摘要:

AbstractNineteen patients with colorectal adencarcinoma, three with cholangiocarcinoma, two with hepatocellular carcinoma, and one with carcinoid were treated with hepatic artery infusion chemotherapy. An implantable pump system was used to deliver floxuridine (FUdR), starting at 400 mg for 2 weeks with 2 weeks of rest. Eleven of 15 (73%) measurable patients with colorectal carcinoma responded. Of 6 complete responses, 4 were documented by laparotomy, including 1 with choleangiocarcinoma. Toxicity included dyspepsia and elevated liver function tests in all patients, gastric ulcer in 2, cholecystitis in 2, and sclerosing cholangitis in 3. Overall median survival for the colon cancer patients has not been reached at 16 months. Regional disease was controlled in the majority of patients treated with this regimen with acceptable toxicity and good quality of life.

ISSN:0735-7907    

DOI:10.3109/07357908909038262

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractThe proliferative and plaque-forming cell (PFC) responses of unseparated mononuclear cells (MNC) and B- and T-cell-enriched populations of cells were analyzed in 15 patients with lung cancer to determine the mechanisms involved in the functional abnormality of their B cells. The PFC responses of the MNC of the patient group were significantly lower than those of normal controls. In addition, the enriched B cells of several patients showed a further decrease in their PFC responses after coculture with autologous Tcells compared with their respective MNC responses. The proliferative response against phytohemagglutinin (PHA) was also lower in many of the patients after similar cocultures. Cocultures of patients' B cells with T cells from normal controls significantly enhanced the PFC responses in 7 patients. In most of the normal controls, B lymphocytes showed a significant decrease in their PFC responses after coculture with the patients' T cells. Although the percentages of total T cells, T-helper, and B cells were within the normal range, the number of suppressor T cells was significantly higher in the patient group. These results indicate that a combination of insufficient T-cell help, excessive suppression by both T and non-T cells, and a possible intrinsic B-cell abnormality are responsible for the B-cell functional deficiency observed in patients with lung cancer.

ISSN:0735-7907    

DOI:10.3109/07357908909038263

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractMurine plasmacytoma MOPC 104E-KI81 is a tissue culture cell line of MOPC 104E derived from BALB/c mice. MOPC 104E-KI81 implanted subcutaneously in syngeneic normal mice regresses spontaneously after an initial growth of about 10 mm. Mice that regressed tumors or mice immunized intraperitoneally with mitomycin C-treated MOPC 104E-KI81 myeloma could reject subsequent challenge of viable KI81 myeloma cells. In contrast to euthymic mice, T-cell-deficient athymic nude mice developed subcutaneous tumors after challenge and died from progressive tumor growth, suggesting the critical role of T cells in tumor regression. In vitro induction of cytotoxic cells was used to define the immunologic mechanism by which the host can suppress tumor growth. Spleen cells from immune mice did not show cytolytic activity in51Cr release cytotoxicity assay, but showed inhibitory action of tumor proliferation in vitro at an effector cell to target cell ratio of 500:1 in a [3H]thymidine incorporation assay. To determine if cytotoxicity could be induced against MOPC 104E-KI81 cells, in vitro sensitizing cultures were studied. We have demonstrated that normal BALB/c spleen cells became cytotoxic against MOPC 104E-KI81 cells after 5 days cultivation with mitomycin C-treated stimulator cells at an optimal responder to stimulator cell ratio of 5:1. Treatment of anti-Thy-1.2 serum plus complement abolished cytotoxic activity of effector cells. Cytotoxic cells lysed not only MOPC 104E-KI81 cells used for stimulation but also H-2kosteosarcoma cells. It was concluded that Thy-1.2-positive cytotoxic cells with nonspecific anomalous reactivity could be induced in murine plasmacytoma-stimulating cultures.

ISSN:0735-7907    

DOI:10.3109/07357908909038264

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractRequirements for the induction of anomalous killer (AK) cells to syngeneic MOPC 104E-KI81 plasmacytoma, and their pattern of reaction were investigated. The AK cells are Thy-1.2 positive and were induced by cocultivation of normal BALB/c spleen cells for 5 days in vitro with mitomycin C-treated MOPC 104E-KI81 cells in RPMI 1640 medium supplemented with fetal calf serum and 2-mercaptoethanol. The pattern of reactivity was investigated by direct cytotoxicity and indirect cold target inhibition assays using a panel of target cells. The results from cold target inhibition show that anomalous killer cells react with various tumor targets in the same preferential order as the results shown in direct cytotoxicity assay, and indicates that the AK cell population may be detecting the same determinants expressed to different degrees on panels of target cells. Kinetic study showed that peak cytotoxic responses were observed on day 5 and day 4, for primary and secondary sensitizing cultures, respectively. Cytotoxicity was not generated when nude mouse spleen cells were used as responder cells, suggesting the essential role of T cells in the induction. Nylon wool-column-purified splenic T cells from mice primed in vivo with intraperitoneal injection of MMC-treated stimulator cells, but not from normal mice, were able to generate AK cells in vitro. These results indicate that generation of AK cells with NK-cell-like reactivity needs inductive factors provided by the immune reaction between sensitized T cells and stimulatory MOPC 104E-KI81 cells.

ISSN:0735-7907    

DOI:10.3109/07357908909038265

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractDespite a steady decline in incidence over the past five decades in this country, gastric carcinoma continues to represent a major health problem. From the turn of the century through the 1930s, gastric cancer was the leading cause of death in the United States (1). Despite the subsequent decline, the American Cancer Society estimated that approximately 25,000 new diagnoses of gastric cancer would be made in 1988, and that deaths due to this malignancy would exceed 14,400 in the same year. At present, it is the eighth most common cause of cancer death in this country.

ISSN:0735-7907    

DOI:10.3109/07357908909038266

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractSince the development of the first polyclonal antiserum to human milk fat globule (HMFG) membranes (1), this immunogen has been used by numerous workers to produce polyclonal and monoclonal antibodies. These reagents have been extremely useful in identifying markers of breast epithelial differentiation and have had a number of clinical applications. In addition, monoclonal antibodies to HMFG and to many tumour-associated antigens have brought into focus a group of highly immunogenic glycoproteins which have the characteristics of mucins and are expressed by many carcinomas. In this review we will discuss mainly work which has been done with the human milk fat globule, but it should be borne in mind that the same membranes and their components have been extensively studied in rodents and in the cow.

ISSN:0735-7907    

DOI:10.3109/07357908909038267

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractChromosome analyses in leukemias and cancers have yielded a body of cytogenetic information which has led to the hypothesis that specific (primary) chromosomal abnormalities exist in specific types of leukemia and cancer, findings of value in the diagnosis, prognosis, and classification of each condition (1-6). In hematopoietic neoplasia such nonrandom chromosome abnormalities are often and consistently associated with a particular disease process, making it possible to subdivide the acute leukemias and myelodysplastic syndromes into distinct categories. Furthermore, the primary cytogenetic change may serve as an independent variable in the prognosis, apparently unrelated as to how these diseases are classified according to the criteria of the French-American-British (FAB) Cooperative Group (7).

ISSN:0735-7907    

DOI:10.3109/07357908909038268

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractThe assumption that family relationships play an important role in the care and well-being of the cancer patient may be overlooked simply because it is so universal. Patients live in families, become sick in families, and receive medical care in families. Indeed, as Griffin (1) has noted, almost all medical treatment eventually becomes the obligation of family members:

ISSN:0735-7907    

DOI:10.3109/07357908909038269

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractChronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from neoplastic transformation at the level of the pluripotent hematopoietic stem cell (1). The hallmark of CML is a shortened chromosome 22, termed the Philadelphia (Ph) chromosome, which results from a reciprocal translocation between chromosomes 9 and 22—t(9;22)(q34;q11) (2,3). Ph-positive CML is characterized by a multistep evolutionary course. The disease inexorably progresses from a benign or chronic phase lasting an average of 3.5 years to a terminal blast transformation phase (4). The invariably fatal outcome of CML cannot be altered by chemother-apeutic agents which control the proliferative thrust of the benign phase but do not affect the Ph chromosome. Although ablative chemoradiotherapy followed by allogeneic bone marrow transplantation can be curative, this option is only available to young patients with histocom-patible siblings. Therefore, exploration of other therapeutic approaches is warranted.

ISSN:0735-7907    

DOI:10.3109/07357908909038270

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor

摘要:

AbstractUntil the publication of a report by Wagner et al. in 1960 (1) describing 33 cases of diffuse pleural mesothelioma in South Africa, this tumor was considered a clinical rarity. Since then, the relevant medical and epidemiological literature has grown substantially, with recent reports providing evidence that the incidence of this tumor has been increasing steadily. This increase has been particularly striking among asbestos-exposed occupational cohorts.Several issues have complicated epidemiological studies of diffuse pleural mesothelioma as well as hindered the recognition of malignant mesothelioma as a distinct pathological entity. Among these are the rare occurrence of this malignancy in the early part of this century; the existence of two forms of the tumor, namely the localized and benign versus the diffuse and malignant; and the contention that apparently primary tumors of the mesothelium may actually be metastases from a primary tumor located elsewhere in the body (2). Over the last 40 years its increased occurrence and the implication of asbestos as an etiologic factor have resulted in the standardization of diagnostic criteria and acceptance of mesothelioma as a distinct neoplasm (3).

ISSN:0735-7907    

DOI:10.3109/07357908909038271

出版商:Taylor&Francis    

年代:1989

数据来源: Taylor