1.Management consideration in nonpulmonary visceral metastatic seminoma of testis.
Dong Soo PARK ; Debra M PROW ; Robert J AMATO ; Christopher J LOGOTHETIS
Journal of Korean Medical Science 1999;14(4):431-437
To develop a more appropriate therapeutic strategy for treatment of nonpulmonary visceral metastatic testicular seminoma based on the International Germ Cell Consensus Classification, we reviewed the medical records of patients with nonpulmonary visceral metastatic testicular seminoma who were treated over a 20-year period. Only 15 (2.2%) of the 686 cases of testicular seminoma were nonpulmonary visceral metastatic seminoma. The median age of patients was 38 years (range, 22-53 years). Ten (67%) of the patients had an initial diagnosis of supradiaphragmatic or visceral metastatic disease. In addition to nonpulmonary visceral metastasis, all patients had lymph node metastasis as well, the majority of which involved the retroperitoneal lymph nodes. The median and mean progression-free survival durations after chemotherapy for advanced disease were 19 months and 63.7 months, respectively. Six patients (40%) survived, five relapsed after radiation therapy and four died of chemorefractory disease not dependent on the specific regimen. Although the number of cases reviewed in this study was small, we conclude that the choice of chemotherapeutic regimen among the current treatments for nonpulmonary visceral metastatic seminoma of testis primary does not present a different outcome. Therefore, multimodality therapies using new strategies or new agents are well indicated.
Adult
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Antineoplastic Agents, Combined/administration & dosage*
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Bone Neoplasms/secondary
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Bone Neoplasms/radiotherapy
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Bone Neoplasms/drug therapy
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Combined Modality Therapy
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Human
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Lung Neoplasms/secondary
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Lung Neoplasms/radiotherapy
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Lung Neoplasms/drug therapy
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Lymphatic Metastasis
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Male
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Middle Age
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Retroperitoneal Neoplasms/secondary*
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Retroperitoneal Neoplasms/radiotherapy
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Retroperitoneal Neoplasms/drug therapy*
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Retrospective Studies
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Seminoma/secondary*
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Seminoma/radiotherapy
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Seminoma/drug therapy*
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Testicular Neoplasms/pathology*
2.Progressive Multiple Cystic Changes in Both Lungs in a Patient Treated with Gefitinib for Lung Adenocarcinoma with Multiple Lung Metastases.
Yon Ju RYU ; Eun Mi CHUN ; Soon Nam LEE ; Sung Shin SHIM
Korean Journal of Radiology 2014;15(2):300-304
Gefitinib is regarded as a relatively safe agent for the treatment of an advanced non-small cell lung cancer (NSCLC). Pulmonary toxicity such as interstitial lung disease associated with gefitinib is uncommon with an estimated all time incidence around 1% worldwide. Moreover, a case of gefitinib associated with pulmonary cystic changes has not been reported yet. In this report we present a case of progressive multiple air cystic changes in both lungs in a patient with NSCLC and intrapulmonary metastases who underwent a gefitinib therapy.
Antineoplastic Agents/*adverse effects
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Brain Neoplasms/secondary
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Carcinoma, Non-Small-Cell Lung/*drug therapy/secondary
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Cysts/*chemically induced
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Female
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Humans
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Lung/pathology
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Lung Diseases/*chemically induced
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Lung Diseases, Interstitial
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Lung Neoplasms/*drug therapy
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Middle Aged
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Quinazolines/*adverse effects
3.A Case of Benign Metastasizing Leiomyoma with Multiple Metastasis to the Soft Tissue, Skeletal Muscle, Lung and Breast.
Ji Hoon JO ; Jin Hwa LEE ; Dae Cheol KIM ; Sung Hyun KIM ; Hyuk Chan KWON ; Jae Seok KIM ; Hyo Jin KIM
The Korean Journal of Internal Medicine 2006;21(3):199-201
Benign metastasizing leiomyoma (BML) is composed of well-differentiated smooth muscle cells and dense connective tissue. BML affects middle-aged women who have had previous hysterectomies due to a histologically benign-appearing uterine leiomyoma. We report here on a case of BML from the uterine leiomyoma in a 39-year-old woman that involved the soft tissues, skeletal muscles, lungs and breasts. She underwent a hysterectomy for the uterine leiomyoma, double oophorectomy for hormonal ablation and lung wedge resection to confirm the diagnosis. The microscopic findings of the breast and lung tumor were similar to those of the benign uterine leiomyoma. Therefore, we consider that these lesions were breast and pulmonary metastases of the uterine leiomyoma. We report here on a rare case of benign metastasizing uterine leiomyoma that involved the soft tissue, skeletal muscles, lungs and breasts, and we include a review of the relevant literature.
Uterine Neoplasms/*pathology/surgery
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Tamoxifen/therapeutic use
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Soft Tissue Neoplasms/*secondary
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Muscle, Skeletal/pathology
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Muscle Neoplasms/*secondary
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Lung Neoplasms/*secondary
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Leiomyoma/drug therapy/*pathology
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Hysterectomy
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Humans
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Female
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Breast Neoplasms/*secondary
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Antineoplastic Agents/therapeutic use
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Adult
4.Combination of lapatinib with chlorogenic acid inhibits breast cancer metastasis by suppressing macrophage M2 polarization.
Jie-qiong ZHANG ; Zhang-ting YAO ; Gui-kai LIANG ; Xi CHEN ; Hong-hai WU ; Lu JIN ; Ling DING
Journal of Zhejiang University. Medical sciences 2015;44(5):493-499
OBJECTIVETo determine the effect of the combination of lapatinib with chlorogenic acid on metastasis of breast cancer in mouse model.
METHODSThe classical macrophage M2 polarization model induced by interlukin13in vitro was adopted in the study. Flow cytometric analysis was performed to detect the expression of M2 marker CD206. The transcription of M2-associated genes was measured by RT-PCR. HE staining was used to analyze the metastatic nodes of breast cancer in lungs of MMTV-PyVT mice. Immunostaining analysis was used to detect the expression of related proteins in breast cancer.
RESULTSThe combination of lapatinib and chlorogenic acid inhibited the expression of CD206 induced by IL-13[(42.17%±2.59%) vs (61.15%±7.58%), P<0.05]. The combination more markedly suppressed expression of M2-associated gene Ym1 than lapatinib alone[(0.9±0.1) vs (1.8±0.0), P<0.05]. The combination of lapatinib and chlorogenic acid significantly reduced metastatic nodes in lung[P<0.05], and also significantly decreased the percentage of CD206(+) cells in breast cancer compared to controls[(6.08%±2.60%) vs(29.04%±5.86%), P<0.05].
CONCLUSIONThe combination of lapatinib and chlorogenic acid can effectively inhibit macrophage M2 polarization and metastasis of breast cancer.
Animals ; Chlorogenic Acid ; pharmacology ; Female ; Lung Neoplasms ; drug therapy ; secondary ; Macrophages ; drug effects ; Mammary Neoplasms, Experimental ; drug therapy ; Mice ; Neoplasm Metastasis ; drug therapy ; Quinazolines ; pharmacology
5.Micropapillary Lung Cancer with Breast Metastasis Simulating Primary Breast Cancer due to Architectural Distortion on Images.
Kyungran KO ; Jae Yoon RO ; Eun Kyung HONG ; Seeyeon LEE
Korean Journal of Radiology 2012;13(2):249-253
A 47-year-old Korean woman with right middle lobe lung adenocarcinoma, malignant pleural effusion, and multiple lymph node and bone metastases, after three months of lung cancer diagnosis, presented with a palpable right breast mass. Images of the right breast demonstrated architectural distortion that strongly suggested primary breast cancer. Breast biopsy revealed metastatic lung cancer with a negative result for estrogen receptor (ER), progesterone receptor (PR) and mammaglobin, and a positive result for thyroid transcription factor-1 (TTF-1). We present a case of breast metastasis from a case of lung cancer with an extensive micropapillary component, which was initially misinterpreted as a primary breast cancer due to unusual image findings with architectural distortion.
Adenocarcinoma/drug therapy/*secondary
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Antineoplastic Combined Chemotherapy Protocols/therapeutic use
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Biopsy, Needle
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Bone Neoplasms/secondary
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Breast Neoplasms/drug therapy/*secondary
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Diagnosis, Differential
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Female
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Humans
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Lung Neoplasms/*pathology
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Lymphatic Metastasis
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Mammography
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Middle Aged
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Neoplasm Staging
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Tomography, X-Ray Computed
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Ultrasonography, Mammary
6.Effects of chemotherapy on circulating angiogenic factor levels in patients with breast cancer.
Jin-hai TANG ; Jian-hua ZHAO ; Jian-ping GONG ; Jian-wei QIN ; Li-qun PAN ; Zhi-yin XU
Chinese Journal of Oncology 2007;29(3):210-214
OBJECTIVETo study the changes in circulating VEGF and endostatin (ES) levels during chemotherapy for patients with breast cancer, and their correlation with efficacy of chemotherapy.
METHODS40 breast cancer patients with metastases were included in this study. They received TAC/TEC, CAF/CEF, NP, CAP, CMF, TFP, TA or TC regime chemotherapy, respectively. Totally 120 serum samples were collected from the patients at three time points: before chemotherapy, the end of 1 and 5-6 chemotherapy cycles, and analyzed for VEGF and ES levels using ELISA. Tumor agiogenesis activity was evaluated by serum soluble vascular cell adhesion molecule (VCAM - 1) measured by ELISA as a surrogate marker.
RESULTS(1) Before chemotherapy, the median level of VEGF in patients with breast cancer was 496.6 pg/ml, 4.7 times higher than that of healthy controls (P <0.001). The median level of ES was 95.5 ng/ml, 18.3% lower than that of healthy controls (P = 0.183). VCAM-1 was 1077.1 ng/ml and higher than that of controls (P <0.001). The serum VEGF levels correlated with VCAM-1 levels, tumor staging and metastatic sites (P <0.05). (2) At the end of 1 cycle of chemotherapy, the serum VEGF level (median 524.8 pg/ml) was higher than the pretreatment values (P = 0.047), whereas the levels of ES and VCAM-1 were not significantly altered (110.5 ng/ml, P = 0.055; and 975.6 ng/ml, P = 0.27). (3) At the end of 5-6 cycles, the changes in VEGF correlated with the response to chemotherapy. Serum VEGF levels in 27 patients with chemotherapy-responsive and stable disease showed a significant decrease (median 287.4 pg/ml) , but not observed in 13 patients with progressive disease. VCAM-1 also showed a treatment-related change like VEGF. However, chemotherapy might only have a minor effect on ES, because there was no significant difference in the ES levels among 5-6 cycle patients, 1 cycle patients and healthy controls, and neither between therapy-responsive patients.
CONCLUSIONIntensive chemotherapy for breast cancer results in a significant decrease of serum VEGF level, which might be an indicator of the controlled disease status, and following the treatment-induced response or stabilization, the tumor angiogenesis seems to change into an anti-angiogenesis direction.
Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Bone Neoplasms ; blood ; drug therapy ; secondary ; Breast Neoplasms ; blood ; drug therapy ; pathology ; Carcinoma, Ductal, Breast ; blood ; drug therapy ; secondary ; Endostatins ; blood ; Female ; Humans ; Liver Neoplasms ; blood ; drug therapy ; secondary ; Lung Neoplasms ; blood ; drug therapy ; secondary ; Lymphatic Metastasis ; Middle Aged ; Neoplasm Staging ; Remission Induction ; Vascular Cell Adhesion Molecule-1 ; blood ; Vascular Endothelial Growth Factor A ; blood
8.A clinical study of reasonable doses of docetaxel salvage therapy for patients with metastatic breast cancer.
Shi-kai WU ; Yan MA ; Xiang-ying MENG ; Bing SUN ; Tao WANG ; Shao-hua ZHANG ; Ze-fei JIANG ; San-tai SONG
Chinese Journal of Oncology 2012;34(10):764-769
OBJECTIVETo evaluate the correlation of clinical effects and reasonable doses of docetaxel salvage therapy for patients with metastatic breast cancer.
METHODSWe reviewed retrospectively the clinical records of patients with metastatic breast cancer treated with docetaxel and statistically analyzed the correlation between clinical effects and reasonable doses of docetaxel.
RESULTSThe objective response rate and clinical benefit rate of docetaxol in patients with metastatic breast cancer were 27.0% and 35.0%, respectively, and the median progression free survival (PFS) was 5.0 (3.8 - 6.3) months. In the analysis at a single dose level, the clinical benefit rate and PFS of the ≥ 90.0 mg/m(2) docetaxel group were superior to that of the < 90.0 mg/m(2) group (P = 0.008, P = 0.045). Multi-dose level group stratified analysis showed that the docetaxel < 75.0 mg/m(2) group was better than the 75.0 - 84.9 mg/m(2) PFS group (P = 0.018), and the ≥ 95.0 mg/m(2) group was better than the 75.0 - 84.9 mg/m(2) group (P = 0.048). In patients who received >third line treatment or previously received paclitaxel adjuvant therapy, the PFS of the ≥ 94.9 mg/m(2) docetaxel group was 6.0 months, better than the 3.0 months of the 75.0 ∼ 84.9 mg/m(2) group (P = 0.031; P = 0.021).
CONCLUSIONThere is a clear correlation between clinical effects and reasonable doses of docetaxel salvage therapy in patients with metastatic breast cancer.
Adult ; Aged ; Antineoplastic Agents ; administration & dosage ; therapeutic use ; Bone Neoplasms ; drug therapy ; secondary ; Breast Neoplasms ; drug therapy ; pathology ; Disease-Free Survival ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Female ; Follow-Up Studies ; Humans ; Liver Neoplasms ; drug therapy ; secondary ; Lung Neoplasms ; drug therapy ; secondary ; Middle Aged ; Remission Induction ; Retrospective Studies ; Salvage Therapy ; Taxoids ; administration & dosage ; therapeutic use ; Young Adult
9.Single-agent Xeloda in the treatment of recurrent and metastatic breast cancer.
Tao WANG ; Ze-fei JIANG ; San-tai SONG ; Shao-hua ZHANG ; Ge SHEN ; Jing-xin YU
Chinese Journal of Oncology 2004;26(6):379-381
OBJECTIVETo evaluate the efficacy and adverse reactions of Xeloda in the treatment of recurrent and metastatic breast cancer.
METHODSThis clinical study was designed to treat 69 patients with recurrent and metastatic breast cancer with Xeloda, 2500 mg/m(2)/d, twice daily for 2 weeks followed by a 1-week rest period, repeated every 3 weeks.
RESULTSSixty-nine patients received Xeloda for more than 1 cycle. The overall response rate (CR + PR) was 16.0%, clinical benefit rate (CR + PR + SD > or = 24 months) was 27.5%, disease control rate (CR + PR + SD) was 75.4%. The median time to failure (TTF) was 3 months (range: 0.7 - 11 months). The median time to progression (TTP) was 2 months (range: 0.7 - 11 months). The median duration of response (CR + PR) was 6 months (range: 4 - 11 months). The most common treatment-related adverse events were hand-foot syndrome (HFS) that occurred in 60.8% (42/69) patients mostly as grade I-II. Fifty-five percent (22/40) of patients who had received high dose preventive Vit B6 developed HFS without grade III; while 69% (20/29) of patients who had not received such treatment did develop HFS including 2 patients with grade III. However, there was not significant difference between the two groups.
CONCLUSIONXeloda is an effective and well tolerated treatment in patients with recurrent and metastatic breast cancer. The symptoms of HFS may be relieved by high dose Vit B6 as prevention.
Adult ; Aged ; Antimetabolites, Antineoplastic ; therapeutic use ; Bone Neoplasms ; drug therapy ; secondary ; Breast Neoplasms ; drug therapy ; pathology ; Capecitabine ; Deoxycytidine ; analogs & derivatives ; therapeutic use ; Drug Administration Schedule ; Female ; Fluorouracil ; analogs & derivatives ; Humans ; Liver Neoplasms ; drug therapy ; secondary ; Lung Neoplasms ; drug therapy ; secondary ; Lymphatic Metastasis ; Middle Aged ; Neoplasm Recurrence, Local ; drug therapy
10.Antimetastatic effects of genistein on salivary adenoid cystic carcinoma in vivo.
Chinese Journal of Stomatology 2004;39(5):373-375
OBJECTIVETo study the antimetastatic effects of genistein on salivary adenoid cystic carcinoma (ACC-M) in vivo.
METHODSACC-M cells were exposed to genistein for 3 days. The treated cells and control cells were then injected into the tail vein of 20 nude mice, which were randomized into 2 groups. The mice were sacrificed at the sixth week after implantation. The lung metastasis rates and the number of metastases were detected. Apoptosis index (AI), the expression of VEGF and MMP-9 of the lung metastases were also observed.
RESULTSCompared to the control groups, the number of metastases was significantly reduced in genistein treated group (P < 0.05). The AI of ACC-M cells was higher in the treated group than in the control group (P < 0.05). The level of VEGF and MMP-9 expression were decreased in the treated groups (P < 0.05).
CONCLUSIONSGenistein has a moderate inhibitory effect on metastasis of ACC. Inducing apoptosis, inhibiting the expression of VEGF and MMP-9 are the mechanisms of antimetastatic effects of genistein on ACC-M in nude mice.
Animals ; Antineoplastic Agents ; administration & dosage ; Carcinoma, Adenoid Cystic ; drug therapy ; secondary ; Female ; Genistein ; administration & dosage ; Lung Neoplasms ; drug therapy ; secondary ; Mice ; Mice, Nude ; Random Allocation ; Salivary Gland Neoplasms ; drug therapy ; pathology