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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The recent 5-year survival rate of patients with lung cancer who underwent resection is significantly higher than that in the previous decade. The main reason for the improved survival rate seems to be due to more accurate staging, however, we cannot detect micrometastases so that distant relapses in many patients occur after operation. In order to control micrometastases, various kinds of surgical adjuvant therapy have been studied. In an attempt to improve resectability rate and survival in patients with locally advanced disease of non-small cell lung cancer, we initiated a pilot study of neoadjuvant (preoperative) therapy. Most of the 31 patients who were entered into the study clinically showed enlarged mediastinal lymph nodes, with or without direct invasion of the primary tumors to mediastinal organs. The response rate of the treatment was 64.5%. Complete resection of the tumor was performed in 14 of 31 (45%) patients and exploratory thoracotomy was done in one patient. Postoperative complications occurred in 6 of those 15 patients who underwent thoracotomy. Three patients suffered from severe complications such as empyema, pulmonary edema or respiratory failure, but recovered eventually. At present, of 15 patients who underwent operation, 9 are alive and free from disease, 2 are alive with relapse and 4 died of relapses. The median survival time was 11.5 and 19 months in non-resected cases and all cases, respectively. Although we cannot draw a conclusion because of the short observation time, we consider that neoadjuvant therapy is worthy of studying.
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PMID:[Surgical adjuvant therapy, especially neoadjuvant therapy of lung cancer]. 216 42

Receptors for granulocyte-macrophage colony-stimulating factor (GM-CSF) were identified on 9 of 35 (26%) human nonhematopoietic tumor cell lines including non-small cell lung cancer, stomach cancer, colon cancer, and osteosarcoma cells. GM-CSF receptors distributed on these human tumor cells were low affinity types with an equilibrium dissociation constant of 1.5-10.0 nM. Cross-linking studies revealed that the molecular weights of the low affinity GM-CSF receptors were 65-85 kilodaltons. The high affinity receptors identified on hematopoietic cells were not detected on human nonhematopoietic tumor cells which we studied, and we could detect no effects of GM-CSF on cell growth of these tumor cells.
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PMID:Frequent expression of receptors for granulocyte-macrophage colony-stimulating factor on human nonhematopoietic tumor cell lines. 216 48

Ploidy and growth fraction were analyzed by means of a computer-assisted image processor in surgically resected non-small cell lung cancer (NSCLC). This study was done in order (a) to evaluate the distribution of anti-Ki-67 immunostaining and (b) to correlate this distribution to ploidy status and pTNM stage of NSCLC. Thirty-two patients underwent a surgical resection for primary NSCLC following complete staging. Indirect immunoperoxidase reactions of monoclonal antibody Ki-67 were done on frozen tissue sections. Integrated optical density and index of stained nuclear surface were calculated by means of a computer-assisted image processor in 120 fields of each preparation in order to quantify the Ki-67 immunostaining. DNA content was determined by means of cytometry of Feulgen-stained cytological prints. The ploidy status was defined for each tumor by DNA index, percentage of hypodiploid cells, and type of DNA content histogram (near diploid, hyperdiploid, hypodiploid, and multiploid). Reproducibility of immunostaining quantitative analysis was demonstrated by iterative measurements of the same slide. Intratumoral heterogeneity of Ki-67 immunostaining induced integrated optical density variation assessed on six nonconsecutive tissue sections from at least two regions of the same tumor. This intratumoral variability was 15 times lower than integrated optical density variability between tumors. The Ki-67 immunostaining varied significantly according to the DNA content histogram type (P less than 0.05, Kruskal-Wallis test); most of the specimens with high Ki-67 immunostaining were multiploid or hypodiploid. Moreover, Ki-67 immunostaining correlated to the percentage of hypodiploid cells. Ki-67 immunostaining and ploidy status did not vary significantly according to the tumor-nodes-metastasis stage. We conclude that (a) quantitative analysis of Ki-67 immunostaining is a reliable evaluation of growth fraction in NSCLC if a large number of fields are analyzed to take into account intratumoral variability, (b) hypodiploidy and multiploidy are frequent abnormalities of DNA content, (c) Ki-67 immunostaining is significantly higher in hypodiploid and multiploid tumors. Thus, determination of growth fraction and ploidy in surgically resected NSCLC specimens may be considered as complementary prognostic parameters independent of the stage of the disease.
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PMID:In situ evaluation of growth fraction determined by monoclonal antibody Ki-67 and ploidy in surgically resected non-small cell lung cancers. 216 48

The p53 gene initially was thought to be an oncogene, but recent evidence suggests that wild-type p53 can function as a tumor suppressor gene in lung, colon, and breast cancer as well as less common malignancies. This study reports the first identification of intronic point mutations as a mechanism for inactivation of the p53 tumor suppressor gene. Abnormally sized p53 mRNAs found in a small cell and a non-small cell lung cancer cell line were characterized by sequence analysis of cDNA/PCR products, the RNase protection assay and immunoprecipitation. These mRNAs were found to represent aberrant splicing leading to the production of abnormal or no p53 protein. Sequence analysis of genomic DNA revealed that a point mutation at the splice acceptor site in the third intron or the splice donor site in the seventh intron accounts for the abnormal mRNA splicing. In one patient the same intronic point mutation was found in the tumor cell line derived from a bone marrow metastasis and in multiple liver metastases but not in normal DNA, indicating that it occurred as a somatic event before the development of these metastases. These findings further support the role of inactivation of the p53 gene in the pathogenesis of lung cancer and indicate the role of intronic point mutation in this process.
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PMID:Identification of intronic point mutations as an alternative mechanism for p53 inactivation in lung cancer. 216 47

The alpha subunits of the GTP-binding proteins, Go and Gi2, in sera, tissues, and pleural effusions have been studied, using an enzyme immunoassays system. The Gi alpha concentrations were found increased in the pleural effusions of patients with a small cell lung cancer, as compared to patients with a nonsmall cell lung cancer. Both GTP-binding proteins, however, were not elevated in the sera of patients with a lung cancer. Thus, an evaluation of the amount of Go alpha in the pleural effusion is thought to be a useful tumor marker of small cell lung cancers, elevating the specificity of a combination assay with other markers, NSE or CKBB.
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PMID:[The alpha subunits of the GTP-binding proteins, Go and Gi2 in lung cancer]. 216 12

A Phase II trial of carboplatin (CBDCA) was performed in 33 patients with advanced lung cancer, including 15 patients with inoperable Stage III non-small-cell (NSCLC) and 18 patients with relapsed small-cell (SCLC) lung cancer. Initial dosage was 320 mg/m2 infused over 24 h; in the absence of hematologic toxicity, subsequent doses were escalated to 400 mg/m2. Patients received a median of two cycles (range 1-13 for NSCLC and 1-5 for SCLC) of therapy. There were no complete or partial responses among the NSCLC patients. Among the SCLC patients, two had a partial response. In vitro analysis of the cytotoxicity of CBDCA and its parent compound cisplatin by two different methods for 20 NSCLC cell lines suggested that equivalent tumor cell kill is achieved by the two compounds, but this occurs at a log lower concentration of cisplatin than of CBDCA. The in vitro cytotoxicity against NSCLC of CBDCA at a concentration predicted to be in the range produced by the dose employed in this Phase II study correlated well with the resulting very modest in vivo benefit. In vitro, a continuous dose-response relationship exists for CBDCA, suggesting that if higher doses could be administered safely to patients, greater clinical benefit might occur. We conclude that single agent CBDCA in the dosage and schedule administered has less than 20% activity (95% confidence intervals 0-19%) in NSCLC and an 11% response rate in SCLC (95% confidence intervals 2-34%). Despite this outcome, in vitro data in human NSCLC cell lines suggest higher dosages should perhaps be evaluated before discounting a role for CBDCA in the management of NSCLC.
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PMID:A phase II trial of carboplatin (CBDCA) in small-cell and non-small-cell lung cancer with correlation to in vitro analysis of cytotoxicity. 216 37

From 1970 through 1987, 77 patients with Stage I lung cancer were treated with definitive radiation therapy (RT) alone at the Fox Chase Cancer Center or the Hospital of The University of Pennsylvania. All patients had a pathologic diagnosis of non-small cell lung cancer and were not candidates for surgical resection because of premorbid medical problems or patient refusal. The median age was 72 years, although 10 patients were over 80. The histologic cell type was squamous in 44, adenocarcinoma in 15, large cell in 3, adenosquamous in 1, non-small cell in 11, and bronchioli-alveolar in 3. Tumor size was retrievable in 75 patients and 25 were less than or equal to 3 cm, 41 from 3-6 cm, and 9 greater than 6 cm. Diagnostic staging varied during the study period. Twelve patients, evaluated with a CT scan of the chest, including the liver, and a bone scan were classified as having "excellent" staging, 24 patients with conventional tomography, liver-spleen scan and a bone scan had "good" staging, and 41 patients were staged less rigorously. The RT was of megavoltage energy in all patients. The median dose was 60 Gy. The mediastinum was treated in all but eight patients who had poor pulmonary function. Survival was measured from the date of pathologic diagnosis. The actuarial 3-year survival rate of the entire group of patients is 17% with a median survival time of 20 months. Of the 61 deaths, 51 were due to disease and 10 were due to intercurrent disease without evidence of tumor recurrence. The actuarial 3-year disease-specific survival (DSS) was 22%. The 3-year disease-specific survival for patients with tumors less than 3 cm and from 3-6 cm was 30% and 17%, respectively. All nine patients with tumors greater than 6 cm were dead of disease. Local progression occurred in 33 patients, resulting in a 44%, 3-year actuarial freedom from local progression. The median time to local failure was 28 months and there were no local failures after 3 years in the 18 patients eligible for observation beyond this point. Of the patients with "excellent" staging, only 2 of 12 were dead of disease compared with 22 of 24 with "good" staging and 30 of 41 of the remainder. In this large group of Stage I non-small cell lung cancer, thorough pre-treatment staging and smaller tumor size are associated with a more favorable outcome.
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PMID:The influence of tumor size and pre-treatment staging on outcome following radiation therapy alone for stage I non-small cell lung cancer. 216 20

The vast majority of patients have disseminated non-small cell lung cancer (NSCLC) at the time of diagnosis. Data from numerous studies clearly indicate that the disease is metastatic in asymptomatic patients who appear to have clinically resectable tumors. Adenocarcinoma is the histologic subtype that is most frequently metastatic, and its incidence appears to be increasing in a manner relative to other tumors. Of all of the prognostic factors, performance status appears to be most directly related to response rates. In other words, the higher the performance status, the higher the response rates. Tumor burden has been found to have an effect not only on performance status, but also on response to chemotherapy. Therefore systemic chemotherapy is urged as adjuvant treatment early in the course of NSCLC when performance status is highest and tumor burden lowest.
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PMID:Rationale for the use of chemotherapy in non-small cell lung cancer. 216 44

The treatment of unresectable non-small cell lung cancer remains a frustrating clinical dilemma. Objective response rates with single agents are brief and rarely complete. Although response rates are higher for combination chemotherapy regimens, they remain disappointing. Since patients with more advanced disease typically have a greater tumor burden, with concomitant decreases in performance status and weight, few studies have demonstrated a survival benefit with chemotherapy. Nevertheless, selected patients should be offered the option of treatment with combination chemotherapy. Candidates for chemotherapy include individuals with good performance status, minimal weight loss, and minimal bulk disease. Patients should understand the limitations of cisplatin-based chemotherapy. Treatment should be discontinued after two to three cycles in the absence of obvious improvement.
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PMID:Chemotherapy for unresectable non-small cell lung cancer. 216 46

Five-year survival rates for patients with non-small cell lung cancer have changed only minimally over the past 20 years. Although systemic chemotherapy has not yet proved to be of major clinical value, suggestions of improving efficacy have been noted over the past decade. A small but real fraction of complete responses has been obtained with combination chemotherapy in patients with favorable prognostic characteristics. A few studies of adjuvant chemotherapy, given after surgery or in conjunction with definitive irradiation, have demonstrated improved disease-free or overall survival periods. Future approaches suggested by laboratory observations of tumor cell biology, such as identification of patients more likely to respond to chemotherapy and early detection of patients at high risk, to develop lung cancer, may eventually prove useful.
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PMID:Future directions in the treatment of non-small cell lung cancer. 216 48


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