Gland Metastasis Research Articles

Multidisciplinary Management of a Rare Case of Esophageal Adenocarcinoma with Cardiac, Pulmonary, Liver, Adrenal Gland and Brain Metastasis

Multidisciplinary Management of a Rare Case of Esophageal Adenocarcinoma with Cardiac, Pulmonary, Liver, Adrenal Gland and Brain Metastasis

Efficacy of Imiquimod Cream Administered Intraperitoneally for Ovarian Metastases in Colorectal Cancer

In this case report, we sought to determine the efficacy of intraperitoneal Imiquimod cream for the treatment of persistent ovarian metastases in colorectal cancer after Avastin-based chemotherapy failure. Topical Imiquimod cream is an immune response modifier. It could trigger skin Langerhan cells (naive dendritic cells) as the priming responsive cell type and initiate a strong Th1-switched anti-tumor cellular immune response. This is a 50-year-old woman with rectal cancer with liver, lung, left adrenal gland and ovarian metastasis, and pelvic carcinomatosis. CEA level decreased after the initial optimal debulking surgery and 12 cycles of chemotherapy. However, CEA level persistently elevated, and CT scan showed progressed carcinomatosis, malignant ascites and diffused metastasis. After intraperitoneal immunomodulatory therapy (IMT) administration with intraperitoneal Interleukin-2 mix Thymoxin on Day 1, and intraperitoneal Imiquimod cream (5% 250 mg in normal saline 2 ml) on Day 2, the amount of drainage ascites gradually decreased, and CEA level dramatically decreased after IMT.

Outcome After SBRT of Adrenal Gland Metastases: A Multicenter Retrospective Analysis of 60 Adrenal Metastases

Outcome After SBRT of Adrenal Gland Metastases: A Multicenter Retrospective Analysis of 60 Adrenal Metastases

Abstract IA27: Cell fate determinants as regulators of cancer metastasis

Abstract An emerging class of genes dictating malignant behavior is cell fate regulators. In the orderly development of a given tissue, the balance between cellular differentiation and division/migration is precisely controlled by a number of lineage specific transcription factors to maintain normal tissue architecture. Deregulation of such cell fate determinants have been increasingly linked to cancer metastasis, and have been shown to play critical roles in regulating cancer stem cell activity, epithelial-mesenchymal transition (EMT), tumor invasion and metastatic colonization. In our study of the mammary gland development, we found that the transcription factor Elf5, a key regulator of alveologenesis in the mammary gland, also plays a critical role in regulating the stem/progenitor function of the mammary epithelium. Targeted deletion of Elf5 in the mammary glands leads to accumulation of cell types with dual luminal/basal properties such as coexpression of K8 and K14 and an increase in CD61(+) luminal progenitor population during pregnancy. Further interrogation suggests that the abnormal increase in K14(+) K8(+) cells may represent the CD61(+) luminal progenitors blocked in differentiation. Remarkably, Elf5 deficiency in mammary epithelium also triggers an increase of adult mammary stem activity as evidenced by the accumulation of mammary stem cell (MaSC)-enriched cell population in both pregnant and virgin mice and further confirmed by mammosphere and transplantation assays. In addition to controlling cell fate determination, Elf5 also inhibits EMT in both mammary gland development and metastasis. This specific role for Elf5 in suppressing EMT and metastasis was uncovered via analyses of Elf5 conditional knockout animals, various in vitro and in vivo models of EMT and metastasis, an MMTV-neu transgenic model of mammary gland tumor progression, and clinical breast cancer samples. Furthermore, we demonstrate that this role of Elf5 is mediated by the direct transcriptional repression of Snail2/Slug, a master regulator of mammary stem cells and a known inducer of EMT. These findings establish a broad molecular function of Elf5 that extends from being a key cell lineage regulator during normal mammary gland development to serving as a suppressor of EMT and metastasis in breast cancer. Citation Format: Yibin Kang. Cell fate determinants as regulators of cancer metastasis. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr IA27.

Abstract IA02: Tumor plasticity and reactive stroma in breast cancer metastasis

Abstract Metastasis represents the most devastating stage of cancer progression. The multi-step cascade of cancer metastasis is driven by both intrinsic changes of cancer cell properties, as well as the stromal reaction to tumor cells. Epithelial-mesenchymal transition (EMT) is a complex process that is associated with dramatic changes in cell adhesion, polarity, and migratory properties, and is intimately associated both with cell fate transitions during embryonic development and with the acquisition of invasive properties during early steps of cancer metastasis. We found that the transcription factor Elf5, a key regulator of alveologenesis in the mammary gland, regulates EMT in both mammary gland development and metastasis. This specific role for Elf5 in suppressing EMT and metastasis was uncovered via analyses of Elf5 conditional knockout animals, various in vitro and in vivo models of EMT and metastasis, an MMTV-neu transgenic model of mammary gland tumor progression, and clinical breast cancer samples. Furthermore, we demonstrate that this role of Elf5 is mediated by the direct transcriptional repression of Snail2/Slug, a master regulator of mammary stem cells and a known inducer of EMT. These findings establish a broad molecular function of Elf5 that extends from being a key cell lineage regulator during normal mammary gland development to serving as a suppressor of EMT and metastasis in breast cancer. The growth of disseminated tumor cells at distant organs represents a critical final stage of metastasis development. Bone metastasis is a frequent occurrence in breast cancer, affecting more than 70% of late stage cancer patients. Increasing evidence suggest that the development of bone metastasis relies on the positive feedbacks from stromal components of the bone microenvironment. Using in vivo imaging technology, we showed that TGFβ is released from bone matrix upon bone destruction, and signals to breast cancer to further enhance their malignancy in developing bone metastasis. We furthered identified Jagged1 as a TGFβ target genes in tumor cells that engaged bone stromal cells through the activation of Notch signaling to provide a positive feedback to promote tumor growth and to activate osteoclast differentiation. More recently, we identified osteoclast-derived miRNAs as biomarkers and therapeutic targets of osteolytic bone metastasis. Importantly, pharmaceutical inhibitors against TGFβ and Notch signaling pathways and miRNAs blocking osteoclast differentiation significantly reduce the development of bone metastasis, suggesting novel avenues for clinical management of skeletal complications of breast cancer. Citation Format: Yibin Kang. Tumor plasticity and reactive stroma in breast cancer metastasis. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications; Oct 3-6, 2013; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2013;11(10 Suppl):Abstract nr IA02.

Human papillomavirus–associated adenocarcinoma of the base of the tongue

Human papillomavirus (HPV) is a major cause of oropharyngeal squamous cell carcinoma with characteristic clinical and pathologic features relative to their non-HPV-associated counterparts. Here we describe 2 cases of HPV-associated adenocarcinoma of the oropharynx. Both cases arose at the base of the tongue, and neither had the histologic or immunohistochemical features of a primary salivary gland tumor or metastasis from another location. One patient had metastases to neck lymph nodes and the lungs and died of disease 37 months after diagnosis. Evidence for an HPV association consisted of strong diffuse expression of p16, polymerase chain reaction-based detection of HPV16 DNA sequences, and localization of HPV by in situ hybridization within tumor cells of both primary and metastatic lesions. These results further expand the spectrum of HPV-associated head and neck malignancy. This rare entity should be distinguished from primary salivary gland adenocarcinoma and may be a candidate for HPV-specific targeted therapies.

Abstract IA6: Epithelial-mesenchymal plasticity in breast cancer metastasis

Abstract Increasing evidence suggests that the normal genetic programs underlying various developmental processes can often be usurped in pathological conditions such as cancer metastasis. Epithelial—mesenchymal transition (EMT) is a complex process that is associated with dramatic changes in cell adhesion, polarity, and migratory properties, and is intimately associated both with cell fate transitions during embryonic development and with the acquisition of invasive properties during cancer metastasis. Several transcription factors, including the Snail, Zeb and Twist families, have been identified as major drivers of EMT by repressing the transcription of E-cadherin. However, our knowledge about the regulatory network and pleiotropic effects of epithelial-mesenchymal plasticity remains largely incomplete, and the importance of reverse process, mesenchymal-epithelial transition (MET), is poorly understood. In our study of the early stage of breast cancer metastasis, we found that the transcription factor Elf5, a key regulator of alveologenesis in the mammary gland, regulates EMT in both mammary gland development and metastasis. This specific role for Elf5 in suppressing EMT and metastasis was uncovered via analyses of Elf5 conditional knockout animals, various in vitro and in vivo models of EMT and metastasis, an MMTV-neu transgenic model of mammary gland tumor progression, and clinical breast cancer samples. Furthermore, we demonstrate that this role of Elf5 is mediated by the direct transcriptional repression of Snail2/Slug, a master regulator of mammary stem cells and a known inducer of EMT. These findings establish a broad molecular function of Elf5 that extends from being a key cell lineage regulator during normal mammary gland development to serving as a suppressor of EMT and metastasis in breast cancer. Focusing on non-coding RNAs as potential novel regulators of EMT, we identified the miR-200 family miRNAs as suppressors of EMT and tumor invasion that function via direct targeting of Zeb1 and Zeb2. Contrary to the expectation that miR-200s should inhibit metastasis, we found that miR-200 overexpression is in fact associated with poor metastasis-free survival of breast cancer patients and functionally promotes metastatic colonization in mouse models. Through an integrated genomic/proteomic analysis, we identified the Sec23a secretory pathway as a prominent functional target of miR-200s with an active role in suppressing metastatic colonization. Secretome analysis further identified IGFBP4 and TINAGL1 as important Sec23a-dependent secreted proteins with metastasis suppressive functions. Thus, the dichotomous functions of miR-200s in inhibiting early steps of invasion while promoting late step of metastatic colonization is achieved through targeting of both tumor cell-intrinsic and —extrinsic regulatory pathways. Taken together, these findings support dynamic and pleiotropic roles of epithelial-mesenchymal plasticity in early and late stages of metastatic progression: while EMT is necessary for initial invasion, MET may be required for efficient colonization. Citation Format: Yibin Kang. Epithelial-mesenchymal plasticity in breast cancer metastasis. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr IA6.

ALK and MET genes in advanced lung adenocarcinomas: The Lung Cancer Mutation Consortium experience.

7589 Background: The Lung Cancer Mutation Consortium (LCMC) consisting of 14 US Cancer Centers was established to evaluate a panel of molecular mutations in advanced lung adenocarcinoma. ALK gene fusions and MET gene amplification were assessed by FISH in CLIA certified laboratories. Methods: Molecular tests were performed in stage IIIB or IV lung adenocarcinoma. To date, FISH assays have been completed in 901 patients for ALK (ALK break-apart, Abbott Molecular) and in 654 patients for MET (in house/Abbott Molecular reagents). ALK+ specimens were defined by split 3’ALK/5’ALK signals (gap >2 signal diameters) or single 3’ALK signals in >15% of tumor cells. MET gene amplification (MET+) was defined by ratio mean MET/mean CEP7 ≥2. Results: The ALK+ patient subset (N=75, 8.3%) compared to the ALK- had significantly lower age at diagnosis (52 vs. 60, p<0.001) and less frequent heavy smoking history (61% never-smokers among ALK+ vs. 31% among ALK-, p<0.001; pack-year for current/former smokers 17 vs. 40, p=0.003). Liver metastases were significantly more frequent among ALK+ than ALK- (23% vs.10%, p=0.004); no difference was detected in bone, brain and adrenal gland metastases. MET+ (N=29, 4.4%) was significantly associated with female sex (72% female among MET+ vs. 39% among MET-, p<0.001) and marginally more frequent in patients with adrenal metastasis; no difference was detected for age at diagnosis and smoking history. Follow-up on 73 ALK+ patients indicated that 56% received crizotinib as targeted therapy. Response was unknown in 8% and unreportable in 22% patients enrolled in ongoing randomized trials. Among patients with evaluable response, complete response, partial response, stable disease, and progressive disease were found respectively in 3%, 66%, 28%, and 3%. Conclusions: The LCMC successfully tested ALK and MET FISH in a large number of lung adenocarcinomas. It was demonstrated that directing positive patients to specific interventions is feasible, and that grouping of testing and trials within consortia may maximise relevant trial accrual in rare molecular subtypes. Supported by NCI-GO award. Submitted on behalf of the LCMC.

Abstract 991: The DNA methylome of castration-resistant prostate cancer

Abstract Lethal prostate cancer is predominantly a castrate-resistant disease. However, castrate-resistant prostate cancer (CRPC) is clinically heterogeneous and a classification that is predictive of outcome and response to therapies is lacking. Previous epigenetic profiling studies in CRPC have been limited to a small number of genes or sequences and therefore we explored the DNA methylome of CRPC and its capacity to classify the disease. We performed methylated CpG island amplification microarrays (MCAMs) using a panel of xenografts derived from 24 patients with CRPC tumors, 8 prostate tumors, 1 local recurrence, 5 liver metastases, 3 pleural fluid samples, 2 adrenal gland metastases and 1 each of the following: bone, subcutaneous tissue, retroperitoneal lymph node, ascitic fluid and brain. The xenograft morphology consisted of 15 adenocarcinomas, 11 small cell carcinomas, 3 large cell neuroendocrine carcinomas, 1 squamous cell carcinoma, 2 mixed morphologies and 2 unknown. The Lowess-normalized M values were used for analysis and the MCAM results were validated by pyrosequencing of 20 sequences associated with 12 genes with a sensitivity of 61.9%, a specificity of 84.3%, a positive predictive value of 73.6% and a negative predictive value of 75.7%. An unsupervised hierarchal clustering analysis using M values for probes located in CpG islands was performed and these results were compared with the clinicopathological features of the tissues. We observed that, different xenograft sublines derived from the same donor tumor clustered together suggesting that the DNA methylome is homogenous throughout a given tumor mass, despite the presence of histological heterogeneity, and that it is maintained through serial passages in mice. Unsupervised hierarchal clustering classified the xenografts into 3 groups, which showed trend towards distinct clinicopathological features including overall survival and androgen receptor (AR) status. In summary, we found that DNA methylation is a frequent event in CRPC and well preserved in xenograft tumors. Furthermore, the methylation profile of CRPC may represent a marker of clinicopathological subgroups with differential survival and AR status. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 991. doi:1538-7445.AM2012-991

99mTc-DMSA complex preparation: the effect of pH and tin(II) chloride amount on reaction

Labelling of meso-2,3-dimercaptosuccinic acid (DMSA) with technetium-99m was reinvestigated. Depen- dence of the 99m Tc-DMSA complex formation on the molar ratio of DMSA:reducing agent (SnCl22H2O) and pH was studied. Five different types of 99m Tc-DMSA complexes were determined. Especially three different complexes were established in the clinically used and prepared DMSA kit labelled with 99m Tc under alkaline condition. This radio- pharmaceutical is used as imaging agent of the primary medullary carcinoma in the thyroid gland and different metastasis types. The existence of all complexes was observed by paper chromatography, paper electrophoresis and high performance liquid chromatography.

Mouse Mammary Tumor Expressing MMTV-SmoM2 as a Tool To Study Lung Metastasis.

Abstract Background: The hedgehog signaling network regulates pattern formation, proliferation, cell fate and stem/progenitor cell self-renewal in many organs. Altered hedgehog signaling is implicated in 20-25% of all cancers, including breast cancer. We demonstrated previously that expression of activated human SMO (SmoM2) under the mouse mammary tumor virus (MMTV) promoter in transgenic mice leads to increased proliferation, altered differentiation, ductal dysplasias, and increase the proportion of mammosphere-forming cells, with reduction of stem cell pool, in virgin mice.Material and Methods: We isolated and established a tumor line from this mouse line (named TU505). To investigate the role of hedgehog signaling in mammary tumorigenesis and metastasis we transplanted TU505 fragments (1-2mm3) to a cleared fat pad of 3 week-old mice. After 10 days we removed the primary tumors and let the mice recover for another 3 weeks, which at that time the animals were sacrificed and the lungs removed under stereomicroscope. The lung metastases visible at naked eyes were snap frozen for RNA isolation, and the remaining lungs fixed in 4%PFA.Results: The TU505 is a tumor expressing MMTV-SmoM2, triple-negative (ER-, PR-, and HEB2-), hormone independent, highly metastatic to the lung, and with a robust expression of Ptch1, Ptch2, Smo, Gli2, and Gli3. The gene expression of primary tumor and metastasis are compared.Discussion: The hedgehog signaling networks has been associated with metastasis. The TU505 is a strong tool to study mammary gland tumorigenesis and metastasis. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 2165.

Massive bilateral adrenal gland metastases from melanoma diagnosed by F18-FDG-PET/CT

We report a case of a 75-year-old man with a history of a malignant melanoma with massive bilateral adrenal gland metastases diagnosed by F18-FDG-PET/CT after 10 years of negative follow-up.

A Case of Complete Clinical Response with Sorafenib in a Patient with Thyroid Gland Metastases from Renal Cell Carcinoma 17 Years from Diagnosis

A Case of Complete Clinical Response with Sorafenib in a Patient with Thyroid Gland Metastases from Renal Cell Carcinoma 17 Years from Diagnosis

Parotid gland metastasis of a breast cancer

Parotid gland metastases from malignant tumors are extremely rare. A 61-year-old woman was diagnosed with an early breast cancer with no expression of oestrogen and progesterone receptors. Five years later the patient presented a tumour in parotid gland. After total parotidectomy, microscopic analysis of the gland demonstrated an invasive duct carcinoma (IDC) with positive expression of oestrogen receptor. The patient was treated with chemotherapy followed by complementary local radiotherapy. Diagnosis of a metastasic tumour in parotid gland poses a challenge. In our case an immunohistochemical study of oestrogen receptor was fundamental to establish a diagnosis.

IRS Cancer Connection

Two groups (Dearth et al . and Ma et al .) examined the role of insulin receptor substrate (IRS) in mouse mammary gland tumorigenesis and metastasis. Dearth et al . used transgenic mice forced to overexpress IRS-1 or IRS-2, or an immortalized but nontumorigenic cell line (MCF-10A) also forced to overexpress one of these two proteins. In the MCF-10A cells, overexpression of either protein caused an increase in phosphorylation (and activation) of Akt and an increase in proliferation in response to insulin growth factor-1 (IGF-1). Only the IRS-1-overexpressing cells showed enhanced phosphorylation of extracellular signal-related kinases 1 and 2. Both IRS proteins disrupted acinar formation in three-dimensional Matrigel cultures, and both IRS proteins coimmunoprecipitated with β-catenin. In the transgenic mice, there was no effect on lactational capacity, but both groups of mice formed tumors in the mammary glands. The IRS-2-overexpressing mice had more rapid tumor formation than did the IRS-1-overexpressing mice; however, IRS-2 was overexpressed to a greater extent than was IRS-1. Both groups exhibited lung metastasis. The histology of the tumors was quite diverse, and many contained cells that were highly differentiated, which is similar to phenotypes associated with activation of β-catenin. In the tumors from the IRS-1- or IRS-2-overexpressing mice, β-catenin coimmunoprecipitated with the IRS proteins, and there was increased abundance of cyclin D, which is encoded by a β-catenin target gene. In the overexpressing MCF-10A cells, IGF-1 stimulated the association between IRS-1 or IRS-2 and β-catenin. Ma et al . examined the different functions of IRS-1 and IRS-2 in tumorigenesis and metastasis by generating tumors in IRS-1-deficient mice using polyoma virus middle-T (PyV-MT:: Irs1 −/− ) and comparing these tumors to those formed in wild-type mice (PyV-MT) or in IRS-2-deficient mice (PyV-MT:: Irs2 −/− ). It was previously known that mammary tumors formed in PyV-MT:: Irs2 −/− mice exhibited decreased metastasis. The tumors from the PyV-MT:: Irs1 −/− mice showed increased lung metastasis compared with PyV-MT mice. This effect was intrinsic to the PyV-MT:: Irs1 −/− tumors, because the tumors grew faster and showed increased lung metastasis even when injected into wild-type mice. The PyV-MT:: Irs1 −/− tumors showed elevated microvascular density compared with the PyV-MT tumors and the PyV-MT:: Irs1 −/− tumors, and serum from these mice had increased concentrations of vascular endothelial growth factor A (VEGF-A). The tumors from the PyV-MT:: Irs1 −/− mice also showed increased signaling through the mTOR pathway, which regulates protein production and may explain the increase in VEGF-A production. The tumors from the PyV-MT:: Irs1 −/− mice also showed decreased abundance of apoptotic cells compared with tumors from the PyV-MT mice. IRS-2 abundance and tyrosine phosphorylation were increased in the tumors from the PyV-MT:: Irs1 −/− mice, and there was increased interaction between IRS-2 and the p85 regulatory subunit of phosphinositide 3-kinase, suggesting that in the absence of IRS-1, signaling through IRS-2 is enhanced. Further, these results suggest that IRS-1 may have an inhibitory effect of tumor metastasis, yet promote tumor formation and growth. Metastatic tumors from PyV-MT:: Irs2 −/− or PyV-MT mice had increased serine phosphorylation of IRS-1, which prevents tyrosine phosphorylation and thereby inhibits IRS-1 function. Small interfering RNA (SiRNA) used to decrease IRS-1 in cells from PyV-MT tumors increased IRS-2 abundance in those cells, suggesting that IRS-1 may inhibit IRS-2 signaling, and siRNA of IRS-2 in cells from PyV-MT:: Irs1 −/− decreased the phosphorylation of S6 kinase, a marker for activation of the mTOR pathway. Thus, it appears that IRS-1 and IRS-2 antagonize each other's activity and that inactivation of IRS-1 may contribute to the increased metastatic potential of mammary tumors. R. K. Dearth, X. Cui, H.-J. Kim, I. Kuiatse, N. A. Lawrence, X. Zhang, J. Divisova, O. L. Britton, S. Mohsin, D. C. Allred, D. L. Hadsell, A. V. Lee, Mammary tumorigenesis and metastasis caused by overexpression of insulin receptor substrate 1 (IRS-1) or IRS-2. Mol. Cell. Biol. 26 , 9302-9314 (2006). [Abstract] [Full Text] Z. Ma, S. L. Gibson, M. A. Byrne, J. Zhang, M. F. White, L. M. Shaw, Suppression of insulin receptor substrate 1 (IRS-1) promotes mammary tumor metastasis. Mol. Cell. Biol. 26 , 9338-9351 (2006). [Abstract] [Full Text]

Prognostic factors in patients with stage IV non-small cell lung cancer

Objective: To investigate the prognostic factors for stage IV non-small cell lung cancer (NSCLC) with distant metastasis and establish a reliable model of clinical prognostic index. Methods: From January 1990 to April 2005, 313 primary NSCLC patients with metastasis, who had been treated in Shanghai Chest Hospital, were reviewed. Survival time was estimated according to the Kaplan-Meier method. Cox proportional hazard regression model was used for multivariate analysis. Results: Among the 313 cases of non-small cell lung cancer (NSCLC) at stage IV, there were 218 and 95 patients with metastasis to single and different organs, respectively. The overall median survival time for all 313 cases of NSCLC patients was 10.8 (9.00, 12.30) months and the overall 1-, 2-, 3-, 4-and 5-year survival rate was 45%, 18%, 12%, 4% and 0%. There were 63, 174, 127, 36, 18, 11 and 5 patients with metastasis to brain (20.13%), bone (55.59%), lung (40.58%), liver (11.50%), adrenal gland (5.75%), subcutaneous (3.51%) and others, respectively. The survival time was shortest in subcutaneous metastasis (4.6 months), and liver 7.0 months, brain 8.0 months, adrenal gland 8.6 months, bone 10.6 months, lung 11.8 months. Kaplan-Meier estimation showed that patients anatomic typing, KPS, numbers of organ with metastasis, appetite, liver, adrenal gland and subcutaneous metastasis, body weight loss, smoking, index of smoking, chemotherapy, cycles of chemotherapy were the predictors of survival. Multivariate analysis showed survival statistically significant correlation with anatomic typing, KPS, appetite, liver and subcutaneous metastasis, body weight loss, cycles of chemotherapy. The relative risk (RR) was 1.51, 1.97, 1.55, 1.67, 2.56, and 2.56 respectively. Conclusion: Survival time decreases distinctly in patients who had distant metastasis to more than two different organs (P<0.01). Bone is the commonest organ for distant metastasis in lung cancer. The prognosis is poor when lung cancer appears subcutaneous metastasis and liver metastasis. Independent prognostic factors in patient with stage IV non-small cell lung cancer were liver and subcutaneous metastasis, anatomic typing, KPS, appetite, body weight loss, cycles of chemotherapy.

Tc-99m MDP Uptake by Adrenal Metastases From Nonsmall Cell Carcinoma of the Lung

In a 51-year-old male patient with nonsmall cell lung cancer (NSCLC), masses were detected with ultrasonography and computed tomography in both adrenal glands. The results of fine needle aspiration biopsies from both adrenal glands diagnosed metastases from lung cancer. Whole-body bone scan of the patient revealed metastatic lesions in the left hemipelvis and left femur together with Tc-99m MDP uptake in both adrenal gland metastases.

Laparoscopic anterior adrenalectomy for the treatment of adrenal metastases.

Aim of this study was to evaluate the results in 6 patients undergoing laparoscopic adrenalectomy for the treatment of solitary adrenal gland metastases. One hundred forty-five patients underwent laparoscopic adrenalectomy by transperitoneal anterior approach. In 6 patients the indication was the presence of a solitary adrenal gland metastasis. Primary tumors were the following: truncal melanoma, gastric cancer, renal cancer, lung cancer, and breast cancer. Mean age was 57 years (range 44-70 years). Three patients underwent right adrenalectomy and 3 patients a left adrenalectomy. No conversion to open surgery occurred. No mortality or intraoperative complications were observed. Mean operative time was 103 minutes (range 70-150) for right adrenalectomy and 170 minutes (range 90-280) for left adrenalectomy. No postoperative complications occurred. Mean diameter of the tumor was 3.5 cm (range 2-5 cm). Tumor free margins were obtained in every case. Mean hospital stay was 2 days (range 2-3 days). At follow-up, 2 patients have died of systemic dissemination of the disease, one 15 months and one 24 months after the operation. The remaining 4 patients are alive and disease free at a mean follow-up of 7 months (range 4-11 months). So far, no port site metastases or local recurrence have been observed. In our experience adrenal gland metastasis can be treated safely and effectively by the laparoscopic transperitoneal anterior approach.

Cancer of the Prostate

THE purpose of this paper is to evaluate the results of roentgen-ray and radium treatment for 152 cases of cancer of the prostate in the Radiological Department of the Philadelphia General Hospital. Since nearly every case required admission to the hospital when first seen, the study obviously resolves itself into an analysis of the palliative benefits of radiation for clinically advanced cases. The question is often raised: How much value is high voltage radiation for the late and advanced cases? Is it really worth while? With this object in view it seemed necessary: (a) to associate the relevant clinical data of age, duration of symptoms, diagnosis, extent of involvement, bone and gland metastasis as well as pathologic characters, and (b) to outline and discuss the technical procedures of radiation employed. For the study of the irradiation group, 82 cases were selected because they were known to have received an adequate dose of high voltage roentgen rays as compared with a clinically similar group of ...