stochastic, vary widely among cells and are therefore difficult to detect using standard methods because each change is so rare. If, however, a tissue such as the breast undergoes considerable clonal expansion, particularly if relatively late in life, normal tissue may have accumulated many thousands of detectable mutations. Since breast cancers are clonal and have almost certainly undergone many more cell divisions than normal cells, each tumour may have many millions of mutations, most of which are entirely innocent and some of which have accumulated in the cell of origin prior to tumorigenesis. Despite some claims to the contrary, even at normal mutation rates, clonal expansion within a tumour is quite sufficient to account for the mutations of five or six genes that are generally supposed necessary for carcinogenesis to occur. Hypermutability does, however, contribute to the pathogenesis of many cancers and, although evidence is indirect in breast cancer, may take forms such as karyotypic instability via centrosome amplification.     

Glycolytic enzymes in breast cancer, benign breast disease and normal breast tissue

The activities of hexokinase, phosphofructokinase, aldolase, enolase and pyruvate kinase were studied in breast cancer tissues, in comparison to benign breast disease and normal breast tissues. The enzyme activities in breast cancer were significantly increased compared to normal and benign breast tissues (p less than 0.001). Also the increase in activity in benign disease compared to normal was statistically significant (p less than 0.001). Within the group of benign diseases, fibroadenomas could be distinguished from fibrocystic disease, the former generally showing higher activities compared to the latter (p less than or equal to 0.05). Carcinoma subgroups, classified according to their histology, could not be recognized enzymologically. In addition, isozyme composition of pyruvate kinase and enolase was studied. We did not find a significant shift towards K type pyruvate kinase expression in benign disease compared to normal breast tissues. Also fibroadenomas did not differ from fibrocystic disease. However, the amount of K type pyruvate kinase in carcinomas proved to be significantly higher in comparison to benign disease and normal breast tissues (p less than 0.001). Expression of alpha gamma-enolase in normal breast tissue was virtually absent. In benign disease only a minority of specimens did show the hybrid alpha gamma-enolase. Nearly all carcinomas had alpha gamma-enolase expression and in 20% of the carcinomas gamma gamma-enolase could be detected (so-called neuron-specific enolase). By discriminant analysis, the function giving the best discrimination compared to the histological data was based on natural logarithm aldolase and the total of gamma-enolase subunits. Contrary to expectation, the regulator enzymes of glycolysis; i.e., hexokinase, phosphofructokinase and pyruvate kinase were not included in this discriminant function. The best fit produced a 90% correct classification in both benign and malignant disease. If these findings are confirmed to a larger series, the discrimination is sufficiently strong to form the basis of a clinically useful tool.     

Estrogen and progesterone receptors in breast carcinoma and in nonmalignant breast tissue

Since 1983 we have studied the relationship, in the same patient, between receptor status in breast carcinoma and in nonmalignant breast tissue. Fifty patients have been evaluated to date. The total unoccupied cytosol estrogen and progesterone receptors were determined by a dextran-coated charcoal method. In nonmalignant breast tissue we found a measurable receptor concentration above the sensitivity of the method in 62% of cases for estrogen receptors and in 44% of cases for progesterone receptors. No relationships were found between the receptor level of each tumor and that of the corresponding benign tissue. The data suggest that the levels of the receptors in the tumor and in the nonmalignant tissue are totally independent.     

Familial breast cancer and genes involved in breast carcinogenesis

Breast cancer has often been reported to run in families, and the most important risk factor for the disease is a family history of breast cancer. Numerous pedigrees and segregation analyses have suggested an autosomal dominant transmitted susceptibility to breast cancer. Familial breast cancer occurs alone or associated with other cancers in clinically distinguishable syndromes. Such cases may be characterized by early onset, bilateral disease, prolonged survival, and anticipation, mainly seen as a higher penetrance or earlier onset in subsequent generations. Studies of patients and tumors from these families as well as sporadic cases have led to localization and/or identification of a number of genes implicated in breast carcinogenesis of familial and sporadic breast cancer.     

Prostate specific antigen in breast cancer,benign breast disease and normal breast tissue

Prostate specific antigen (PSA) is a tumor marker used widely for the diagnosis and monitoring of prostatic adenocarcinoma. Recently, we provided evidence that PSA may also be produced by breast tumors. In this report we examined quantitatively the PSA levels in 199 breast tumors, 48 tissues with benign breast disease (BBD, 34 fibroadenomas), and 36 normal breast tissues. Significant amounts of PSA (≥ 0.030 ng of PSA per mg of total protein) were found in 28% of breast tumors, 65% of BBD tissues, and 33% of normal breast tissues. PSA positivity in breast tumors was highest in stage I disease (34%) and decreased with disease stage (24% in stage II and 18% in stage III–IV). Using polymerase chain reaction amplification we have shown PSA mRNA presence in patients with PSA protein-positive tissues (benign and malignant) but not in patients with PSA protein-negative tissues. Our data suggest that PSA is expressed frequently by normal breast tissue, by tissue of benign breast diseases, and by breast cancer tissue. Highest expression is seen in benign breast disease and lowest expression in advanced stage cancerous tissue. As PSA production is mediated by steroid hormones and their receptors, we propose that PSA may be a new marker of steroid hormone action in the normal or diseased female breast. The role of this enzyme in the development of breast diseases including breast cancer is currently unknown.     

Histochemically demonstrable phosphotyrosyl-protein phosphatase in normal human breast, in benign breast diseases and in breast cancer

The activity of phosphotyrosyl-protein phosphatase enzyme was investigated by a histochemical method in the normal human breast and in breast diseases in order to evaluate its possible significance in the genesis and in the growth of benign and malignant epithelial proliferative. In normal human breast tissue only a weak enzyme activity was present. The activity was elevated in benign disease in actively proliferative lesions and in 71% of the cases of breast cancers. When enzyme activity of breast cancers was compared with the content of receptors for epidermal growth factor and insulin-like growth factor-I, no association was found. It is concluded that phosphotyrosyl-protein phosphatase is increased in actively proliferating human breast diseases. Thus the putative increase in phosphotyrosyl-proteins mediating benign and malignant epithelial proliferations is rather caused by an increase in protein-tyrosine kinase activity than by a decrease in phosphotyrosyl-protein phosphatase activity.     

Tyrosine kinase activity in breast cancer, benign breast disease, and normal breast tissue

Tyrosine specific protein kinase activity was determined in 70 specimens of the human mammary gland. These included 28 cancers of the breast, 21 benign breast diseases, and 21 normal breast tissues. We measured tyrosine kinase activity in the cytosol fraction and in the membrane fraction of the homogenates. In addition cytosolic aldolase activity was measured. Tyrosine kinase activity was determined using poly(glutamic acid:tyrosine = 4:1) as an artificial substrate. Cancers of the breast exhibited considerable higher tyrosine kinase activities in both cytosol and membrane fractions, compared to benign breast tumors (P less than or equal to 0.001). Benign tumors demonstrated increased activities in cytosol in comparison to normal breast tissues (P less than 0.001). Furthermore, there appears to be a strong association of an enhanced expression of activity of tyrosine kinase in cytosol of primary carcinomas and early systemic relapse. In combination with aldolase activity a nearly complete discrimination is achieved between malignant specimens on one hand and benign and normal tissues on the other.     

Exposure to breast milk in infancy and risk of breast cancer

Early life exposures, such as being breastfed in infancy, may influence the risk of breast cancer in adulthood. We evaluated the risk of breast cancer in relation to ever having been breastfed in infancy among 9,442 women who participated in a population-based, case–control study. Cases were identified through cancer registries in three states (Massachusetts, New Hampshire, and Wisconsin); controls were identified through statewide drivers’ license lists or medicare lists. Data on known and suspected risk factors were obtained through telephone interview. We used unconditional logistic regression to assess the relation of breast cancer with ever having been breastfed and with breastfeeding duration (available for only 19% of breastfed women) in premenopausal women (1,986 cases and 1,760 controls) and postmenopausal women (2,600 cases and 2,493 controls). We found no evidence that ever having been breastfed in infancy was associated with breast cancer risk in either premenopausal women (odds ratio [OR] = 0.96; 95% confidence interval [CI] = 0.83–1.10) or postmenopausal women (OR = 0.98; 95% CI = 0.87–1.10). The association did not differ according to breast cancer stage, mother’s history of breast cancer, or any other reproductive factor assessed. Likewise, we found no association between breastfeeding duration and risk of breast cancer. Our results did not support the hypothesis that exposure to breast milk in infancy influences the risk of adult breast cancer.