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Cancer hospital还是tumor hospital

探讨与争鸣Cancer hospital 还是tumor hospital欧周罗(复旦大学肿瘤医院，上海200032)中图分类号:N04;R73文献标识码:A文章编号:1673－8578(2012)02－0033－02收稿日期:2012－02－07作者简介:欧周罗(1958—)，男，陕西凤翔人，博士，复旦大学教授，研究方向为肿瘤分子生物学。

通信方式:ouzhouluo@yahoo．com．cn．复旦大学肿瘤医院的英译名一为Fudan Uni-versity Cancer Hospital (FUCH )，二为Fudan Univer-sity Shanghai Cancer Center (FUSCC )，后者大概是为了同国外为数众多的癌症中心(cancer center )如得克萨斯大学MD 安德生(MD Anderson )癌症中心(MDACC )、纽约斯挪恩－柯特林(Sloan-Kettering )纪念癌症中心(MSKCC )、新加坡的国立癌症中心(NCC )等取得一致的英文名称，但多数学者提到肿瘤医院时首先想到的还是cancer hospital ，不久前当我初次听到法国专家将本院简称为“复驰”(FUCH )的时候甚至还有点诧异。

然而，路过肿瘤医院门前的49路公交车英文报站时用的却不是cancer hospital 而是tumor hospital ，其他公交线路亦然。

不言而喻，由于无数次反复强化的关系，tumor hospital 已经印在了许多乘客的脑海中。

究竟是学术界的cancer hospital 更准确，还是民间人士的tumor hospital 较贴切呢?如果将英文的“cancer ”“tumor ”分别直译为中文的“癌”“肿瘤”的话，看似简单明了，但cancer hospital 倒译回来可就成了“癌医院”，而国人显然已经接受并习惯于肿瘤医院这一称谓，很多人也许未曾听说过“癌医院”。

含有car的英语单词

以下是一些含有"car"的英语单词：
1.Carriage - 这个词通常用来描述一种四轮马车，或者火车的车厢。

2.Caramel - 是一种焦糖或糖蜜制品，也可以作为动词使用，意为“把……做成
焦糖色”。

3.Carcass - 指动物（尤其是家畜）的躯体，尤指去掉头、腿和内脏之后的躯
体。

4.Carcinoma - 这是一种恶性肿瘤，尤其是上皮组织的癌症。

5.Cardiac - 这个词与心脏有关，如“cardiac arrest”（心脏骤停）。

6.Cargo - 通常指船、飞机或车辆等运输工具装载的货物。

7.Carillon - 是一种大型钟琴，也指一组教堂钟。

8.Caribou - 这是一种生活在北美洲的驯鹿。

9.Carjacking - 指强行抢劫汽车的犯罪行为。

10.Carnal - 这个词通常用来描述与性有关的，或者肉体的。

请注意，这些词的含义可能会根据上下文的不同而有所变化。

所以，在使用这些词时，一定要清楚其含义，并根据上下文来正确理解。

特殊毒性试验

三、人群流行病学调查
➢ 动物致癌试验，根据阳性结果检出潜在的人类致癌物
➢ 描述流行病学调查或临床观察发现怀疑人类致癌物
➢ 病例-对照研究 ➢ 队列研究
四、致癌作用模型
转基因动物 (transgenic animal)
借助基因工程技术将确定的外源基因通过生殖细胞或早期胚胎导入动物个体的染色体上，在其基因组内稳定地整合经导入的外源基因，并能遗传给后代的一类动物
化学、物理或生物等致癌因素作用于细胞后，引起原癌基因突变使之激活，转变成癌基因后才会导致细胞癌变
2．抑癌基因 (anti-oncogene)
正常细胞分裂生长的负性调节因子，其编码的蛋白质能够降低或抑制细胞分裂活性，或称为肿瘤抑制基因(tumor suppressor gene)、肿瘤易感基因(tumor susceptibility gene)
致癌毒性试验
肿瘤(tumor，neoplasm) ：有分裂潜能的细胞受致癌因素作用后发ቤተ መጻሕፍቲ ባይዱ恶性转化和克隆性增生所形成的新生物
良性肿瘤：呈膨胀生长，与周围组织有明显的界限，多有包膜，它们生长常有“自限性”，对机体破坏较小
恶性肿瘤：癌和肉瘤
癌(carcinoma)：由上皮细胞来源的恶性肿瘤
肉瘤(sarcoma)：由间质细胞来源的恶性肿瘤
第三节
观察化学毒物致癌作用的基本方法
化学致癌物的判别
➢ 人群流行病学调查：两项以上由不同研究者在不同地点、不同对象中以不同调查方法获得的结论相符的证据；
➢ 动物实验证据：两项按现行常规设计进行，符合GLP（good laboratory practice），在不同物种动物中所得结果一致的动物致癌物鉴定资料。

结肠癌-carcinoma colon

USG of Whole Abdomen Chest X-Ray X-Ray of specific site involving bone pain CT- Scan MRI
-For local invasion - To see the extent
Other Investigations : - Carcino-Embryonic Ag (CEA) - Stool Cytology - IHC markers (KERATIN) - - DNA flow Cytometry - Immunoscintigraphy
CT scan is also used for the TNM staging of Ca Colon .
It is helpful for detecting distant metastases.
DUKE’S STAGING
A- lesion confined to bowel wall, mucosa & submucosa.
Morphological Types 1. Annular Stricture 2. Tubular 3. Cauliflower 4. Excavated or Ulcerated
Clinical Features Depend upon1. Tumor Location 2. Tumor Size 3. Presence of Metastases
Proctoscopy Sigmoidoscopy / Procto-Sigmoidoscpy with
Biopsy Flexible Sigmoidoscopy Colonoscopy with Biopsy ( GOLD STANDARD) Barium Enema CT Colonography

Nasopharyngeal-carcinoma_2015_The-Lancet

SeminarNasopharyngeal carcinomaMelvin L K Chua, Joseph T S Wee, Edwin P Hui, Anthony T C ChanEpidemiological trends during the past decade suggest that although incidence of nasopharyngeal carcinoma isgradually declining, even in endemic regions, mortality from the disease has fallen substantially. This ﬁ nding isprobably a re sult of a combination of life style modiﬁ cation, population scre e ning couple d with be tte r imaging,advances in radiotherapy, and eﬀ ective systemic agents. In particular, intensity-modulated radiotherapy has driventhe improvement in tumour control and reduction in toxic eﬀ ects in survivors. Clinical use of Epstein-Barr virus(EBV) as a surrogate biomarker in nasopharyngeal carcinoma continues to increase, with quantitative assessmentof circulating EBV DNA use d for population scre e ning, prognostication, and dise ase surve illance. Randomise dtrials are inve stigating the role of EBV DNA in stratiﬁcation of patie nts for tre atme nt inte nsiﬁ cation anddeintensiﬁ cation. Among the e xciting de ve lopme nts in nasopharynge al carcinoma, vascular e ndothe lial growthfactor inhibition and novel immunotherapies targeted at immune checkpoint and EBV-speciﬁ c tumour antigensoﬀ er promising alternatives to patients with metastatic disease.IntroductionNasopharyngeal carcinoma is a cancer arising from the nasopharynx epithelium. Within the boundaries of the nasopharynx, the tumour epicentre is frequently seen at the fossa of Rosenmüller, from where the tumour invades adjacent anatomical spaces or organs. Despite being of a similar cell or tissue lineage, distinct diﬀ erences exist between nasopharyngeal carcinoma and other epithelial tumours in the head and neck region. Compared with other cancer types, nasopharyngeal carcinoma is uncommon, albeit with a very unique pattern of geographical distribution. Worldwide, 86 500 cases of nasopharyngeal carcinoma were reported in 2012, accounting for only 0·6% of all cancers diagnosed in that year. 71% of new cases were in east and southeast parts of Asia, with south-central Asia, and north and east Africa accounting for the remainder (appendix).1Besides geographical variation, some ethnic groups also seem to have a predisposition for nasopharyngeal carcinoma—eg, the Bidayuh in Borneo, Nagas in northern India, and Inuits in the Artic, in whom age-standardised incidence is reportedly higher than 16 per 100 000 person-years in men.2 In terms of demographic trends, men are two to three times more likely to develop the disease than are women, and peak age of disease occurrence is between 50 and 60 years. In view of the heterogeneous epidemiological patterns, it is possible that other factors, not limited to genetic susceptibility, are implicated in the pathogenesis of nasopharyngeal carcinoma.Pathology and risk factorsMorphologically, an abundance of lymphoid cells is often seen intermixed with transformed epithelial cells, but nasopharyngeal carcinoma is widely regarded to be squamous in origin. Depending on the degree of diﬀ erentiation, nasopharyngeal carcinoma is categorised into three pathological subtypes on the basis of WH O criteria. Diﬀ erentiated tumours with surface keratin are deﬁned as type I, whereas types II and III refer to non-keratinising diﬀerentiated and undiﬀ erentiated tumours, respectively. In 1991, types II and III werecombined into a single category of non-keratinisingcarcinoma. The use of the numerical categorisation wassubsequently dropped, and a third category, the basaloidsquamous carcinoma, was added (ﬁ gure).3 Each of thesedeﬁnitions is also closely related to geographicaldistribution and epidemiological factors. In regionswhere nasopharyngeal carcinoma is endemic, non-keratinising subtypes constitute most cases (>95%)4,5 andare invariably associated with Epstein-Barr virus (EBV)infection, whereas type I disease is more common inother parts of the world.EBV infection is perhaps the most extensively studiedaetiological factor for nasopharyngeal carcinoma. On thebasis of in-situ hybridisation techniques to EBV-encodedRNAs, the virus is detected exclusively in all tumour cellsbut not in normal nasopharyngeal epithelium, suggestingthat EBV activation is necessary in the pathogenesis ofnasopharyngeal carcinoma. This notion is furthersupported by reports that similar techniques undertakenon preinvasive lesions identiﬁ ed the presence of EBV evenduring the initial phases of malignant transformation.6,7Yet, the inability to detect EBV in nasopharyngeal biopsySearch strategy and selection criteriaWe searched the PubMed and MEDLINE databases for articlespublished in English from Jan 1, 2000, to Dec 31, 2014, withthe keywords “nasopharyngeal carcinoma”, “epidemiology”,“pathology”, “genetics”, “Epstein-Barr virus”, “humanpapilloma virus”, “staging”, “imaging”, “functional magneticresonance imaging”, “positron emission tomography”,“radiotherapy”, “intensity-modulated radiotherapy”,“adaptive radiotherapy”, “chemotherapy”, “salvage therapy”,“immunotherapy”, “clinical trials”, and “meta-analysis”.Priority was given to large contemporary clinical trials orstudies in human beings. Selected references were judged onrelevance and mainly consisted of publications from the past5 years, but did not exclude widely referenced and highlyregarded older seminal work. Abstracts of recent pertinentmedical conferences were also included for latest updates.Published OnlineAugust 28, 2015/10.1016/S0140-6736(15)00055-0Division of Radiation Oncology,National Cancer CentreSingapore, Singapore(M L K Chua FRCR,J T S Wee FRCR); Duke-NUS,Graduate Medical School,Singapore (M L K Chua,J T S Wee); and State KeyLaboratory of Oncology inSouth China, Sir Y K Pao Centrefor Cancer, Department ofClinical Oncology, Hong KongCancer Institute, The ChineseUniversity of Hong Kong,Hong Kong, China (E P Hui FRCP,Prof A T C Chan FRCP)Correspondence to:Dr Melvin L K Chua, Division ofRadiation Oncology, NationalCancer Centre Singapore,11 Hospital Drive,Singapore 169610, Singaporemelvin.chua.l.k@.sgSeminarsamples from high-risk individuals suggests that other factors are needed for the EBV-infected epithelial cell to undergo malignant transformation. Recent work has proposed that deregulation of cell-cycle checkpoint through p16 inactivation and cyclin D1 overexpression promotes maintenance of the viral genome, favouring transition of low-grade dysplasia to higher grade lesions.8,9 Intrinsic genetic determinants such as 3p and 9p deletions have also been suggested as mechanisms of susceptibility to EBV infection and its downstream eﬀ ects.10 Epigenetic modiﬁ cations that are associated with a tumorigenic phenotype have been identiﬁ ed in EBV-infected epithelial cells and were shown to persist even in the absence of the virus (appendix).11Another viral cause for nasopharyngeal carcinomaperhaps more associated with the non-endemic form ishuman papillomavirus (HPV). Limited evidence on viralepidemiology is available for H PV and nasopharyngealcarcinoma because the non-endemic form has a lowprevalence worldwide. Nonetheless, small-scale studies have suggested that HPV might be a contributing factor in keratinising and even non-keratinising nasopharyngeal carcinoma in white people.12–16 These studies also suggest that EBV and HPV infection are nearly always mutually exclusive. Prognosis diﬀ ered between EBV-associated and HPV-associated nasopharyngeal carcinoma; patients with H PV-associated tumours had poorer survival and local control, whereas distant failures were more common with EBV-associated tumours.16 Nevertheless, patients with non-viral-associated nasopharyngeal carcinoma (ie, H PV-negative, EBV-negative tumours) had worse outcomes than patients with viral-associated tumours (table 1). Such ﬁ ndings lend further support to the notion that non-viral-related oncogenic signalling contributes to a more aggressive tumour phenotype, but the exact underlying mechanisms remain elusive.Apart from viruses, there is also substantial interest in genetic susceptibility as a determinant of risk for nasopharyngeal carcinoma in endemic regions. Studies have mainly been small-scale case-control comparisons reporting associations of genes involved in immune responses, DNA repair, and metabolic pathways.17,18 Nonetheless, with the advent of high-throughput whole-genome sequencing, genome-wide association studies of large cohorts of patients with nasopharyngeal carcinoma and high-risk individuals have now identiﬁ ed a susceptibility locus within the MH C region of chromosome 6p21 that codes for the HLA genes (HLA-A , HLA-B , HLA-C , HLA-DQ , HLA-DR , HLA-F ).19–24 Other non-HLA susceptibility loci that were also identiﬁ ed from genome-wide association studies were GABBR1 (on chromosome 6p21), HCG9 (6p21), TNFRSF19 (13q12), MECOM (3q26), and CDKN2A and CDKN2B (9p21).19,20 Additionally, a systematic review of 83 related studies further highlighted the relevance of a few other genes involved in DNA repair (RAD51L1), cell-cycle checkpoint regulation (MDM2, TP53), and cell adhesion and migration (MMP2).18 Among them, the DNA double-strand break repair pathway has been validated in a cohort of 2349 individuals from H ong Kong as a potential determinant of nasopharyngeal carcinoma risk.25Large-scale epidemiological studies have proposed associations between several dietary and social practices and an increased risk of nasopharyngeal carcinoma. Most notably, a history of salted ﬁ sh consumption has been reported to be common in patients with nasopharyngeal carcinoma.26 Speciﬁ cally, N-nitrosamine is believed to be the associated carcinogen, and long-term exposure is associated with a two-fold increase in risk of developing the disease. Other risk factors are consumption of preserved foods, herbal teas, slow-cooked soups, and alcohol, and smoking habits; however, such links were often inconsistent between studies, and even when present, were weaker than that seen for salted ﬁ sh. In a proof-of-concept study, exposure of cells to nicotine in vitro promoted EBV replication and expression of its lytic gene products.27Figure: Light microscopic appearance of nasopharyngeal carcinoma(A) Keratinising squamous cell carcinoma; haematoxylin and eosin (H&E) stain, magniﬁ cation 200×. (B) Non-keratinising carcinoma, diﬀ erentiated subtype; H&E stain, magniﬁ cation 400×. (C) Non-keratinising carcinoma,undiﬀ erentiated subtype; H&E stain, magniﬁ cation 400×. (D) Detection of Epstein-Barr virus-encoded small RNA by in-situ hybridisation.A BC D Epidemiology Overall survival Local control Distantmetastasis-free survivalHPV-negative/EBV-positive Endemic regions Most superior Most superior LowestHPV-positive/EBV-negative Non-endemic regions Moderate Moderate ModerateHPV-negative/EBV-negative Non-endemic regions Lowest LowestModerate HPV=human papillomavirus. EBV=Epstein-Barr virus.Table 1: Characteristics of the diﬀ erent types of viral-associated nasopharyngeal carcinomaSee Online for appendixSeminarPopulation screening in endemic areasIn view of the prevalence of nasopharyngeal carcinoma in southern China, population screening presents an attractive strategy for early diagnosis and, consequently, better outcomes. Immunoserology (IgA antibodies against EBV capsid antigen [VCA-IgA], early antigen [EA-IgA], EBV nuclear antigen 1 [EBNA1-IgA], and EBV-speciﬁc DNase antibodies) and EBV DNA-based screening methods have been studied. From the early studies consisting of case-control and prospective testing, immunoseropositivity is estimated to be predictive of nasopharyngeal carcinoma susceptibility after a year, and detection sensitivity is enhanced when combining a panel of markers (appendix).28 Nonetheless, false-positive rates of 2–18% have been reported with serological testing alone.29 A promising method to reduce false-positive rates could entail use of a conﬁ rmatory non-invasive test after positive serology. In a study that incorporated this strategy, the combination of serum VCA-IgA antibody and circulating EBV DNA had an overall sensitivity (deﬁ ned as positive result of either marker) of 99%, but EBV DNA accurately identiﬁ ed 75% of false-positive VCA-IgA-detected cases.30 A large-scale prospective screening study (NCT02063399) for nasopharyngeal carcinoma with use of plasma EBV DNA is in progress and plans to recruit almost 20 000 healthy men aged between 40 and 60 years (appendix). Symptoms and diagnosisClinical presentation of nasopharyngeal carcinoma is correlated with the extent of primary and nodal disease. Possible routes of primary tumour invasion are anterior spread into the nasal cavity, pterygoid fossa, and maxillary sinuses; lateral involvement beyond the pharyngobasilar fascia into the parapharyngeal and infratemporal spaces; and base of skull, clivus, and intracranial structures when the disease extends posteriorly and superiorly. H ence, depending on the anatomical structures aﬀ ected, clinical presentation varies accordingly, ranging from non-speciﬁ c symptoms of epistaxis, unilateral nasal obstruction, and auditory complaints to cranial nerve palsies (cranial nerves third, ﬁfth, sixth, and 12th being most aﬀ ected). Nodal metastasis in the neck is a frequent clinical ﬁ nding in nasopharyngeal carcinoma, occurring in roughly three-quarters of all patients. Retropharyngeal and level 2 neck nodes are typically the ﬁ rst and second echelons of spread, respectively, and skipped metastasis does not usually occur in the lower neck in the absence of disease at the upper nodal stations.31Nasendoscopy is routine in eliciting a tumour in the nasopharynx. Biopsy samples are obtained for pathological diagnosis, and in the rare instance when no tumour is visible, blind or radiology-guided targeted biopsies, or both, are done if the index of suspicion is high. Diﬀ erential diagnoses of a malignant tumour in the nasopharynx are lymphoma, extramedullary plasma c ytoma, melanoma, rhabdomyosarcoma, and adenoid cystic carcinoma. Benign condition-like tuberculosis of the nasopharynx could also present with a similar range of symptoms, and ought to be considered in immuno c ompromised individuals. Characteristic histological features constitute the microscopic morphology of nasopharyngeal carcinoma, but at times, distinguishing between the undiﬀ erentiated subtype and lymphoma might be diﬃ cult. In such instances, immuno h istochemical markers speciﬁ c to individual tumour types (leucocyte common antigen, lymphoma; S100, melanoma; MNF116, a pancytokeratin marker) and in-situ hybridisation to EBV-encoded RNAs can supplement haematoxylin and eosin staining. Other useful investigations for conﬁ rming a diagnosis of naso-pharyngeal carcinoma are quantitative assessments of plasma immunoserology and EBV DNA.32,33Staging and prognosisNasopharyngeal carcinoma is classiﬁ ed by the joint Union for International Cancer Control TNM Classiﬁ cation of Malignant Tumours and the American Joint Committee on Cancer staging system. This classiﬁ cation system was updated in 2009 and introduced several modiﬁ cations to the staging of primary and nodal disease for the seventh edition (appendix).34Besides tumour burden as reﬂ ected by the TNM stage classiﬁcation, other clinical and molecular prognostic variables have also been proposed. A history of smoking, low-penetrance allelic variation of DNA repair genes, overexpression of serglycin and p53, chromatin modiﬁcation, ERBB-PI3K signalling, and raised plasma EBV DNA are among some highlighted determinants of prognosis.35–39 Notably, quantiﬁ cation of plasma EBV DNA before treatment has been shown to independently predict for odds of recurrence and survival, complementing the TNM stage classiﬁ cation.40,41 Large cohort studies have further qualiﬁed that strength of prognostication with EBV DNA is enhanced when combined with other unrelated biomarkers such as ﬁ brinogen, plasma D-dimer, and C-reactive protein.42–44Imaging studiesOptimum imaging is crucial for staging and radiotherapy planning of nasopharyngeal carcinoma. MRI provides better resolution than CT in terms of assessing parapharyngeal spaces, marrow inﬁ ltration of the skull base, intracranial disease, and deep cervical nodes. The advent of functional MRI adds a biological dimension. Parameters of cellularity (diﬀ usion) and perfusion have been correlated to clinical stage of nasopharyngeal carcinoma.45 Likewise, ¹⁸F-ﬂ uorodeoxyglucose (¹⁸F-FDG)-PET provides metabolic parameters (maximum standardised uptake value and total lesion glycolysis) that could be interpreted to represent tumour biology and predict clinical outcomes.46,47 It is also sensitive and accurate for the detection of nodal metastasis, but lacks the soft-tissue resolution of MRI for assessment of primary tumour.48,49SeminarIn terms of distant metastasis staging, several studies have concluded that ¹⁸F-FDG-PET is substantially more sensitive (70–80% vs about 30%) and accurate (>90% vs 83–88%) than conventional work-up consisting of chest radiography, abdominal ultrasound, and skeletal scinti g raphy.50,51 In the assessment of bone metastasis, also the most common site of distant spread, a direct comparison between ¹⁸F-FDG-PET and skeletal scintigraphy showed that ¹⁸F-FDG-PET is substantially more sensitive with similar speciﬁ city. Thus, MRI and ¹⁸F-FDG-PET are recommended as the preferred modalities for staging in patients with TNM stage III, IVA, or IVB nasopharyngeal carcinoma, or raised plasma EBV DNA load of 4000 copies per mL or more.52Radiotherapy in the management of nasopharyngeal carcinoma Radiotherapy is the primary and only curative treatment for nasopharyngeal carcinoma. In centres where modern radiation technology is available, intensity-modulated radiotherapy (IMRT) is the preferred method. Brieﬂ y, this technique caters for delivery of tumoricidal doses to gross tumour and subclinical disease, while minimising doses to adjacent normal tissues. Such a technology is particularly advantageous in nasopharyngeal carcinoma, in view of the late toxic eﬀ ects reported in patients treated with crude two-dimensional (2D) radiotherapy techniques (appendix).53The recent improvement in disease control and survival in patients with nasopharyngeal carcinoma is partly attributable to IMRT. Early studies by independent groups reported 3-year local control and survival rates of 80–90%, even for advanced stages.54,55 In a randomised study by Peng and colleagues,56 IMRT contributed to an absolute improvement in 5-year locoregional control of 7·7% compared with conventional 2D radiotherapy. Additionally, a review of 1593 patients who were treated at a single institution with progressive radiotherapy techniques (2D radio t herapy, 3D radiotherapy, and IMRT) over two decades (1994 to 2010) also showed increased disease-speciﬁ c and overall survival in individuals who received IMRT (disease-speciﬁ c survival: 85% with IMRT vs 81% with 3D radiotherapy vs 78% with 2D radiotherapy; overall survival: 80% with IMRT vs 73% with 3D radiotherapy vs 71% with 2D radiotherapy; appendix).57The clinical yield of modifying fraction size (hyper-fractionation) and overall treatment time (acceleration) in patients with nasopharyngeal carcinoma is uncertain. Early studies testing a hyperfractionated, twice-daily regimen did not show a beneﬁ t in tumour control, and even more concerning, reported increased incidences of late eﬀ ects compared with conventionally fractionationated radiotherapy.58,59 Nonetheless, two other prospective trials did suggest eﬃ cacy with altered fractionation schedules. Pan and colleagues 60 showed that a hyperfractionated radiotherapy regimen resulted in absolute improvements of 11·7% in locoregional control and 16·1% in overall survival at 5 years, without incurring incremental late neurological toxic eﬀ ects, compared with conventionally fractionated radiotherapy. The NPC-9902 trial compared an accelerated regimen of six times a week with conventional fractionation, with or without concurrent chemotherapy, in patients with T3–4N0–1 nasopharyngeal carcinoma.61 Although concurrent chemotherapy and accelerated fractionation reduced the risk of treatment failure compared with conventionally fractionated radiotherapy alone (hazard ratio [H R] for failure-free survival 0·35, 95% CI 0·14–0·84), neither accelerated radiotherapy alone nor the combination of chemotherapy plus conventional radiotherapy improved outcomes compared with the control group. Since concurrent chemoradiotherapy is the established standard treatment of locally advanced nasopharyngeal carcinoma, the ﬁ ndings of the NPC-9902 trial are certainly peculiar and the question remains whether altered fractionation improves the therapeutic ratio over and above combination chemotherapy. The NPC-0501 trial was a study designed in part to address this clinical conundrum.62 Preliminary results suggest that accelerated radiotherapy fractionation provides no therapeutic beneﬁ t in patients with advanced disease receiving concurrent systemic treatment compared with conventional fractionation (H R for progression-free survival 1·13, 95% CI 0·82–1·54; appendix).Chemotherapy in non-metastatic disease The strategy of combining chemotherapy with radio-therapy is another pivotal advancement in the treatment of locally advanced nasopharyngeal carcinoma. Since the publication of the seminal INT-0099 trial, several trials have substantiated the beneﬁ ts in disease control and survival reported with chemoradiotherapy, henceforth establishing this treatment as the standard of care in this subgroup (table 2).63–71 Combination regimens varied between studies, but for the most part, cisplatin was the chemotherapy of choice. In terms of dosing schedules, either 30–40 mg/m² once a week or 100 mg/m² every 3 weeks is accepted practice; however, these schedules were never prospectively compared. Nonetheless, any diﬀ erences in radiosensitisation eﬀ ects and toxic eﬀ ects proﬁ les between dosing schedules are likely to be negligible relative to the importance of cisplatin dose intensity, for which 200 mg/m² is the threshold for optimum eﬃ cacy.72–74 Other concurrent agents with similar eﬃ cacy to cisplatin are uracil plus tegafur (a prodrug of ﬂ uorouracil) and oxaliplatin.69,70 Overall, meta-analyses examining the eﬀ ects of chemoradiotherapy in nasopharyngeal carcinoma have consistently generated HR estimates of 0·64–0·79 for overall survival, 0·67–0·71 for distant metastasis-free survival, and 0·59–0·73 for locoregional control in favour of chemoradiotherapy over radiotherapy alone.75–77 For TNM stage II nasopharyngeal carcinoma, Chen and colleagues 71 reported a beneﬁ t inSeminaroverall survival with chemoradiotherapy compared with radiotherapy alone mainly through improvement in distant failures. Nonetheless, because local control remains excellent with radiotherapy alone in this subgroup, some centres prefer to restrict chemoradiotherapy to individuals with a presumed high risk of distant metastasis (single or unilateral bulky node[s] 4–6 cm or EBV DNA >4000 copies per mL).Part of the current controversy around supportive evidence for combination treatment relates to the roles of induction and adjuvant chemotherapy. Regarding adjuvant chemotherapy, it typically consisted of cisplatin (20 mg/m² daily for 4 days) and ﬂ uorouracil (1 g/m² daily for 4 days) given every 4 weeks for three cycles. Trends seen in speciﬁ c trials of adjuvant chemotherapy showed that additional treatment after radiotherapy was poorly tolerated, with 55–75% compliance at best.63–65,71 Compounding the clinical dilemma, several trials designed speciﬁ cally to investigate the beneﬁ ts of adjuvant treatment largely did not show a survival advantage.69,78 These results contradict the ﬁ ndings of other retrospective analyses that suggested an improvement in survival and reduction of distant metastasis when two or more cycles of adjuvant chemotherapy were delivered.73,79 Notably, in the trial byChen and colleagues,78 despite selecting for patientswho were at risk of developing distant metastasis (deﬁ ned as clinical presentation of T3–4N1 or N2–3disease), the results of preliminary analyses after amedian follow-up of 37·8 months suggested similarclinical endpoints irrespective of treatment assignment(2-year outcomes for chemoradiotherapy vschemoradiotherapy plus adjuvant chemotherapy,failure-free survival 84% vs 86%; distant metastasis-freesurvival 86% vs 88%; overall survival 92% vs 94%).While we await long-term results, further evidenceregarding the eﬀ ectiveness of adjuvant chemotherapycan be inferred from published meta-analyses. Independent pooled analyses of chemoradiotherapy trials based on whether adjuvant chemotherapy wasincorporated in the test group suggested similar beneﬁ tsin overall survival with either approach compared withradiotherapy (H R 0·66–0·80 for chemoradiotherapy; 0·64–0·83 for chemoradiotherapy with adjuvant).75–77However, an updated network meta-analysis reported afavourable trend for overall survival (H R 0·84, 95% CI0·67–1·03) and distant failure-free survival (H R 0·90,0·69–1·17), and a signiﬁcant advantage in terms ofSeminarSeminarlocoregional failure-free survival (H R 0·67, 0·46–0·95) with chemoradiotherapy followed by adjuvant chemotherapy compared with chemoradiotherapy alone.80 The probabilities for being ranked as the most eﬀ ective treatment for overall survival were 84% for chemoradiotherapy followed by adjuvant chemotherapy and 3% for chemoradiotherapy alone. None of the meta-analyses included the latest trials from Singapore (NCT00997906) and Guangzhou (NCT01245959), which adopted chemoradiotherapy alone as the standard treatment (table 3).Induction chemotherapy was once thought to be a potentially more feasible and eﬀ ective strategy of treatment intensiﬁ cation than adjuvant sequencing. H owever, early phase 3 studies assessing various combinations of induction chemotherapy before radiotherapy alone have mostly been inconclusive. Generally, despite suggestions of better disease control, none of the studies actually reported an improvement in overall survival, although a combined exploratory analysis of the Asian Oceania Clinical Oncology Association (AOCOA) and Guangzhou trials did later report a beneﬁ t in survival and distant failures in patients with T1–2N0–1 disease.84 Interest, however, was subsequently renewed after promising reports of 2-year and 3-year overall survival of 71–95% from smaller phase 2 studies that used induction chemotherapy and chemoradiotherapy.81,85–88 In a randomised phase 2 comparison of chemoradiotherapy (cisplatin) with or without induction cisplatin and docetaxel, H ui andcolleagues 81 reported that 3-year progression-free survival and overall survival was 88% and 94% in the experimental group compared with 60% and 68% in the control group, respectively. By contrast with these ﬁ ndings, a series of randomised trials have yet to reproduce these favourable results (table 3). Fountzilas and colleagues 82 tested an induction regimen consisting of epirubicin, cisplatin, and paclitaxel, and reported no diﬀ erence in response rates, progression-free survival, and overall survival when the triplet combination was added to chemoradiotherapy. Tan and colleagues 83 recently reported a phase 3 study of 172 patients with advanced nasopharyngeal carcinoma and reported that locoregional control, distant metastasis-free survival, and overall survival did not diﬀ er between groups with the addition of induction gemcitabine, carboplatin, and paclitaxel to chemoradiotherapy. Finally, the six-arm NPC-0501 study (a 2 × 3 factorial study of concurrent cisplatin and conventional or accelerated radiotherapy, in combination with induction cisplatin plus capecitabine, or induction cisplatin plus ﬂ uorouracil, or adjuvant cisplatin plus ﬂ uorouracil) showed that overall chemotherapy tolerance was similar between patients who received induction or adjuvant chemotherapy, and variation in sequencing of cisplatin and ﬂ uorouracil did not achieve a statistically signiﬁ cant improvement in progression-free survival and overall survival.62 In summary, the role of induction chemotherapy in the management of locally advanced nasopharyngeal carcinoma remains investigational, and current evidence precludes its routine use in patients planned for chemoradiotherapy.A better patient stratiﬁ cation for treatment intensiﬁ cation and deintensiﬁ cation is clearly needed. A subgroup analysis of the Taiwanese chemoradiotherapy trial showed that chemoradiotherapy was beneﬁ cial in patients without high-risk features such as N3 or T4N2 disease or bulky nodal metastases (at least one node >4 cm), whereas patients harbouring any of these disease characteristics had poorer outcomes with chemo-radiotherapy.89 These ﬁ ndings might be preliminary, but they highlight the importance of improvising patient stratiﬁ cation beyond the TNM staging system. The incorporation of prognostic biomarkers is a potential strategy. Two phase 3 trials are underway, in which patients are randomly assigned to adjuvant regimens of diﬀ ering intensities depending on whether EBV DNA is detectable after chemoradio t herapy (NRG-N001, NCT02135042; NPC-0502, NCT00370890). Findings that persistent EBV DNA detection is strongly associated with a high likelihood of tumour recurrence and poor prognosis lend support to both trials.40,41,90–92 Coincidentally, a retrospective analysis from Taiwan showed that in a cohort of 85 patients who had persistent EBV DNA titres after radiation, adjuvant tegafur and uracil substantially reduced distant failure and improved survival (appendix).93Disease surveillance and toxic eﬀ ectsInitial post-treatment assessment entails monitoring of acute eﬀ ects and tumour response. Common acute radiotherapy-related eﬀ ects include mucositis, dysphagia, dermatitis, and xerostomia. Clinical symptoms typically improve within weeks after treatment cessation, but in instances of grade 3 or 4 reactions, these can persist, leading to consequential late eﬀ ects. Chemoradiotherapy is invariably associated with higher incidences of haematological and non-haematological acute toxic eﬀ ects compared with radiotherapy alone.94,95 Unlike its beneﬁ ts in reducing late eﬀ ects, IMRT seems to have a limited role in mitigating acute toxic eﬀ ects. Pharmacological interventions for acute xerostomia and mucositis are mostly ineﬀ ective, although studies have suggested eﬀ ective relief of mucositis with palifermin (recombinant human keratinocyte growth factor) and doxepin rinse (tricyclic antidepressant).96–98Comprehensive assessment of tumour response includes clinical examination, nasendoscopy with or without biopsy, EBV DNA titre measurement, and radiological imaging.99 Nasendoscopy is restricted to assessing superﬁ cial lesions and a positive biopsy sample 10 weeks after treatment has been shown to probably represent persistent residual disease.100 For deeper lesions within the skull base, radiological assessment is necessary, but it might pose a challenge。

简述良性肿瘤与恶性肿瘤的区别9、简述cancer、carcinoma、sarcoma的

1、简述良性肿瘤与恶性肿瘤的区别9、简述cancer、carcinoma、sarcoma的定义和关系（请各举例３个carcinoma、sarcoma）。

简述细胞原癌基因的分类以及激活机制23、简述cancer、carcinoma、sarcoma的定义和关系（请各举例３个carcinoma、sarcoma）。

24、简述肿瘤浸润的途径有哪些25、简述肿瘤对机体有哪些影响？26、细胞凋亡（apotosis）在细胞生长发育过程中具有十分重要意义，请简述其生物学意义以及包括的阶段27、癌基因有多种分类方法，根据癌基因产物的功能分类有哪几种？28、叙述细胞凋亡的形态学和生化特征。

1．试述化学致癌物影响人类健康、导致人类肿瘤的主要途径，并各举2例2．简述基因与肿瘤形成的关系3．简述遗传性肿瘤综合症的特点4．试述癌基因的定义，并举例。

（至少3个）5，试简述抑癌基因的可能功能。

1、肿瘤流行病学研究可归纳为哪几个主要方面？2、分子流行病学研究中生物标志物的分类？3、研究肿瘤流行病学的意义？4、当前我国癌症发病增高的主要原因有哪些？呼吸系统的内镜包括哪些？22.消化系统的内镜包括哪些？23.内镜诊断的常用方法？24.内镜的发展史上，依次出现过那些种类的内镜？25.胶囊内镜的优点？26. 气管镜检查的并发症包括哪些？27. 气管镜检查的范围。

28.胃镜检查的范围。

29.胃镜检查的适应证。

30.胃镜检查的禁忌证。

31.结肠镜检查的适应证。

32.结肠镜检查的禁忌证。

33.十二直肠镜的应用有哪些？34. ERCP 的适应证。

35.ERCP的禁忌证。

36.小肠镜的检查方法。

37. 小肠镜检查适应证。

38. 结肠镜肠穿孔类型。

39. 介入超声诊断的意义。

40. 腹腔镜的适应证。

5、在肿瘤病理学中，目前有较多的新技术、新方法，它们多有哪些方面？20、对于实体肿瘤一般形态学表现在哪几方面？21、病理学检查诊断诊断时，存在的不足，其主要可能有哪方面？22、简述良性肿瘤与恶性肿瘤的区别23、外科病理学医师提高冰冻切片诊断准确性的措施有哪些？24、病理申请单的填写规范与病理诊断的准确性是相关的，申请单应该填写哪些内容？25、简述冰冻切片的指征？1．肿瘤的临床诊断应该包括哪3个方面?2．常用肿瘤标志物有哪些？3．AFP，中文名称甲胎蛋白，英文名称是什么？可用于诊断什么恶性肿瘤?4．PSA，中文名称前列腺特异性抗原，英文名称是什么？可用于诊断什么恶性肿瘤？5．肿瘤的高危因素的定义是什么？6．肿瘤的发生与生活习惯密切相关。

癌细胞CancercellPPT课件

这是癌细胞的基本特征。
●在分化程度上癌细胞低于良性肿瘤细胞，且失去了
许多原组织细胞的结构和功能
3.细胞间相互作用改变（识别改变；表达水解酶类；产生新的表
面抗原）
4.蛋白表达谱系或蛋白活性改变（胚胎细胞蛋白、端粒酶活性升
高）
5.mRNA转录谱系的改变（少数基因表达不同；突变位点
不同，表型多变）
6.染色体非整倍性
去分化现象；对生长因子需要量降低；代谢旺盛线粒体功能障碍：即使在氧供应充分的条件下也主要是糖酵解途径获取能量。
与三个糖酵解关键酶（己糖激酶、磷酸果糖激酶和丙酮酸激酶）活性增加和同工酶谱的改变，以及糖原异生关键酶活性降低有关。可移植性：正常细胞移植到宿主体内后，由于免疫反应而被排斥，多不易存活。但是肿瘤细胞具有可移植性，如人的肿瘤细胞可移植到鼠类体内，形成移植瘤。
致癌因素
内因：恶性肿瘤的形成往往涉及多个基因的改变外因：多种理化因子致癌
根据其性质分为：化学、生物和物理致癌物三大类根据它们在致癌过程中的作用，可分为；
1.启动剂：可直接改变DNA的成分或结构。 2.促进剂：本身不能诱发肿瘤，但有促进作用。
如糖精可促进膀胱癌的发生，苯巴比妥促进肝癌的发生。 3.完全致癌物：兼具启动和促进两种作用。
(2)如果我们把原癌基因切除，就会避免癌症的发生，对吗？为什么？
鼠白血病毒 Mouse Leukemia Virus
三、物理因素
（一）、电离辐射辐射致癌的机制： ①染色体或基因的突变； ②基因表达改变； ③激活潜伏的致癌病毒。
（二）、紫外线可引起细胞DNA断裂、交联和染色体畸变，抑制
皮肤的免疫功能，诱发皮肤癌、基底细胞癌和黑色素瘤。
癌发生涉及的基因及其作用

医学词根

carcino- 癌：carcinoma atypical 不典型癌alb- 白：alba lochia 白色恶露leuco- 白，白细胞，褪色，无色：leucoagglutinin白细胞凝集素；leuco base无色基leuko- 白，白细胞，褪色，无色: leukocytes白细胞; leukoblast白细胞母细胞,成白细胞细胞centi- 百分之一,厘: centimeter厘米,公分hect- 百：hectare 公顷hemi- 半,偏侧,单侧: hemiablepsia偏盲; hemialgia偏侧痛semi- 半，一半：semiantigen半抗原dorsi- ,dorso- 背，背侧: dorsibronchus背支气管; dorsispinal脊柱背侧的opistho- 背，后面：opisthocheilia唇后缩naso- 鼻：nasoantrostomy 鼻上颌窦造口术rhino- 鼻，鼻样结构：rhinoantritis 鼻上颌窦炎prop- 丙：Prop acil丙基硫氧嘧啶patho- 病理：pathoanatomy病理解剖学；pathobolism新陈代谢异常,病理性代谢morbido- 病：morbid oberity病理性肥胖-igo 病：aurigo黄疸；bullous impetigo大疱性脓疱病-metry 量度法,测量法: acidimetry 酸量滴定法,酸量法lamino- 层：laminograph体层照像机,断层照像机longi- 长度：Longicil苄星青霉素(长效青霉素)entero- 肠,肠道: entero-adenitis肠腺炎; enteroantigen肠抗原intesino- 肠：intestinalization肠化生-plasty 成形术,整复术,整形术,形成: Angioplasty 血管成形术gingivo- 齿龈：gingivoectomy龈切除术; gingivolabial龈唇的ulo- 瘢,瘢痕,龈,牙龈,齿龈: ulocace 龈溃疡; ulodermatitis成瘢痕皮炎hapto- 接触，结合，触觉：haptospore附着孢子thigmo- 触或机体接触的: thigmocyte血小板; thigmomorphosis接触膨大-centesis 穿刺: abdominocentesis 腹腔穿刺术hypophyso- 垂体：hypophysoma垂体瘤；hypophysoprivic垂体分泌缺乏的cheilo- 唇：cheiloplasty 唇成形术；cheilotomy 唇切除术labio- 唇：labiomental 唇颏的-ol 醇，酚：allyl guaiacol丁香油酚,丁香酸anti- (against):antibiotics 抗生素，antioxidants 抗氧化物antiseptic n. 杀菌剂,adj. 防腐的hyper-(above): hypertension 高血压，hyperoxia 高氧症hyperthermia过热sym- ,syn- (together): symphony交响乐，symptom n. 症状,症候,征兆syndrome 综合征pre-(before,in front of): predispose使易害,造成…的因素, premature早熟的,过早的infra-(beneath): infrastructure 基础，基础结构，infrared adj. & n.红外线(的)，infrasonic 听域下的physi-(nature): physiopathologic 病理生理的，physiotherap物理治疗psych-(mind): psychosocial精神社会的,社会心理的,心理社会的, psychiatric 精神病的,精神病学的,psychoactive对精神起作用的,影响精神行为的,精神活性药,精神活性的pedia-（child）：pediatrics 儿科学，pediatrist 儿科学家dent- （tooth）：dentistry 口腔医学,牙科学，denture假牙-iatrics（treatment，healing）：amblyopiatrics 弱视矫正法morpho-（form）：morphocytology细胞形态学，morphologic形态学的，morphography形态论chromo-（color）：chromosome染色体，chromogenesis 色素生成chrono-（time）：chronic慢性的；chronological 年代学的bio-（life）：biochemical生物化学的；biopsy活组织检查biomedical生物医学的necro-（dead）：Necrosis坏死；necropsy尸检necrology死亡统计,死亡统计学-genesis（origination，production）：pathogenesis发病机制；Biogenesis 生源论Cytogenesis细胞发生-plasm，-plasia（a thing formed，forming）：hyperplasia增生aplasia不发育neoplasm肿瘤lipo-（fat）：hyperlipoprotein emia高脂蛋白血症lipoarthritis关节脂肪组织炎lipoprotein脂蛋白proteo-（protein）：proteolipid蛋白脂,含蛋白脂质；proteopeptic蛋白质消化的；proteometabolism蛋白代谢；glyco—（sweet，sugar）：hypoglycaemia低血糖glycogenesis糖原生成；glycolysis糖酵解chole-（bile胆汁）：cholesterol胆固醇；cholelith 胆石；cholemia 胆血症医学英语词汇通常拼写较长而复杂，且与普通的英文词汇有较大的差异，不容易记忆。

(完整)肿瘤学英语名词

1, AIDS [eidz]abbr. 获得性免疫缺乏综合症；爱滋病（Acquired Immune Deficiency Syndrome）2， acidophilic cell carcinoma 嗜酸细胞癌3, ACTH cell adenoma 促肾上腺皮质激素细胞腺瘤4, AML abbr. 急性髓细胞性白血病（Acute Myelocytic Leukemia）5, acidophilic cell adenoma 嗜酸性细胞腺瘤6，adenocarcinoma [’ædənəu，kɑ：si'nəumə]n。

［肿瘤] 腺癌；恶性腺瘤7, adenomatous polyp 腺瘤性息肉8, adenoma ［,ædi'nəumə］ n. [肿瘤］腺瘤9， adenosquamous carcinoma 腺鳞癌10， adrenocortical adenoma 肾上腺皮质腺瘤11， adrenocortical carcinoma 肾上腺皮质癌12， angiosarcoma ［，ændʒiəusɑ：'kəumə］n。

［肿瘤] 血管肉瘤13, apudoma n. 胺前体摄取与脱羧细胞瘤14, architectural atypia 结构异型性15, astrocytoma ［,æstrəsai’təumə］n. ［肿瘤］星形细胞瘤16, atypia n. 异型性；非典型；不标准17, dysplasia ［dis'pleiziə]n. 异生18, basal cell carcinoma [肿瘤］基底细胞癌19， basophile cell adenoma 嗜碱性细胞腺瘤20, benign tumor 良性肿瘤21， borderline tumor 交界性肿瘤22, primary bronchogenic carcinoma 原发性支气管肺癌23, bronchioloalveolar carcinoma 细支气管肺泡癌24， Burkitt lymphoma [肿瘤］伯基特淋巴瘤25， cachexia ［kə’keksiə］n. [内科］恶病质26， cancer ［’kænsə］n。

医学英语疾病介绍——Gastric Carcinoma(胃癌)

(1)息肉型或蕈伞型 (2)溃疡型 polypoid or fungating type Ulcerative type
Polypoid:['pɔlipɔid]息肉样 Fungating:['fʌngeit] [医]真菌样生长
(3)浸润型 Infiltrating type
Ulcerative:[ˈʌlsərətiv] adj. 溃疡（性）的
隶属浸润型进展期胃癌
Linitis plastica 革囊胃
Exams and Tests
Diagnosis is often delayed(被推迟) because symptoms may not occur in the early stages of the disease(疾病早期阶段). Or, patients may self-treat symptoms(自己治疗出现的一些症状) that gastric cancer has in common with other, less serious gastrointestinal disorders(相对不那么严重的胃肠道疾病) (bloating(胃气胀), heartburn(胃灼热), and a sense of fullness(腹胀感)).
• The cancer have not invaded the muscularis propria(肌层) and are therefore limited to the mucosa(黏膜层) and submucosa(黏膜下层).
Advance gastric carcinoma:进展期胃癌
Gastric sarcoma 5% (Arising from Mesenchymal tissue 来源于间叶组织) 胃肉瘤（教材未提及）

简述良性肿瘤与恶性肿瘤的区别9、简述cancer、carcinoma、sarcoma的

小细胞型等多种类型。
Sarcoma
定义
Sarcoma指的是来源于间叶组织的恶性肿瘤，如骨肉瘤、脂肪肉瘤等。
特点
Sarcoma通常具有浸润性生长和转移的特点，其恶性程度较高，对患者的生命威胁较大。
分类
根据细胞的来源和特征， Sarcoma可以分为纤维肉瘤型、骨肉瘤型和脂肪肉瘤型等多种类型。
恶性肿瘤
指生长迅速、边界不清、无包膜、易发生转移、对人体影响较大的肿瘤。
形成原因
良性肿瘤
形成原因较为复杂，可能与环境、遗传、生活方式等多种因素有关。
恶性肿瘤
形成原因尚未完全明确，可能与基因突变、环境因素、感染等多种因素有关。
对机体的影响
良性肿瘤
一般对人体影响较小，症状较轻，生长缓慢，不发生转移，治疗难度相对较小。
恶性肿瘤
对人体影响较大，症状严重，生长迅速，易发生转移，治疗难度较大，危及生命。
02
Cancer、Carcinoma、Sarcoma的简述
Cancer
定义
Cancer指的是一组疾病，包括上皮组织的恶性肿瘤，如肺癌、胃癌等，以及间叶组织的恶性肿瘤，如淋巴瘤、白血病等。
特点
Cancer通常具有浸润性生长和转移的特点，其恶性程度较高，对患者的生命威胁较大。
标题为《简述良性肿瘤与恶性肿瘤的区别9、简述cancer、 carcinoma、sarcoma的》的 ppt大纲 xx年xx月xx日
目录
• 良性肿瘤与恶性肿瘤的区别 • Cancer、Carcinoma、Sarcoma的简述
01
良性肿瘤与恶性肿瘤的区别
定义与概念
良性肿瘤
指生长缓慢、边界清楚、包膜完整、不发生转移、对人体影响较小的肿瘤。

TRIM59靶向调控PPMIB对鼻咽癌侵袭和迁移的作用

鼻咽癌（NPC）是一种上皮细胞的恶性肿瘤［1］，中国是世界鼻咽癌发病率和死亡率水平较高的国家之一，我国鼻咽癌的死亡率占全国恶性肿瘤死亡率的 2.81%，发
收稿日期：2021-02-21 基金项目：安徽省高等学校自然科学研究项目（KJ2019A0400， KJ2020A0568）作者简介/通信作者：王文忠，主任医师，硕士生导师，E-mail: 13955259093@
1 材料和方法 1.1 材料 1.1.1 细胞人正常鼻黏膜上皮细胞系（HNEpC）和人鼻咽癌细胞 6-10B、CNE-2、HNE1 均购自上海细胞库。 1.1.2 药品与试剂 TRIM59 抑制物（si-TRIM59）、 TRIM59 模拟物（mimic-TRIM59）、PPM1B 模拟物（mimic-PPM1B）以及 Lipofectamin2000（上海吉玛基因）；RNA 提取试剂盒，逆转录试剂盒，荧光定量PCR试剂盒，引物 (赛默飞）；双荧光素酶报告基因系统及报告载体（Promega）；Mateigel 基质（上海前尘生物科技）； TRIM59，PPM1B，β-actin 及兔/鼠二抗（上海艾博抗）。 1.2 方法 1.2.1 标本来源蚌埠医学院第一附属医院收集癌旁组织及鼻咽癌组织 10 例，所有患者术前均未接受过靶向、放化疗或内分泌等辅助治疗，所有患者均签署知情同意书，实验方案由蚌埠医学院第一附属医院伦理委员会审核批准。 1.2.2 细胞培养人正常鼻黏膜上皮细胞系（HNEpC）和人鼻咽癌细胞6-10B、CNE-2、HNE1培养在含100 U/mL 青霉素、100 mg/L 链霉素、10 %胎牛血清的 DMEM 培养基中，37 ℃、5% CO2饱和湿度的细胞恒温培养箱中进行细胞培养。 1.2.3 细胞转染分组取 HNE1 细胞株接种于六孔板，待细胞融合度为整个六孔板的 60%严格按照说明书对 HNE1 细胞中 TRIM59 进行下调，实验按照如下分组： Control 组（Lip2000 处理 HNE1 细胞）、NC 组（Lip2000+ inhibitor NC 序列转染 HNE1 细胞）、si-TRIM59 组（Lip2000 + inhibitor TRIM59 转染 HNE1 细胞）；对

c开头r结尾的单词

c开头r结尾的单词
（大全）
1.c adave r n.尸体
2.c ampe r n.露营者
3.c aniste r n.罐；筒
4.c aesa r n.凯撒；暴君
5.c ando r n.坦白；直率
6.c apacito r n.电容器
7.c anke r n.溃疡；弊害
8.c ante r n.慢跑；流浪汉
9.c andou r n.公正；坦率
10.c ampho r n.樟树；樟脑
11.c ance r n.癌；癌症；肿瘤
12.c ape r n./v.雀跃；欢蹦
13.c apto r n.捕捉者；逮捕者
14.c arpente r n.木工；木匠
15.c arrie r n.运输工具；运载工具
16.c alibe r n.口径；才干；器量
17.c alle r n.访客；召集员；传唤员
18.c artographe r n.绘制地图者
19.c arve r n.雕刻匠；雕工；切肉刀
20.c alculato r n.计算器；计算者
21.c alenda r n.日历；历书；历法
22.c ampaigne r n.从军者；出征者；竞选者
23.c anvasse r保险经纪人；推销员
24.c arbureto r n.汽化器；化油器
25.c ardiovascula r a.心血管的
26.c aree r n.生涯；职业；经历
27.c aretake r n.管理人；看管者；看守人
28.c a r n.汽车；小卧车；（这里指）运货马车；轿车；
电车；车；火车厢。

浅析cancer与carcinoma的区别_粟陶

·医学英语视角·浅析cancer 与carcinoma 的区别Analysis of the difference between “cancer ”and “carcinoma ”随着医学的繁荣和发展，许多医学中的英语专业词汇也运用的更加广泛，如人们谈及色变的癌的英文单词“cancer 【拉】”，我们已十分的熟悉。

但由于字面翻译的相近，另一个词“carcinoma【希】”却时常被人们甚至专业医师们所混淆。

Cancer 虽然译为癌，但实质应译为癌症。

所谓癌症这是一个广义词，首先它代表为一种恶性肿瘤，是一种临床用语，它主要包括上皮来源的癌，也包括其他组织来源的肉瘤。

例如：肺癌（lung cancer ）、皮样癌（dermoid cancer ）等都使用cancer 来表达。

Cancer 也适用于表达内皮癌（epidermal cancer ）、分支状癌（ramose cancer ）。

例如句子“那位病人最终死于癌症”译为“The patient finally died from cancer ”中的“cancer ”为癌症的总称。

Carcinoma 虽然也译为癌，但只限于上皮组织来源的恶性肿瘤，其他组织如：间叶组织、淋巴组织、骨组织等来源的恶性肿瘤不能称为carcinoma 。

例如胃癌（gastric carcinoma ）、支气管肺癌（bron-chogenic carcinoma ）、食道癌（esophagus carcinoma /carcinoma of the esophagus ）、原发性肝癌（primary carcinoma of the liver ）、胰腺癌（carcinoma of pancreas ）、子宫体癌（cropus carcinoma ）、胚胎性癌（em-bryonal carcinoma ）、腺泡癌（acinosum carcinoma ）、粘液癌（mucosum carcinoma ）等都适用于用carci-noma 来表达。

胆囊腺鳞癌临床病理分析

胆囊腺鳞癌临床病理分析方三高;张渝;肖蔚;马强;杜娟;肖华亮【摘要】Objective To study the characteristics of morphologic and immunohistochemical of adenosquamous carcinoma ( ASC )of gallbladder. Methods Clinical pathological and immunohistochemical analyses were carried out in 2 cases of ASC, and related literatures were reviewed to discuss the diagnosis and differential diagnosis. Results The patients were both female with the age of 62 and 67 respectively. The main clinical manifestation was dull pain in the right upper quadrant after meals. The type - B demonstrated the cholelithiasis with irregular thickening of gallbladder wall. The pathological examination showed mucosal atrophy of gallbladder and fibrosis combined with focal calcification of the gallbladder wall in case one. And within the gallbladder cavity in case 2, there was a polypoid mass which infiltrated the adjacent organs such as bile duct and liver. The tumors in the two cases consisted of two malignant components of adenocarcinoma and squamous carcinoma, i. e. glandular tube configurations with or without mucin and spindle - shaped cells with the nests and mosaic array in which keratin pearls, individual keratinization, and intercellular bridges could be observed. Immunohistochemical examination showed the adenocarcinoma cells were positive for CK7, and the cells of squamous epithelium were positive for CK5/6. Both were intermingled in the transitional zones. Conclusion Adenosquamous carcinoma of the gallbladder is rare but special. Its prognosis of ASCs isworse than that of ordinary adenocarcinomas.%目的研究胆囊腺鳞癌(ASC)的形态学和免疫组化特征.方法对2例ASC病例进行临床病理和免疫组化分析,并结合文献讨论其诊断与鉴别诊断.结果患者均为女性,年龄分别为62和67岁.临床表现为餐后右上腹钝痛.B超显示胆囊结石伴囊壁不规则增厚.病理检查见例1患者的胆囊黏膜萎缩,囊壁纤维化伴灶性钙化;例2的胆囊腔内肿物呈息肉状生长,浸润毗邻器官如胆管和肝脏.两例肿瘤镜下均由腺癌和鳞癌两种成分构成:既有腺管状结构(黏液可有可无),又有呈巢状镶嵌排列的梭形细胞团,可见角化珠、单个细胞角化及细胞间桥.免疫组织化学检查腺癌细胞表达CK7,鳞状上皮表达CK5/6,而在移行带两者兼而有之.结论胆囊腺鳞癌罕见,但形态学很有特点.预后较单纯腺癌差.【期刊名称】《西南国防医药》【年(卷),期】2013(001)001【总页数】4页(P25-28)【关键词】胆囊;腺鳞癌;病理;免疫组化;鉴别诊断【作者】方三高;张渝;肖蔚;马强;杜娟;肖华亮【作者单位】400042,重庆,第三军医大学大坪医院野战外科研究所病理科;400042,重庆,第三军医大学大坪医院野战外科研究所病理科;江苏省泰州市人民医院病理科;400042,重庆,第三军医大学大坪医院野战外科研究所病理科;400042,重庆,第三军医大学大坪医院野战外科研究所病理科;400042,重庆,第三军医大学大坪医院野战外科研究所病理科【正文语种】中文【中图分类】R735.8胆囊腺鳞癌是胆囊癌组织学的一个特殊类型，较罕见〔1-4〕。

13.cancer细胞生物学英文课件

• 393 amino acids
• Play an important role in cell activity, such as a transcript factor
•Loss-of-function in most cancer，reason： mutations in the TP53 gene or binging to viral proteins or other proteins
• ① Intracellular proteins that regulate or restrain cell cycle (e.g.p16 and Rb)
• ② Receptors or signal transducers for secreted hormones or developmental signals that inhibit cell proliferation (e.g.TGF)
In-vivo Environment Hormone Immune system Chronic inflammation Oxygen Radicals （ reactive oxygen intermediates, ROI; or
reactive oxygen species, gens
（4） lymphoma and leukemia, derived from bone marrow and affects the lymphatic system. In leukaemia, lymphocytes cells do not mature properly and become too numerous in the blood and bone marrow. Leukaemias may be acute or chronic. The most common type is acute lymphoblastic leukaemia (ALL). There are a number of other less common acute types which may be grouped together as acute non-lymphoblastic leukaemia (ANLL), this includes acute myeloid leukaemia (AML). （5）Myelomas Myelomas are cancers of specialized white blood cells, involving the white blood cells responsible for the production of antibodies (B lymphocytes or B-cells).

口腔科(牙科)常用英文词汇

精心整理口腔科(牙科)常用英文词汇alveolarbone牙槽骨alveolarabscess牙槽脓肿ameloblastoma造釉细胞瘤apicalinfection根尖感染apicalcyst根尖囊肿branchialcleftcyst肋裂囊肿carcinomaofmaxillarysinus上颌窦癌carcinomaoftongue舌癌cellulitisofthefloorofthemouth口底蜂窝织炎cementum牙骨质carcinomaofbuccalmucosa颊粘膜癌carcinomaofgingiva牙龈癌carcinomaoflip唇癌caries龋齿circumvallatepapillae轮廓乳头crownfracture冠折deciduousteeth乳牙dentalimpaction牙掼生dentalplaque菌斑dentalrootfracture根折denticulus，denticle髓石dentoalveolarabscess牙槽脓肿drug-inducedgingivitis药物性龈炎dentalcrown牙冠dentaldefect牙体缺损dentalnecrosis牙坏死dentalsac牙囊dentin牙本质dentalarch牙弓epulis龈瘤enamel牙釉质endodontics牙体牙髓病学extraction拔牙术fascialspaceinfection间隙感染fluoride氟化物fractureofmaxillary上颌骨骨折filiformpapillae丝状乳头fistulaapicalis根尖瘘管foliatepapillae叶状乳头fungiformpapillae菌状乳头gingivalabscess牙龈脓肿gingivitis牙龈炎gingivitisinleukemia白血病龈炎gum，gingiva牙龈herpeticstomatitis疱疹性口炎infraorbitalspace框下间隙injuryofteeth牙损伤jaw颌骨juvenileperiodontitis青少年牙周炎luxatedtooth牙脱位lymphoepitheliallesions淋巴上皮病leukoplakia白斑lichenplanus扁平苔藓localanesthesia局麻mucouscyst粘液囊肿missingtooth牙脱失mixeddentition混和牙列mixedtumorofsalivarygland涎腺混和瘤mumps流行性腮腺炎nevi色素痣occlusion咬heodontoclasis燕羡oralcandidiasis口腔念珠菌病oralhygiene口腔卫生oralpathology口腔病理学oralsurgery口腔外科orthodontics正畸学osteomyelitisofthejaws颌骨骨髓炎palate腭paradontoma牙周膜瘤parageusia味觉异常paraglossa舌肿paraglossia舌下炎paralalia出语障碍，构音倒错parotitis腮腺炎periapicalabscess根尖脓肿periapicaldisease根尖周病pericoronitis冠周炎periodontitis牙周炎permanentteeth恒牙pulphorn髓角pediatricdentistry口腔儿科学periodontalligament牙周韧带periodontalmembrane牙周膜periodontics牙周病学prosthodontics修复学pterygomandibularspace翼颌间隙public-healthdentistry口腔预防医学pulp牙髓pulpexposure牙髓暴露pulpectomy牙髓摘除术pulpitis牙髓炎pyogenicosteomyelitis化脓性骨髓炎radiationosteomyelitis放射性骨髓炎radicularcyst根端囊肿recurrentaphthae复发性口疮rootcanaltherapy根管治疗rootoftooth牙根rootresorption牙根吸收sebaceouscyst皮脂囊肿sialolithiasis涎石病sublinguitis舌下腺炎sublingualglandsyst舌下腺囊肿sublingualspace舌下间隙submassetericspace嚼肌间隙submaxillaryspace颌下间隙tartar牙石teeth牙齿temporomandibularjoint颞颌关节thrush鹅口疮thyroglossaltractcyst甲状舌管囊肿toothdecay龋齿toothreplantation牙再植术torsionofteeth牙扭转tongue舌toothmigration牙移动toothreplacement牙复位toothache牙痛最细颗粒金刚石磨头thefinestgritdiamond橡皮杯(轮)rubbercup(wheel)抛光圆盘(粗、中、细、超细)polishingdisk(coarsemediumfinesuperfine)抛光刷polishingbrush抛光膏polishingpaste(RAPTOR)RapidAdaptingPrecisionTransformerofOcclusalResins锯条sawstrip金刚砂条diamondstrip(打磨临间隙用的)不锈钢打磨条stainlesssteelabrasivestrip(forsmoothingadja2centcontactpointswhendoingfillingsandcrowns) 氧化铝aluminiumoxide(打磨条表面的磨料)聚酯条pllyesterstrip持针器needleholder牛角钳cowhorn刀片scalpel刀柄scalpelhandle牙挺elevator根尖挺apicalelevator骨凿bonechisel骨锉bonefile缝和线suture止血钳hemostaticforcepspeet2mosquitoforcepsKellyforceps 剪刀scissors正畸钳orthoplier三头钳“3jaw”claspbendingpliers弯弓丝钳wirebendingpliers分牙圈separator弓丝archwire压带环器bandpusher带环去除钳bandremovingpliers固定器brace咬和纸articulatingpaper咬和纸柄paperarticulator球状抛光器ballburnisher板状充填器plastic(flatplastic)(白色充填用) 成形片matrixband楔子wedge涂药器applicator或dycalapplicator银汞充填器amalgamplugger树脂输送器compositeapplicator口腔材料输送器dentalmaterialapplicator调刀cementspatula调板mixingpad粘接剂bond小容器welldappensdishes橡皮障rubberdam橡皮障夹钳rubberdamclampforcep橡皮障打孔器rubberdampunch橡皮障弓Young’sArch根管侧压器rootcanalspreader藻酸盐印模材alginate印模托盘impressiontray印模调刀alginatespatula蜡刀waxknives塑料刀plasterknife去冠器crownremover(可调)开口器(adjustable)mouthprop印模材枪impressiongun印模材注射器impressionsyringes印模膏putty高稠度印模膏(取冠印模时用的)heavybody低稠度印模膏lightbody喷砂机sandblaster牙间隙刷interdentalbrushinterproximalbrushes 排牙arrangementofteeth喷灯blowlampr/>边缘封闭区bordersealarea 毛刷轮bristlebrushwheel雕刻刀carvingknife。

Primary Bronchogenic Carcinoma..

>3cm但≤7cm†或肿瘤具有以下任一项‡：侵犯脏层胸膜，累及主支气管、距隆突≥2cm，肺不张/阻塞性肺炎蔓延至肺门但未累及全肺
>3cm但≤5cm† >5cm但≤7cm†
†最长径；‡具有这些特征的肿瘤如果≤5cm分类为T2a
亚组
T1a T1b
T2a T2b
2009 IASLC 肺癌分期：肿瘤原发
瘤复发与肺纤维化的情况。
中央型肺癌
MRI
中央型肺癌
MRI
五、辅助检查——痰脱落细胞检查
❖ 当怀疑肺癌时，胸部X线检查之后的下一个诊断步骤，为获取组织标本进行组织学检查。
❖ 痰细胞学检查的阳性率取决于标本是否符合要求、细胞学家的水平高低、肿瘤的类型以及送标本的次数（以3－4次为宜）等因素，非小细胞癌的阳性率较小细胞肺癌的阳性率高，一般在70％－80％左右。
的危险因素，特别是对女性腺癌。
❖ 烹调时加热所释放出的油烟雾也是致癌因素，不可忽视。
❖ 城市中汽车废气、工业废气、公路沥青都有致
癌物质存在。
4、电离辐射
❖ 美国1978年报告一般人群中电离辐射的来源约49.6%来自自然界，44.6%为医疗照射，来自X线诊断的电离辐射可占36.7%。
❖ 大剂量电离辐射可引起肺癌，辐射的不同射线产生的效应也不同，如日本广岛释放的是中子和α射线，长崎则仅有α射线，前者患
定义
灶 (T)
亚组
T T3
>7cm，
T3>7
或直接侵犯胸壁/膈/膈神经/纵膈胸膜/壁层心包，
T3Inv
或肿瘤位于主支气管、距隆突<2cm≤2cm§，
T3Centr
或全肺肺不张/阻塞性肺炎，

肾集合管癌CT表现

肾集合管癌CT表现翟永川;柴彦军;周俊林;马来阳【摘要】目的探讨肾集合管癌(CDC)的CT特征.方法回顾性分析11例经我院手术病理证实的CDC患者CT资料,观察CDC的CT特征.结果所有患者均为单侧发病,肿瘤边界不清,形态不规则,直径3～12 cm;8例(8/11,72.73％)呈单纯浸润性生长,3例(3/11,27.27％)呈局部膨胀性生长伴浸润性生长;4例(4/11,36.36％)累及肾皮质和髓质,7例(7/11,63.64％)累及肾皮质、髓质及肾盂;7例(7/11,63.64％)呈囊实性,4例(4/11,36.36％)呈实性;增强扫描病灶实性部分呈不均匀轻-中度强化,强化程度低于肾皮质;5例(5/11,45.45％)肾脏体积增大或局部轮廓发生改变;1例(1/11,9.91％)肿瘤内见斑点状钙化;3例(3/11,27.27％)侵犯肾周筋膜,5例(5/11,45.45％)肾门淋巴结转移.结论 CDC的CT表现具有一定特征,有助于临床诊断.【期刊名称】《中国介入影像与治疗学》【年(卷),期】2014(011)009【总页数】4页(P587-590)【关键词】肾肿瘤;肾小管,集合;体层摄影术,X线计算机;病理学【作者】翟永川;柴彦军;周俊林;马来阳【作者单位】兰州大学第二医院放射科,甘肃兰州 730030;兰州大学第二医院放射科,甘肃兰州 730030;兰州大学第二医院放射科,甘肃兰州 730030;兰州大学第二医院放射科,甘肃兰州 730030【正文语种】中文【中图分类】R814.42;R737.11肾集合管癌（collecting duct carcinoma，CDC）起源于肾集合管，发病率极低，恶性程度高，生存期较短，影像学表现不典型，易误诊为肾结核、黄色肉芽肿性肾盂肾炎等。

本研究回顾11例CDC 的影像学资料，探讨其CT 特征。

1 资料与方法1.1 一般资料收集2006年4月—2013年10月11例经我院手术病理证实的CDC 患者的CT 资料，男7例，女4例，年龄32～81岁，中位年龄52岁。