Japanese Journal of Clinical Oncology

doi: 10.1093/oxfordjournals.jjco.a039684pmid: N/A

Abstract The use of lymphokine activated killer (LAK) cells for adoptive transfer therapy has been reported from number of clinical trials. To our knowledge, however, there has been no report concerning the cell cycle progression of LAK cells. Thus, for the present study we have attempted to examine the LAK cell cycle either before or after transfer. In vitro and in vivo analyses of LAK cells labeled with bromodeoxyuridine (BrdU) were carried out using two-parameter flow cytometries of their nuclear staining using fluorescein isothiocyanate(FITC)- conjugated anti-BrdU antibody and propidium iodide (PI). The in vitro growth of BrdU-positive cells showed the cells to divide once in the S phase, continue to the G2-M phase and return to the G0-G1 phase with a similar pattern after 48 or 72 h culture. They formed a definite subpopulation and were of phenotypes, thy-1.2 (+), Lyt-1.1 ( − ), Lyt-2.1 (+), L3T4 ( − ) and AGM1 (+). The percentage of BrdU-positive cells decreased significantly (P< 0.05) when treated with complement plus anti-thy-1.2, anti-Lyt-2.1 or anti-AGM1 anti- bodies, demonstrating BrdU-labeled LAK cells to have the same phenotype as control LAK cells. As in vitro, the in vito cell cycle of LAK cells 48 and 72 h after transfer had a similar pattern, and the LAK cells also continued on to the S phase after the first division. The in vivo growth of the LAK cells treated with interleukin-2 (IL-2) was promoted 24 and 48 h after transfer. In conclusion, the present study showed LAK cells to be capable of dividing following transfer and to keep their own phenotypic characteristics; also, that treatment with IL-2 may promote their division. Adoptive transfer therapy seems to be a viable therapeutic method. Cell cycle, Lymphokine activated killer cell, Interleukin-2 This content is only available as a PDF. © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039685pmid: N/A

Abstract The localization of acidic fibroblast growth factor (aFGF) and basic fibroblast growth factor (bFGF) was investigated immunohistochemically in human benign and malignant thyroid lesions. Immunostaining for aFGF and bFGF displayed diffuse or granular deposits of the reaction products in the cytoplasm of neoplastic cells, especially in the marginal region of follicular adenoma, follicular carcinoma and papillary carcinoma. All lesions except for diffuse hyperplasia, which was completely negative in immunostaining for all antibodies, showed an increased immunostaining for bFGF (Ab-1) over that of aFGF and bFGF (Ab-2). Basement membranes of follicular and papillary structure and the fibroblasts located in the stromal tissues were free from immunostaining for all antibodies. The ratio of positive immunostaining for all antibodies was highest in papillary carcinoma, with an incidence of more than 80.0%, followed, in descending order, by widely invasive follicular carcinoma, minimally invasive follicular carcinoma, follicular adenoma and normal thyroid, in which some follicular cells exhibited weak reaction products. aFGF with a molecular weight of 18 kDa was identified in papillary carcinoma of the thyroid. From these data, we concluded that aFGF is synthesized in the neoplastic follicular cells of the thyroid, and aFGF and bFGF may have important roles in the neoplastic proliferation of follicular cells. Fibroblast growth factor, Human thyroid lesions, Western blot analysis, Immunohistochemistry This content is only available as a PDF. © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039686pmid: N/A

Abstract The introduction of c-erbB-2 protein to clinical medicine as a prognostic indicator and tumor marker is desired. The authors determined the concentration of c-erbB-2 protein in 81 breast cancer tissues by enzyme immunoassay. The concentration of c-erbB-2 protein in breast cancer tissues showed a broad spectrum. A significant correlation was observed between tissue c-erbB-2 protein concentration and estrogen receptor status or immunohistochemical determination. In patients with distant metastases, there was a close association between c-erbB-2 protein concentration in the primary tumor and serum c-erbB-2 protein level. Cases with a high tumor concentration of c-erbB-2 protein (>1000U/mg total protein; 18.5% of cases) had a poor prognosis. From the above, we concluded the measurement of tissue c-erbB-2 protein by enzyme immunoassay to be clinically useful in breast cancer. Breast cancer, c-erbB-2 protein, Enzyme immunoassay This content is only available as a PDF. © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039687pmid: N/A

Abstract Formalin-fixed, paraffin-embedded sections from 92 breast cancers (invasive ductal carcinomas) were immunostained with a monoclonal antibody against proliferating cell nuclear antigen (PCNA). The labeling index of PCNA ranged widely from 2 to 76 (mean 24.8)%. The labeling index was classified into three groups: low (25%), intermediate (25-50%), high proliferation (>50%). Younger patients seemed to have a higher labeling index than older ones. The labeling index for tumors ≤2 cm was lower than that of tumors larger than 2 cm. The labeling index in patients with high estrogen receptor (ER) levels (>100 fmol/mg cytosol protein) was significantly lower than that in patients with low ER levels (< 10 fmol/mg cytosol protein). In relation to histological type, the labeling index of scirrhous carcinoma was significantly lower than that of papillotubular carcinoma or solid-tubular carcinoma. The high proliferating group had a significantly worse overall survival rate than the low proliferating group. Labeling index was shown to be a possible prognostic indicator. Breast cancer, Proliferating cell nuclear antigen, Immunohistochemistry, Prognosis This content is only available as a PDF. © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039688pmid: N/A

Abstract We compared tumor sizes determined by computed tomography (CT) with those of the resected specimens in 26 patients with pancreatic cancer in order to clarify whether or not the size of a pancreatic tumor can be accurately determined by CT. From the precontrast, postcontrast and arterial dominant phases of dynamic CT, the arterial dominant phase was found to yield the highest correlation between CT measured tumor size and that of the resected specimens (P<0.01). The correlation coefficient was, however, not high (r=0.67). CT alone may therefore be insufficient to determine tumor size in pancreatic cancer accurately. Tumor size, Computed tomography, Pancreatic cancer This content is only available as a PDF. © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039689pmid: N/A

Abstract We reviewed 20 children with salivary gland neoplasms treated at the National Cancer Center Hospital between 1964 and 1990. Retrospective analyses of pathological features and the clinical courses of these cases constituted the bases of the present study. The age of onset was late childhood in 19 cases, ranging from 9 to 20 years, but one patient was 1 year old. Approximately half (55%) the neoplasms were malignant. Histologically, all the benign neoplasms were pleomorphic adenomas (nine cases) and the most common malignant neoplasm was mucoepidermoid carcinoma (six cases, 55%), followed by adenocarcinoma (three cases, 27%), adenoid cystic carcinoma (one case, 9%) and malignant mixed tumor (one case, 9%). Recurrences of pleomorphic adenomas occurred only in the three patients initially treated with enucleation; meanwhile, five patients treated with superficial parotidectomy, and one with submandibular glandectomy, had no recurrence. Recurrences of malignant tumors occurred in all six patients initially treated with enucleation only and in one with superficial parotidectomy but not in two patients treated with total parotidectomy. In seven patients treated with prophylactic neck dissection, no metastasis was identified pathologically. The results support no enucleation of the tumor being applied at the first operation for curing both benign and malignant salivary gland tumors. The indication for radical neck dissection appears to be limited. Salivary gland neoplasm, Children, Plemorphic adenoma This content is only available as a PDF. © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039690pmid: N/A

Abstract Head and neck cancer is mostly curable in the early stages by either surgery or radiotherapy alone, but the control rate for advanced stages is low, even with combined surgery and postoperative radiotherapy. From September, 1990, to January, 1992, 35 patients with locoregionally advanced head and neck cancers were entered in a prospective study of concomitant chemoradiotherapy. Thirty-three completed the treatment. There were 29 males and four females with a median age of 53 years. All except one patient were in stage IV. Radiotherapy was delivered using a telecobalt unit and by conventional fractionation (1.8 Gy/fraction, 5 fractions/wk). Chemotherapy with cisplatin (10 mg/m2/day, daily, days 1-5) and 5-FU (500 mg/m2/day continuously infused for five days) was given concurrently during the first and fifth weeks of radiation. Twenty-four among 31 eligible patients achieved complete response (77.4%) and the other seven (22.6%) partial response, resulting in a 100% response rate. The toxicities experienced were increased compared with those caused by radiotherapy alone. The most common side effects were gastrointestinal and hematologic toxicities but the whole treatment was well tolerated. The two-year actuarial survival rate is 45%. We found the primary origin and overall treatment time to affect survival significantly. The survival rate for tumors arising from the nasopharynx or paranasal sinus is better than for those arising from other regions of the head and neck. The shorter treatment times (within eight weeks) had a better survival rate. Our preliminary experience suggests that concomitant chemoradiotherapy is both feasible and effective for head and neck cancer. The optimal scheduling and dosage of concomitant chemoradiotherapy should be further researched. Head and neck cancer, Concomitant chemotherapy, Radiotherapy This content is only available as a PDF. © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039678pmid: N/A

Abstract We have experienced eight patients with advanced bronchogenic carcinomas who underwent resectional surgery after receiving preoperative adjuvant chemotherapy and radiotherapy during the period March, 1990, to February, 1992. Four patients were in stage IDA and four in stage 1MB, of which six had epidermoid carcinomas and two small cell carcinomas. All patients were male with ages ranging from 48 to 73 (mean 56.7) years. The induction chemotherapy for six patients consisted of cisplatin and VP-16 (Etoposide) only, and two patients were given fluorouracil\cyclophosphamide and cyclophosphamide\adriamycin\cisplatin in addition to cisplati\VP-16, respectively. All patients also received four to six weeks of radiotherapy following chemotherapy and were re-evaluated for the possibility of surgery after four weeks of observation. All patients underwent pneumonectomies. Postoperative histological staging revealed complete responses in two patients, partial responses in three and no response in three. Patients were followed-up for seven to 33 (mean 21.5) months after the diagnosis of lung cancer. Six patients died 1, 2, 3, 10, 14 and 26 months postoperatively and two patients are alive, revealing no evidence of tumor recurrence 24 months postoperatively. Induction therapy may induce a better resectability by the conversion of the lung cancer to a lower clinical stage by the time of surgery. Bronchogenic carcinoma, Induction chemotherapy and radiation therapy, Completeresponse, Histological staging This content is only available as a PDF. Author notes *Presented, in part, at the 12th Asian Pacific Congress of Diseases of the Chest, October 7, 1992, Seoul, Korea © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039679pmid: N/A

Abstract A 75-year-old woman presented with anemia, lymphadenopathy, hepatomegaly and lingual tumor, but no constitutional symptoms. The laboratory data showed pancytopenia and polyclonal hypergammaglobulinemia. A bone marrow aspirate represented an apparent myelodysplastic syndrome (MDS) feature, specifically, refractory anemia with excess of blasts. A lymph-node biopsy revealed the disappearance of normal architecture, small arborizing blood vessels, large lymphoid cells with prominent cytoplasm (so-called pale cells) and a clonal proliferation of T-lymphocytes. The patient was diagnosed as having MDS associatd with immunoblastic lymphadenopathy (IBL)-like T-cell lymphoma. She was subsequently treated with cyclophosphamide, adriamycin, vincristine and prednisolone for lymphoma which successfully induced a remission of not only the T-cell lymphoma but also the MDS. The case suggested that MDS might be a paraneoplastic complication of IBL-like T-cell lymphoma. Myelodysplastic syndrome, Immunoblastic lymphadenopathy-like, T-cell lymphoma, Paraneoplastic complication, Chemotherapy This content is only available as a PDF. Author notes Present address and address for reprints requests: Toshihisa Anzai, Department of Internal Medicine, School of Medicine, Keio Univeristy, 35 Shinanomachi, Shinjuku-ku, Tokyo 160 © Oxford University Press

doi: 10.1093/oxfordjournals.jjco.a039680pmid: N/A

Abstract A case of hepatocellular carcinoma (HCC), which developed during chemotherapy for chronic myelogenous leukemia (CML), is presented. A 55-year-old Japanese man, who had received an alkylating agent for 16 years, was diagnosed as having HCC with clinically evident splenic metastases. The patient died of the HCC rupture three months after diagnosis. The autopsy revealed the HCC to have developed from the non-cirrhotic liver. In the present case, DNA damage due to the long-term chemotherapy with the alkylating agent for CML may have endowed the HCC induced by post-transfusion hepatitis and alcohol abuse with an aggressive proliferative potential. This is the first report on HCC in association with CML. Hepatocellular carcinoma, Splenic metastasis, Chronic myelogenous leukemia This content is only available as a PDF. Author notes Present address and address for reprint requests: Masaru Katoh, Genetics Division, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104 © Oxford University Press