兔肺VX2移植瘤放疗前后~（18）F-FDG PET及CT观察

目的：探讨兔肺VX2移植瘤模型用于评估肺部肿瘤放射治疗效果的可行性。方法：12只兔肺VX2移植瘤模型行短期大剂量放疗,放疗前及放疗后第7天行18F-FDGPET及CT检查,以常规病理作为金标准。结果：兔肺VX2移植瘤放疗前PET显像,常规SUVmax为2.95±1.04,延迟SUVmax为3.58±1.32;放疗后第7天PET显像,常规SUVmax为1.47±0.36,延迟SUVmax为1.88±0.44。放疗后PET常规显像较放疗前18F-FDG代谢变化百分率下降60.48±5.66,PET延迟显像18F-FDG代谢变化百分率下降57.18±6.79。兔肺VX2移植瘤放疗前后PET常规显像SUV改变与放疗前后PET延迟显像的SUV改变均以t检验分析,放疗前后SUV变化有统计学意义。病理检查见肿瘤组织内大片凝固坏死。结论：兔肺VX2移植瘤模型短期大剂量放疗后行18F-FDGPET显像,其SUV显著降低,可在兔肺VX2移植瘤出现CT形态学改变之前早期评估兔肺VX2移植瘤对放射治疗的反应。     

MR扩散加权成像和分子成像在卵巢肿瘤微环境中的应用研究进展

卵巢癌是女性生殖系统的常见恶性肿瘤之一,其早期发现困难,确诊时多为中晚期,常有腹膜转移,手术难以完全切除,复发率高。这与由肿瘤细胞、肿瘤基质成分、炎性细胞和间质细胞构筑的肿瘤微环境中启动肿瘤细胞生长、开启肿瘤血管生成、促进肿瘤细胞迁徙和浸润、肿瘤细胞免疫逃逸等决定病人预后的一系列发生机制不明有很大关系。采用结构成像、功能成像和分子成像相结合的医学成像方法,进行实时动态、多元精准和在体无创研究及评估卵巢癌微环境,对监测卵巢癌的生物学行为和疗效以及预后判断具有重要意义。     

肋骨肿瘤和肿瘤样病变的X线和CT表现

目的：讨论肋骨肿瘤和肿瘤样病变的X线和CT表现,总结各自的特点。方法：取经手术和病理证实,或临床动态观察证实的肋骨病变病例100例;所有病例均行X、CT检查。结果：64例为良性病变,其中24例为骨岛,18例为骨纤维异常增殖症,14例为软骨类良性肿瘤,8例为骨感染性病变,（4例为结核,4例为非特异性感染）。恶性病变36例,其中转移瘤20例,骨髓瘤8例,骨巨细胞瘤8例。结论：肋骨肿瘤和肋骨肿瘤样病变一般具有某些有助于诊断的X线和CT表现,据此可以较好的区分常见肋骨肿瘤和肋骨肿瘤样病变。     

重视平坦型大肠肿瘤的临床诊治

平坦型大肠肿瘤包括表浅型大肠肿瘤及凹陷型大肠肿瘤,与大肠癌发生有密切相关的特殊性。表浅型大肠肿瘤以大肠侧向发育型肿瘤(1aterally spreading tumor,LST)为代表;凹陷型大肠肿瘤以凹陷型早期大肠癌(Ⅱc型早期大肠癌)为代表。平坦型大肠肿瘤由于在临床上难以发现,在我国尚未被临床医师普遍认知,因此有关报道极少。近年来,南方医院在做肠镜检查中对平坦型大肠肿瘤的检出和诊疗上创造与积累了一些自己的经验,他们认为,提高大肠平坦型病变征象的识别和染色内镜的应用是发现大肠平坦型病变的关键,黏膜剥离术和分析黏膜剥离术是诊治大肠平坦型病变的最佳方法之一,而且已着手开展对平坦型大肠肿瘤发生发展的基础研究工作。     

原发性腹膜后肿瘤57例分析

目的探讨原发性腹膜后肿瘤的诊断及治疗。方法1990—2004年经手术和病理证实的原发性腹膜后肿瘤57例,就其年龄、临床表现、辅助检查、病理类型及手术方式进行比较。结果首发症状及体征多数为腹痛及腹块。良性肿瘤23例,占40%,恶性肿瘤34例,占60%,平均病程21.6个月,70%恶性肿瘤病程多在1年以内,良性肿瘤病程多在1年以上。术前确诊率为68%,B超及CT的诊断率分别为81.3%,90.9%。本组良性肿瘤切除率91.3%,恶性肿瘤32.4%,术后复发6例,3例再次行根治术。结论本病早期缺乏典型症状,临床早期诊断困难,B超、CT等影像学检查是本病诊断的重要手段。手术切除是治疗的主要手段,对侵犯脏器者采用累及脏器一并切除,不能切除和切除后再发的主张探查活检和再次手术或多次手术切除。     

多次肝动脉化疗栓塞术联合射频消融在肝癌治疗中的临床应用

目的评价多次肝动脉化疗栓塞(TACE)联合射频消融(RFA)治疗肝癌的临床疗效。方法对经多次TACE治疗后仍有肿瘤残余的10例肝癌患者分别行B超引导下射频消融治疗,术后随访监测甲胎蛋白(AFP)的动态变化及肝脏CT表现来评价疗效。结果 RFA治疗后3~6个月,生存率为100%,其中9例患者AFP<400 ng/mL,CT检查无肿瘤复发征象者8例,有肿瘤复发征象者2例。9~12个月复查,8例患者AFP<400 ng/mL,CT增强扫描未发现肿瘤复发征象;有肿瘤复发征象的患者2例,再次行射频消融治疗。8例患者随访时间达到24个月,其中6例患者AFP<400 ng/mL,CT增强扫描未发现肿瘤复发者7例;1例患者死亡。结论多次TACE联合射频消融为中晚期肝癌治疗提供了新的治疗思路与途径。     

Imaging procedures for assessment of the response of mammary carcinoma to preoperative chemotherapy

Summary Neoadjuvant chemotherapy with epirubicin and cyclophosphamide makes breast conserving therapy possible in patients with large tumors, which are primarily not suited for this treatment. The regression of the tumor can be followed by mammography, ultrasound and MRI. Mammography is reproducible and easily available. Tumors, which cannot be measured mammographically, usually can be followed with ultrasound. MR allows imaging of the tumor independent of structure and density of the parenchyma. In addition the measurement of functional parameters is possible. – All methods are restricted in the imaging of tumor residuals after neoadjuvant chemotherapy, because imaging of small microscopic foci of invasive or even non invasive tumorresiduals is hardly possible. Of special concern are tumor specific microcalcifications, which only can be shown on mammograms, in this respect. They do not regress under chemotherapy, even if the invasive tumor regresses, and they typically hint for non invasive tumor residuals. For planning surgery the pretherapeutic tumor extent always has to be taken into account, because of the restricted ability to image small tumor residuals.      

Leydig cell tumors in adults. Value of ultrasonic diagnosis. Apropos of 7 tumors

Leydig cell tumors arise from the gonadal stroma and represent two or three per cent of all testicular tumors. They may occur at any age in contrast with germinal tumor. In adults, about 20 per cent occur with endocrine disturbance: gynecomastia or impotence. Ten per cent are malignant and few cases are bilateral. They are small, yellow, brown tumor. Reinke's crystals are observed in 50 per cent and are pathognomonic. They present no necrosis no hemorrhage, no cyst. A benign tumor is difficult to distinguish from a malignant tumor. A vascular and capsular invasion, an infiltrative margin, a bilateral or multiple tumors must evoke a malignant case. Cryptorchidism, even corrected seems to be partly responsible in tumor induction. Ultrasonography can help for a precocious and reliable diagnosis of tumors, specially in case of occult tumors (2 cases). It also helps to survey the controlateral testis (bilateral tumor: 1 case).     

Solitary fibrous tumor: an update on the spectrum of extrapleural manifestations

Solitary fibrous tumor (SFT) is a rare tumor initially believed to be a benign localized pleural tumor of mesothelial origin. Over the past few years, the literature on this tumor has grown tremendously. The tumor is now reported in diverse bodily locations, and recognized to have a wider range of clinical and radiological features. The most common extrapleural sites of the tumor are the orbits and the extremities. Tumors are often well-circumscribed masses, and vary in size from 1 cm to over 30 cm. The admixture of histological components in the tumor, namely, fibrous tissue, cellular components, and highly vascularized areas consisting of numerous closely packed small to medium-sized blood vessels, influence the imaging appearances of the tumor. On magnetic resonance imaging (MRI), the diagnosis of solitary fibrous tumor is suggested by a well-circumscribed mass that has smooth margins, and focal or diffuse hypointense signal on T2-weighted imaging due to fibrous content in the tumor. SFTs demonstrate strong focal or diffuse contrast enhancement due to the highly vascularized areas in the tumor.     

Individuality of malignant neoplasms

The article concerns the implication of the tumor cell heterogeneity, which is caused by the genetic instability of tumor cells. Thereby, within a given tumor, subpopulations with differing marker profiles may appear in a very irregular fashion. For instance, some populations may show criteria which under normal circumstances are mutually exclusive. In so far, the tumor cell heterogeneity can be viewed as responsible for the fact that tumor classifications are never scientific classifications which are defined by reliable and stable criteria. Furthermore, the tumor cell heterogeneity must be born in mind when malignant tumors are graded. Grading provides usually only statistical results which must not necessarily be valid for the individual case. It is concluded that malignant neoplasias should be considered much more individually if we were to take their biologic behaviour properly into account. This, however, bears considerable difficulties, especially with respect to diagnostic and therapeutic conclusions.     

Regrowth, tumor cell proliferation and morphological alterations of the adenocarcinoma EO 771 following a single dose of 30 Gy 60Co gamma-rays

The effect of irradiation with 30 Gy 60Co gamma-rays on the adenocarcinoma EO 771 has been studied by simultaneously evaluating the effect on tumor growth, on tumor cell proliferation and on the histological structure of the tumor. Inspite of a drastic decrease of tumor cell density by a factor of 2 within one day after irradiation there is practically no tumor regression but only a growth delay lasting about five to six days. The lack of decrease in tumor volume is due to hemorrhages and interstitial oedemas. Regrowth of the tumor starting after about five days concomitantly with the removal of necrotic tissue is followed by a second wave of growth delay. Following the release of the G2 block of the cells tumor cell proliferation is reduced to about half the normal proliferative activity for further three days. Tumor cell proliferation reaches its maximum about eight days after irradiation and then decreases again although higher proliferative activity should be expected comparing the size of the tumor with that in untreated animals. The proliferative activity is much higher in the tumor periphery than in the center suggesting that radiation damage is more rapidly compensated in the tumor periphery. These studies confirm that tumor volume changes are not representative for radiation effects but that there are many processes as damage to the vascular system or the tumor bed effect that influence the effect of irradiation on the tumor.     

Recurrent desmoid tumor arising from latissimus dorsi flap: A case report

Fibromatosis or desmoid tumor in the breast is a very rare benign soft tissue tumor. We report a case of recurrent desmoid tumor arising from latissimus dorsi flap after lumpectomy for breast carcinoma. To our knowledge, this is the first case of desmoid tumor arising from the latissimus dorsi flap. Despite its benignity, desmoid tumor is often locally aggressive, therefore timely diagnosis and proper management are very important. Imaging and pathological diagnosis as well as treatment management are discussed. High clinical suspicion and multidisciplinary approach are essential for prompt diagnosis and management. Wide surgical resection is required, but there is no consensus regarding treatment due to limited data.     

Correlation of size of the primary tumor and axillary node status with the p53 tumor suppressor gene in carcinoma of the breast

Correlation of standard pathomorphological prognostic parameters, primary tumor size and axillary nodal status with new prognostic factor in breast carcinoma: tumor suppressor gene p53 was analyzed. The studied sample included 65 women who underwent surgery for breast carcinoma at the Surgical Clinic of Clinical Center Banja Luka, from January 1st 1997 till January 1st 1999. Statistical data analysis was performed and correlation of prognostic factors was determined. The majority of authors in this field agree that the primary tumor size and axillary nodal status are the two most important prognostic factors. These factors are the best predictors of prognosis and survival of women who had the tumor and were operated on. Tumor markers were immunohistochemically determined in the last ten years and, according to the majority of authors, are still considered the additional or relative prognostic factors in breast carcinoma. Their prognostic value and significance increase almost daily. Most frequently determined tumor markers are bcl-2, pS2, Ki-67 and p53. There was a positive, directly proportional relationship between primary tumor size and tumor suppressor gene p53, but there was no positive correlation between the axillary nodal status and tumor suppressor gene p53. Significance of determination of new tumor markers as the prognostic factors was emphasized. These markers represent a powerful tool in the early detection and prevention of breast carcinoma.     

Concepts for treatment of micrometastases developed in murine systems.

Small tumor cell foci, whether left in situ during primary surgical excision or escaping lethal radiation damage, as well as distant metastases, are the primary reason for treatment failure in man and are the proper targets for the chemotherapist and immunotherapist. Since cure probably requires reduction of the total body burden of tumor cells to very small numbers (possibly to less than one cell), and since first-order kinetics of tumor cell kill by drugs appears to be a natural law in cancer chemotherapy, drug treatment should be started as soon as possible after likely noncurative primary treatment with surgery or radiation. Current knowledge of tumor cell population growth kinetics indicates that the growth fraction (viable tumor cells undergoing active cell replication) is inversely related to population size. Tumor cells in micrometastases should, therefore, be more sensitive to anticancer drugs active against anabolizing cells than are tumor cells in the larger, grossly apparent primary tumor from which they were derived. This indicates the probability that micrometastases will be effectively responsive to more drugs than is the primary and clinically apparent tumor from which they came. Studies with at least four metastatic and uniformly fatal murine solid tumors (lung, breast, colon, and melanoma) have demonstrated significantly improved cure rates with drug treatment following surgical removal of the grossly apparent primary tumor than can be obtained with either surgery or drug treatment when used alone. Further, both disease staging and drug dosage have been shown to influence cure rates of combined-modality treatment. With several mouse tumors, a significantly smaller number of viable tumor cells can establish lethal tumors in the presence of radiation-inactivated tumor cells than in their absence. This suggests that small numbers of residual viable tumor cells in radiation-treated tumor sites may be a greater threat to clinical cure than smaller tumor cell populations remaining in situ after surgery.     

Evidence for and against a tumor type-specific vascularity

Although there are some implications from experimental rodent tumors that the vascular morphology may be characteristic, but not unique for a special tumor, there is clear evidence that in general the histological type of a tumor and the degree of differentiation can only modulate, but not dictate the vascular pattern. Problems arising when trying to identify a certain tumor on the basis of its vascularity or vice versa are aggravated by considerable intra-tumor inhomogeneities of both vascular structure and function of the vascular bed. The same holds true for an individual tumor at different sizes. As a consequence, it is impossible to draw conclusions concerning the tumor vascularity from a known tumor histology.     

肋骨肿瘤和肿瘤样病变

本文报告经手术和病理证实的肋骨肿瘤和肿瘤样病变７２例，其中良性病变５１例，恶性２１例、良性病变以骨纤维异常增殖症和软骨源性肿瘤多见，恶性肿瘤以转移瘤和骨髓瘤多见。本文提出了良恶性肿瘤鉴别要点和有助于某些肿瘤诊断的Ｘ线表现的特点，还报告了几例少见表现为中度膨胀性破坏的转移瘤。少数肋骨慢性骨髓炎易与肿瘤混淆。     

Comparison of changes in tumor metabolic activity and tumor size during chemotherapy of adenocarcinomas of the esophagogastric junction.

We evaluated the temporal relationship between chemotherapy-induced changes in tumor glucose use and tumor size. METHODS: Twenty patients with adenocarcinoma of the esophagogastric junction (AEG) were studied by 18F-FDG PET and CT scans before neoadjuvant chemotherapy, 14 d after the initiation of therapy, and 4 wk after the completion of therapy. RESULTS: The relative change in 18F-FDG uptake was more than 2 times larger than the decrease in tumor size at all time points (P<0.01). At 14 d after the initiation of chemotherapy, there was no correlation between the reduction in 18F-FDG uptake and tumor wall thickness. The change in 18F-FDG uptake after 14 d of therapy was significantly correlated with the reduction in tumor size after the completion of therapy. CONCLUSION: In AEG, changes in tumor metabolism are a more sensitive parameter for assessing the effects of chemotherapy than are changes in tumor size. Early changes in metabolic activity predict the subsequent reduction in tumor size.     

Transient early computed tomographic changes mimicking tumor progression after brain tumor irradiation

Transient computed tomographic (CT) changes occurring within three months after radiotherapy are described in three patients with cerebral gliomas. These changes consist of enlargement of an area of central necrosis, new tumor enhancement, and increased tumor enhancement with adjacent low-density changes. Subsequent scans showed regression of these changes in all patients. It is proposed that these changes are the direct effect of radiation on tumor tissue and adjacent normal brain; possible mechanisms are discussed. These radiation-induced changes mimic tumor progression on CT. The importance of recognizing their transient nature is stressed.     

Circulating tumor markers and nuclear medicine imaging modalities: breast, prostate and ovarian cancer.

Clinical oncologists have always shown great interest in circulating tumor markers. There are several markers that in the clinical routine are a signal of particular tumor types; some of them are strictly tissue-specific such as prostatic specific antigen (PSA) for prostatic cancer, AFP and HCG for germ cell tumors of the testis and ovary, others such as CA 15.3, CA125, CEA or cytokeratins are less specific since their elevations can be found in different varieties of cancers even if they are preferentially associated to a certain tumor type, thus are considered markers for breast, ovarian cancer and colon adenocarcinoma. The most useful clinical applications of these parameters is their determination during the follow-up of the treated patients, in order to detect the tumor recurrence early, and also to evaluate the evolution of the disease by monitoring the treatment responses. During follow-up, increasing levels of tumor markers can be observed even several months before the clinical demonstration of cancer recurrence. The association of tumor marker tests with imaging modalities can lead to several advantages: the first is to confirm the diagnosis of relapses, possibly before the appearence of the related clinical symptoms due to tumor growth; the second is to localize the sites of lesions, while tumor markers provide only a general indication of the existence of metastases; the third is to make possible a correct whole body restaging. In the assessment of cancer response tumor markers are often very reliable and their changes are faster than the morphological ones. Among all the imaging modalities, nuclear medicine plays an important role in detecting recurrences and metastatic localizations as it is able to investigate functional rather than morphological aspects of tumors, and provide different information in comparison to morphologic imaging. In addition, the scintigraphic techniques offer the possibility to evaluate treatment responses, confirming or not the information from biochemical changes. This review aims to show some examples (breast, prostate and ovarian cancer) in which the combination of nuclear medicine imaging modalities and tumor marker tests is proposed for clinical practice. The advantages and some critical aspects are discussed on the basis of the clinical findings and the most important clinical indications are described.     

Tumor markers: essential diagnostic tools for radiologists]

A tumor marker is defined as a substance that is produced by the body in response to cancer or by the cancer tissue itself. Since discovery of the Bence-Jones protein in 1848 and AFP (alpha-fetoprotein), CEA (carcino-embryonic antigen), and SCC (squamous cell carcinoma antigen) in the 1960s and 1970s, a number of tumor markers have been developed for routine clinical laboratory tests. Some tumor markers are specific for one type of cancer, while others are positive for several cancer types. Furthermore, tumor markers are seen in non-cancerous conditions as well as in cancer. A positive result for one tumor marker does not necessarily indicate the presence of a malignant lesion. Because of insufficient sensitivity and specificity, most tumor markers cannot be used in screening for cancer in the early stage. When the presence of cancer is suspected, it must be confirmed using other diagnostic approaches such as radiological tests, pathological tests, or meticulous observation of disease progress. Tumor markers are useful in the follow-up of patients after treatment for malignant lesions, and they are usually superior to radiological tests in detecting recurrent lesions. When cancer is evaluated radiologically, knowledge of tumor markers is of great help to radiologists. Basic knowledge regarding tumor markers and pitfalls in their clinical usage are described.