子宫内膜与卵巢原发双癌的分子机制研究进展

女性生殖道原发双癌约占所有妇科肿瘤的1%～2%,其中最常见的是子宫内膜与卵巢原发双癌(SEOC)。原发双癌约占所有卵巢癌的10%,约占所有子宫内膜癌的5%。相对于单发肿瘤,双癌发病时肿瘤期别较早、病理分级较低,预后较好,因此,临床上对于原发早期双癌的治疗原则也有别与于单发的卵巢或子宫内膜转移癌。但目前原发的诊断标准及与转移癌的鉴别诊断标准尚存在诸多争议。本文旨在探讨SEOC的临床及分子生物学、分子遗传学特点,进而为临床诊疗提供更确切的理论依据。     

同时性多原发肺癌诊治体会(附5例报告)

目的探讨多原发肺癌的手术方式选择。方法对5例诊断为同时性多原发肺癌患者的临床病例资料进行回顾性分析,按肿瘤不同的生长部位采取不同的手术方式。结果本组均行一期胸腔镜手术:无手术死亡;慢性胸腔积液l例,治愈。结论多原发肺癌的治疗主要还是采取手术切除,其前提是最大限度的保证肺功能;胸腔镜手术为同期多肺叶手术提供更大可能。     

双镜联合治疗同时性多原发肺癌13例临床分析

目的评估电视辅助胸腔镜手术(video-assisted thoracoscopic surgery,VATS)联合电磁导航支气管镜(electromagnetic navigation bronchoscopy,ENB)引导微波消融(microwave ablation,MWA)治疗同时性多原发肺癌(Synchronous multiple primary lung cancer,sMPLC)的安全性和可行性。方法回顾性分析2017年3月~2020年9月我院接受VATS联合ENB引导MWA治疗的13例sMPLC病人的临床资料。结果 13例sMPLC总病灶数44个,其中手术切除31个,ENB引导MWA13个。手术方式以肺段切除为主,占46.2%。手术切除主病灶大小为(22.2±12.8)mm。MWA病灶大小为(10.2±5.8)mm。术后第1天引流量为(177.7±93.3)ml,术后胸管拔除时间为(2.8±1.8)天,术后住院时间为(3.7±1.8)天。术后发生1例持续性肺漏气,无其他并发症。术后随访平均时间为(10.6±10.5)个月,无复发及死亡。结论 VATS联合ENB引导MWA治疗sMPLC具有一定的安全性和可行性。通过手术切除主要病灶和淋巴结清扫,精确病理分期,从而指导术后个体化治疗。ENB引导MWA术并不会增加病人围术期风险,可减少手术切除范围,最大限度保留肺功能。     

多原发肺癌的外科治疗

多原发肺癌(multiple primary lung cancer,MPLC)以往认为是一种较少见的疾病,但随着螺旋CT以及PET等影像学技术的发展,临床上越来越多的MPLC被发现.其原因可能为(1)临床上肺癌的发病率逐年增高,MPLC作为一种特殊的肺癌越来越常见;(2)随着新技术、新术式的应用,肺癌患者的生存率较以前提高,患者术后二次原发肺癌的风险也相应增加;(3)新的诊断技术使更多的MPLC被发现.     

肺癌患者多原发恶性肿瘤的诊断和治疗

作者报告本院经手术病理证实的１０３７例肺癌中，多原发恶性肿瘤３６例，占３。５％。多原发肺癌１５例，占１。４％，（其中１４例为双原发癌，１例为三原发癌）；肺癌与其他脏器恶性肿瘤２１例，占２。０％（其中１９例为双原发恶性肿瘤，２例为三原发癌）。作者就多原发肿瘤发病率升高的原因、诊断和治疗等进行了讨论，并认为早期诊断和外科治疗能增加生存率。     

多原发非小细胞肺癌的诊断与外科治疗进展

随着疾病谱变化和技术进步,特别是早期肺癌筛查的开展,非小细胞肺癌(NSCLC)的临床表现发生了巨大的变化,表现为从中心型病变向周围型病变的转变、鳞癌向腺癌的转变、巨块型向小结节的转变、单发病灶向多发病灶的转变。其中,多灶肺癌可为多原发肺癌或肺癌肺内转移,其鉴别诊断与预后是影响治疗策略的重要因素。该文通过总结最新的文献进展,结合该院对此类疾病的研究结果,对多原发肺癌的诊断与外科治疗进展作一综述。     

EB病毒阳性的胃癌与伴有淋巴样间质的胃癌——诊断及分子检测进展

EB病毒阳性的胃癌与伴有淋巴样间质的胃癌均属于胃癌特殊病理亚型。其组织学形态、免疫学与遗传学特征存在部分重叠,却不完全相同。因此,这一组肿瘤不仅引起病理医师诊断上的困惑,同时也不利于临床治疗及后续研究。本文对这两种肿瘤以及与之相近诊断术语作详细介绍及对比,探讨其临床病理特征、遗传学改变、分子检测及治疗进展,并归纳总结现存争议及未来研究方向。     

细胞遗传学与外科(综合报道)

细胞遗传学已成为肿瘤特征的重要部分，有部分的肿瘤细胞遗传学和分子学研究有助于诊断、指导治疗和预测结果。本文介绍了有关淋巴瘤、平滑肌肉瘤、胰腺癌、甲状腺髓样癌、乳腺癌和胃肠道癌肿的细胞遗传学进展。     

5例同侧异时性第二原发肺癌的外科治疗

近年来,随着高分辨率CT的应用和CT复查的普及,第二原发肺癌(second primary lung cancer,SPLC)的患者逐年增多[1],对外科治疗提出了新的课题和挑战.现回顾性分析总结我们手术治疗的5例同侧异时性肺癌患者的临床资料,以探讨同侧异时性第二原发肺癌的诊断和手术方法.@@资料和方法2006年7月至2011年3月间我们为9例第二原发肺癌患者施行手术,占同期收治肺癌(9/830例)的1.1％,其中同侧异时性第二原发肺癌5例.此5例均为男性;平均年龄63.8岁.     

细胞遗传学与外科

细胞遗传学已成为肿瘤特征的重要部分，有部分的肿瘤细胞遗传学和分子学研究有助于诊断、指导治疗和预测结果，本文介绍了有关淋巴瘤、平滑肌肉瘤、胰腺瘤、甲状腺髓样癌、乳腺癌和胃肠道癌肿的细胞遗传学进展 。     

Photodynamic therapy for lung cancer: state of the art and expanded indications

Photodynamic therapy (PDT) has now achieved the status of a standard treatment modality for centrally located, early-stage lung cancer and is introduced on the home page of the US National Cancer Institute. Over the past decade, 145 patients (191 lesions) with central-type early-stage lung cancers have been treated with PDT in our hospital. Overall complete remission was obtained in 86.4% of the total number of lesions. In patients with advanced stage III disease, however, bronchi opening was successful in 61 out of 81 lesions (75%) for the PDT group compared with 143 of 177 (81%) in the Nd-YAG laser therapy group. Although quite recent, treatment using PDT has been introduced for the first time in patients with peripheral lung cancer, who did not previously meet the criteria for surgery. Eight patients underwent this trial, of which 3 achieved partial remission. No serious complications except for one case of pneumothorax, were noted. As increasing number of patients consider quality of life after therapy, the indications for PDT are expected to expand. The success in clinical trials of PDT for cancer treatment offers encouragement for its future use.     

Präventive Chirurgie des vererbten colorectalen Carcinoms als Folge molekularer Diagnostik

Numerous inherited genetic changes predisposing to cancer have already been identified and the number is increasing. Accurate prediction of individual risk by means of molecular diagnosis implies clinical consequences in the treatment of cancer-predisposing syndromes. Using familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC) as an example, we present here the underlying genetic changes that contribute to tumor development. These genetic alterations can be efficiently identified through molecular diagnostic techniques. Identification of the familial germline mutation permits one to distinguish mutation carriers from non-mutation carriers within affected families and results in individually tailored surveillance and prevention. Therefore, molecular diagnosis is making a contribution to the advances in preventive surgical therapy. The indications are discussed.     

肺癌干细胞标志物的研究现状

肺癌具有高度异质性,能够抵抗化疗药物治疗,5年生存率小于15%。尽管我们关于肺癌的知识在不断增多,但仍很难确定肺癌的异质性和耐药性的发病基础。肿瘤干细胞模型近年来吸引了很多注意力,通过这种模型可以解释各种肿瘤的异质性、耐药性、休眠、复发和转移。肿瘤干细胞理论较少涉及肺癌研究。本文综述了肺癌干细胞的鉴定方法,包括其细胞表面标志物和生物学特征,还讨论了肺癌干细胞与肺癌预后的关系,从而为消灭肺癌干细胞、攻克肺癌提供理论依据。     

Molecular targets and targeted therapies in bladder cancer management

Bladder cancer remains a significant health problem. Currently, conventional histopathologic evaluation criteria (tumor grade and stage) are limited in their ability to accurately predict tumor behavior. A significant number of patients with muscle-invasive or extravesical disease treated by radical cystectomy alone die of metastasis. Intense research efforts are being made to better identify and categorize tumors by their molecular alterations and biological characteristics. A majority of the aggressive, invasive bladder carcinomas have alterations in the p53 and retinoblastoma pathways that regulate the cell cycle by interacting with signal transduction pathways. Angiogenesis further contributes to the neoplastic growth by providing a constant supply of oxygen and nutrients. It is becoming apparent that the accumulation of genetic and molecular changes ultimately determines a tumor’s phenotype and subsequent clinical behavior. We provide a contemporary outline of our current understanding of the molecular and genetic events associated with tumorigenesis and progression. We emphasize the ways by which molecular biology is likely to affect the development of future therapies that will be able to target molecular alterations in individual tumors based on their respective profiles. The current status of targeted therapies for bladder cancer is also presented as well as the ongoing clinical trials. R. F. Youssef, A. P. Mitra, G. Bartsch Jr have contributed equally to this work.     

Impact of Smoking Status on the Biological Behavior of Lung Cancer

Cigarette smoking is the most established risk factor for lung carcinogenesis; however, its effects on the progression of lung cancer are still unclear. We reviewed the clinical investigations on this issue, which imply that smoking status is a treatment predictor and prognostic factor for several subtypes of lung cancer. Moreover, gene alterations and various protein expressions of tumor progression were recognized more frequently in the tumor tissues of smokers than in those of the never smokers. A cellular analysis revealed that tobacco-specific chemical compounds cause genetic or epigenetic alterations, modulate expressions of large numbers of genes that include molecules related to proliferation, invasion and metastasis, and deteriorate anti-tumor immunity. Our findings suggest that smoking promotes the progression of lung cancer, and that elucidating the molecular mechanisms may help to clarify the therapeutic targets.     

Molecular genetic parameters in pathogenesis and prognosis of testicular germ cell tumors

Aim of this review article was to critically analyze the recently described cytogenetic and molecular markers for testicular germ cell tumors with regard to their clinical utility. The isochromosme i(12p) represents the most common and characteristic cytogenetic finding which already appears in testicular carcinoma in situ. A number of proto-oncogenes (cyclin D and PTHLH) as well as putative tumor suppressor genes are localized on 12p; however, their role in pathogenesis and prognosis of testicular germ cell tumors has not been defined yet. Clinical characteristics of patients with familial testicular germ cell tumors indicate a genetic background for the development of testicular tumors. Although a number of chromosomal loci encoding potential testicular tumor susceptibility genes have been identified, the genetic basis of testicular cancer pathogenesis is still unknown. With regard to molecular prognostic risk factors most of the reported data on proliferation markers, tumor suppressor genes, proteases and adhesion molecules have to be confirmed in prospective randomized trials prior to their widespread clinical use. Based on the available data on prospective studies the percentage of embryonal carcinoma and vascular invasion appear to be the most significant prognosticators. Investigation and identification of those factors determining the aggressive biologic behavior of embryonal carcinoma compared to all other histological components appear to be most promising in the research for prgnosticators of metastatic disease. In conclusion, the increasing knowledge of molecular genetic events involved in pathogenesis and prognosis of testicular germ cell tumors will not only help to better understand development and progression of testicular cancer, but it will also define new approaches to classification and management of germ cell tumors     

Molecular pathogenesis of lung cancer

Lung cancer is the largest cancer killer of men and women in the united states. In addition to the progress made from antismoking primary prevention measures, new tools to help treat patients with lung cancer are emerging from the rapid advances in knowledge of the molecular pathogenesis of lung cancer. These tools include molecular and cellular biology and are starting to provide an insight into how the tumor cell, by altering oncogenes and tumor suppressor genes, achieves growth advantage, uncontrolled proliferation and metastatic behavior via disruption of key cell-cycle regulators and signal transduction cascades. Moreover, new knowledge is being developed in terms of the molecular definition of individual susceptibility to tobacco smoke carcinogens. These tools are being translated into clinical strategies to complement surgery, radiotherapy, and chemotherapy and also to assist in primary and secondary prevention efforts. This review summarizes current knowledge of the molecular pathogenesis of lung cancer. From this we know that respiratory epithelial cells require many genetic alterations to become invasive and metastatic cancer. We can detect cells with a few such changes in current and former smokers, offering the opportunity to intercede with a biomarker-monitored prevention and early detection effort. This will be coupled with new advances in computed tomography-based screening. Finally, because the molecular alterations are known, new mechanism-based therapies are being developed and brought to the clinic, including new drugs, vaccines, and gene therapy, which also must be integrated with standard therapies.     

Molecular genetics improves the management of hereditary non-polyposis colorectal cancer.

BACKGROUND: The syndrome of hereditary non-polyposis colorectal cancer (HNPCC) can be diagnosed fairly accurately using clinical criteria and a family history. Identifying HNPCC helps to prevent large-bowel cancer, or allows cancer to be treated at an early stage. Once the syndrome has been diagnosed a family member's risk can be judged approximately from a family tree, or it can now be predicted accurately if the causative mutation is known. OBJECTIVE: This study involved attempts to improve the management of a family with HNPCC over a period of 10 years. Clinical diagnostic criteria, colonoscopic surveillance, surgical treatment, genetic counselling, molecular genetic research, and finally predictive genetic testing were applied as they evolved during this time. SUBJECTS AND METHODS: A rural general practitioner first noted inherited large-bowel cancer in the family and began screening subjects as they presented, using rigid sigmoidoscopy at the local hospital. At the time that the disorder was recognised as being HNPCC (1987), screening by means of colonoscopy at our university hospital was aimed primarily at first-degree relatives of affected individuals. After realising how many were at risk, screening was brought closer to the family. A team of clinicians and researchers visited the local hospital to identify and counsel those at risk and to perform screening colonoscopy. Family members were recruited for research to find the gene and its mutation that causes the disease, to develop an accurate predictive test and to reduce the number of subjects undergoing surveillance colonoscopies. RESULTS: There are approximately 500 individuals in this family. In the 10 years of this study the number of subjects who have been counselled for increased genetic risk or who have requested colonoscopic surveillance for HNPCC in this kindred has increased from 20 to 140. After the causative mutation was found in the hMLH1 gene on chromosome 3, a test for it has reduced the number of subjects who need screening colonoscopy by over 70%. A protocol has been devised to inform family members, to acquire material for research in order to provide genetic counselling for (pre-test and post-test) risk, and to test for the mutation. Eventually, identifying those with the mutation should focus surveillance accurately. CONCLUSIONS: The benefits of restricting screening to subjects with the mutation that causes colorectal cancer and of performing operations to prevent cancer are hard to measure accurately. However, it is likely that at least half the family members will be able to avoid colonoscopic screening, some deaths from cancer should be prevented, and the cost of preventing and treating cancer in the family should fall substantially.     

Estimation of the risk of lung cancer in women participating in a population-based breast cancer screening program

IntroductionLung cancer mortality is increasing in women. In Spain, estimates suggest that lung cancer mortality may soon surpass breast cancer mortality, the main cause of cancer mortality among women. The aim of this study was to estimate the proportion of women at high risk of developing lung cancer in a group of participants in a population-based breast cancer screening program.MethodsCross-sectional study in a sample of women who participated in a population-based breast cancer screening program in 2016 in Hospitalet de Llobregat n = 1,601. High risk of lung cancer was defined according to the inclusion criteria of the National Lung Screening Trial (NLST) and the Dutch-Belgian randomized lung cancer screening trial (NELSON).ResultsAround 20% of smokers according to NLST and 40% of smokers according to NELSON criteria, and around 20% of former smokers according to both criteria, are at high risk of developing lung cancer. A positive and statistically significant trend is observed between the proportion of women at high risk and nicotine dependence measured with the brief Fagerström Test.ConclusionsA high proportion of participants in this breast cancer screening program have a high risk of developing lung cancer and would be eligible to participate in a lung cancer screening program. Population-based breast cancer screening programs may be useful to implement lung cancer primary prevention activities.