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Biomedical subjects

D M Shin

Publications and source records attributed to D M Shin.

At least 91 records · Page 5Linked to original sources
PubMed1994

Activation of p53 gene expression in premalignant lesions during head and neck tumorigenesis.

With the goal of identifying a potential intermediate biomarker in the multistep process of head and neck cancer development, we conducted immunohistochemical analyses for p53 expression in 33 patients with head and neck squamous cell carcinomas whose tissue sections contained adjacent normal epithelium, hyperplastic, and/or dysplastic lesions. Fifteen of 33 (45%) squamous cell carcinomas of the head and neck expressed p53, but none of four normal control patients (cancer-free nonsmokers) expressed detectable p53 in oral mucosa specimens. To determine when p53 expression is initiated during head and neck tumorigenesis, we examined the normal and premalignant lesions adjacent to the tumors. Five of 24 (21%) samples of normal epithelium adjacent to tumors, 7 of 24 (29%) samples of hyperplasia, and 9 of 20 (45%) samples of dysplasia expressed p53. Quantitative image analysis demonstrated not only a gradual increase in the amount of p53 expression as tissue abnormalities progressed but also a topological change in expression. Whereas p53 expression, when present, was limited to the basal layer in normal epithelium adjacent to tumor, the expression of p53 expanded into the parabasal and superficial layers in hyperplasia and dysplasia. We conclude that p53 expression can be altered in very early phases of head and neck tumorigenesis. Thus, it may be an excellent candidate for risk assessment and may serve as an intermediate biomarker in chemoprevention trials.

Base Sequence↗
PubMed1994

Phase II clinical trial of didemnin B in previously treated small cell lung cancer.

Didemnin B (NSC 325319), a cyclic depsipeptide isolated from a Carribean sea tunicate, exhibited potent antitumor activity in preclinical studies. After determining the maximum tolerated dose in our previous phase I/II trial, we conducted a phase II study of this drug in patients with previously treated small cell lung cancer; the starting dose was 6.3 mg/m2 intravenously over 30 min every 28 days. The major side effects were in the neuromuscular system and included severe muscle weakness, myopathy and/or myotonia by electromyography, and elevation of creatine phosphokinase and aldolase levels. We also observed modest increases in bilirubin and alkaline phosphatase levels. There were minimal hematologic toxic effects. No response was observed among 15 evaluable patients, leading us to conclude that didemnin B was toxic but inactive in patients with previously treated small cell lung cancer at the stated dose and schedule. A review of the literature revealed no significant antitumor activity in cancers of the colon, breast, ovaries, cervix, or lung (non-small cell) or in renal cell carcinoma. Further clinical trials for didemnin B may not be warranted at the stated dose and schedule.

Adult↗
PubMed1994

Tumor epidermal growth factor receptor studies in patients with non-small-cell lung cancer or head and neck cancer treated with monoclonal antibody RG 83852.

PURPOSE: Tumor tyrosine kinase activity associated with the epidermal growth factor receptor (EGFR) and localization of anti-EGFR monoclonal antibody RG 83852 were studied in patients with non-small-cell lung cancer (NSCLC) and head and neck cancer. PATIENTS AND METHODS: Fifteen patients were treated with escalating doses of RG 83852 by continuous intravenous infusion for 5 days. Fresh tumor specimens were obtained 24 hours after therapy in 10 patients (of whom five had a pretherapy sample taken). Tumor EGFR tyrosine kinase activity was determined in fresh tumor samples by autophosphorylation of EGFR isolated in immunocomplexes with RG 83852. Tumor EGFR saturation with RG 83852 was assessed semiquantitatively by comparing the EGFR tyrosine kinase activity in immunocomplexes of tumor specimens obtained after therapy with total EGFR tyrosine kinase activity assessed by exogenous addition of RG 83852 to tumor lysates. Modulation of EGFR tyrosine kinase activity after the administration of RG 83852 was assessed by comparing EGFR tyrosine kinase activity from the same malignant lesion obtained before and after therapy. Tumor localization of RG 83852 and EGFR saturation were also assessed by immunohistochemistry. RESULTS: No significant side effects were observed up to a total dose of 600 mg/m2. Based on tyrosine kinase activity, a high degree of EGFR saturation (> or = 50%) was observed at doses > or = 200 mg/m2, and EGFR saturation was estimated to be 100% at a dose level of 600 mg/m2 both in tumor tissue and skin used as surrogate EGFR-positive tissue. Immunohistochemistry studies showed that RG 83852 localized in tumor tissue and skin, but not in stroma, at doses > or = 400 mg/m2, and high EGFR saturation was observed at 600 mg/m2. Tumor EGFR tyrosine kinase activity was studied in five patients (four with EGFR-positive tumors) before and 24 hours post-therapy; a threefold to fourfold upregulation of EGFR tyrosine kinase activity in posttherapy specimens was observed in two patients. Moderate upregulation of EGFR itself was suggested in both of these patients and in two additional patients by immunohistochemistry. CONCLUSION: RG 83852 causes no toxic effects at doses that result in high tumor EGFR saturation. Treatment with RG 83852 may enhance EGFR tyrosine kinase activity and/or EGFR expression. Because high EGFR expression by tumors has been associated with increased sensitivity to cytotoxic therapy, the suggestion of antibody-mediated upregulation of EGFR by agents such as RG 83852 may prove useful in enhancing chemotherapeutic efficacy.

Antibodies, Monoclonal↗
PubMed1994

Phase II study of docetaxel for recurrent or metastatic non-small-cell lung cancer.

PURPOSE: We conducted a phase II study to determine the response and toxicity of docetaxel (Taxotere; Rhône-Poulenc Rorer Pharmaceuticals, Inc, Collegeville, PA) in chemotherapy-naive patients with advanced non-small-cell lung cancer. PATIENTS AND METHODS: We treated 41 chemotherapy-naive patients who had stage IIIb or IV non-small-cell lung cancer with 100 mg/m2 of docetaxel intravenously over 1 hour every 3 weeks. Responses were assessed after every one to two treatment courses. Responses of 39 of 41 patients were assessable. The patient's median age was 63 years; 90% of patients had a Zubrod performance status of 0 or 1. The predominant histology was adenocarcinoma (54%), and 90% of patients had stage IV disease. RESULTS: Thirteen patients (33%) achieved a partial response to treatment, and the median response duration was 14 weeks. Grade 3 or 4 neutropenia occurred in 97% of patient; this was usually of brief duration and was associated with serious infection in 17% of patients. Other acute toxic effects included easily treated hypersensitivity reactions (36% of patients) and dermatitis (74%). We also observed fluid retention (with peripheral edema or pleural effusion or both) in 54% of patients. This was a cumulative side effect that generally occurred late in treatment. CONCLUSION: Docetaxel administered at 100 mg/m2 intravenously every 3 weeks has significant activity against non-small-cell lung cancer, with a 33% major response rate. Primary toxicities were neutropenia, hypersensitivity, and fluid retention.

Adult↗
PubMed1994

Biomarkers in chemoprevention for upper aerodigestive tract tumors.

A chemopreventive approach to cancers of the upper aerodigestive tract (including those of head and neck and lung) to reduce the incidence and mortality rates for these cancers has become an important strategy because therapies such as surgery, radiation, and chemotherapy have only marginally improved the five-year survival rate over the last two decades. However, chemopreventive trials have been hampered by serious feasibility problems, including high cost, the requirement of large numbers of patients, and long-term follow-up necessary to determine cancer incidence, which served as the study end point. Thus, the use of biomarkers, the identification of which would serve as an intermediate end point of the study has recently emerged as a subject of great interest. To try to understand the process of tumorigenesis from normal tissues through the premalignant tissue stage to malignant lesions, there has recently been a search for genetic and/or phenotypic changes that qualify as candidates for biomarkers. These candidates include genomic markers, certain specific genetic markers (such as oncogenes, growth factors and their receptors, and tumor suppressor genes), cell proliferation markers, and cell differentiation markers. This review covers genomic markers (including micronuclei and specific chromosomal alterations) and specific genetic markers (such as the ras gene family, the myc family, erb B1, int-2/hst-1, and the p53 tumor suppressor gene). As a consequence of genetic alteration, we also reviewed cell proliferation markers such as proliferating cell nuclei antigen (PCNA) and the squamous cell differentiations markers, including keratins, involucrin, and transglutaminase 1. These biomarker candidates are important adjuncts to the development of the new chemopreventive agents and to the rational design of future intervention trials. However, it should be emphasized that these biomarkers must first be validated in clinical trials; only then can they replace cancer incidence as the sole end point in chemoprevention trials.

Biomarkers, Tumor↗
PubMed1994

Methods in pathology. Optimization of proliferating cell nuclear antigen immunohistochemical staining by microwave heating in zinc sulfate solution.

Immunohistochemical staining of routinely processed formalin-fixed, paraffin-embedded archival tissue sections with proliferating cell nuclear antigen (PCNA) monoclonal antibody has facilitated the understanding of the regulation of cell proliferation. However, false-negative staining due to masking or poor preservation of antigen epitopes by fixatives or other unknown conditions has been a major problem in PCNA immunohistochemical studies. Microwave heating (MWH) has been used to retrieve antigen in archival tissue. However, optimal staining conditions have not yet been defined. We therefore investigated the effect of MWH with or without a metal solution (zinc sulfate) on routinely processed paraffin-embedded tissue to determine the optimal conditions for retrieval of PCNA. The results were compared with routine immunohistochemical staining. We found that MWH in 1% zinc sulfate solution successfully retrieved PCNA; the optimal MWH time was 7.5 mins. In contrast, when MWH was performed in water, the specific intensity of PCNA expression was not increased because MWH not only enhanced the intensity of the antigen staining but also increased the background staining. In summary, MWH technique in zinc-sulfate solution allowed successful PCNA retrieval from formalin-fixed archival tissue and thus facilitated accurate immunohistochemical evaluation of cell proliferative activity in cancers.

Antibodies, Monoclonal↗
PubMed1994

Biomarkers in upper aerodigestive tract tumorigenesis: a review.

Because therapeutic efforts such as surgery, radiotherapy, and chemotherapy have only marginally improved the 5-year survival rate from cancers of the upper aerodigestive tract (including head and neck and lung cancers) over the past 2 decades, chemoprevention has become an important strategy in reducing the rates of incidence and mortality of these cancers. However, chemoprevention trials have been hampered by serious feasibility problems; they require large numbers of subjects and long-term follow-up for accurate determination of cancer incidence and they are very costly. Because the use of intermediate end points would reduce the duration and costs of these studies, biomarkers that could serve as such end points have recently become a subject of great interest. With the strengthening of the assumption that tumorigenesis is a multistep process of transformation from normal tissues to malignant lesions, there has been a great effort to examine each of these steps for genetic and/or phenotypic alterations that might be candidates for such biomarkers. These candidates include genomic markers, certain specific gene alterations, such as tumor suppressor genes, oncogenes, growth factors and their receptors, proliferation markers, and differentiation markers. In this review, we describe several genomic markers, including micronuclei, chromosomal alterations, and specific genetic markers, e.g., the ras gene family, erb B1, int-2/hst-1, and p53 tumor suppressor gene. We also review the proliferation markers, including proliferating cell nuclear antigen, and squamous cell differentiation markers, including keratins, involucrin, and transglutaminase 1. These biomarker candidates have the potential to be important adjuncts to the development of new chemopreventive agents and to the rational design of future intervention trials. However, we can not overemphasize that these markers need to be validated in clinical trials; only then can they replace cancer incidence as the sole end point for chemoprevention trials.

Biomarkers↗
PubMed1993

Sequential increases in proliferating cell nuclear antigen expression in head and neck tumorigenesis: a potential biomarker.

BACKGROUND: Proliferating cell nuclear antigen (PCNA) is a 36-kd nuclear protein whose expression is associated with DNA synthesis and cell proliferation. Tumorigenesis in head and neck squamous cell carcinoma is proposed to be a multistep process; dysregulation of proliferation is a potential marker of this process. PURPOSE: PCNA dysregulation was analyzed in squamous cell carcinoma tissue samples containing premalignant lesions (hyperplasia and/or dysplasia) and in adjacent normal epithelium to better understand proliferative changes during head and neck tumor development. METHODS: Immunohistochemical analysis was performed on formalin-fixed, paraffin-embedded sections by using a monoclonal anti-PCNA antibody. PCNA expression was analyzed in 33 head and neck squamous cell carcinomas and in their adjacent premalignant lesions from different sites and compared with that in the control samples, which had never been exposed to first-hand tobacco smoke. PCNA expression was assessed by semiquantitative scoring (scale 0-3) in three epithelial layers (basal, parabasal, and superficial). The labeling index and the weighted mean index of PCNA expression were calculated. RESULTS: Normal epithelium adjacent to the tumor had much more proliferative activity than the controls: The weighted mean index of PCNA expression was four-fold higher in the basal layer and sixfold higher in the parabasal layer. PCNA expression increased as tissues progressed from adjacent normal epithelium to hyperplasia (P < .001), hyperplasia to dysplasia (P < .001), and dysplasia to squamous cell carcinoma (P = .065); the total increase in PCNA expression ranged from fourfold to 10-fold from adjacent normal epithelium to squamous cell carcinoma. PCNA expression was higher in the parabasal than in the basal layer at all premalignant stages (23 of 25 samples in adjacent normal epithelium, 12 of 13 in hyperplasia, and 17 of 22 in dysplasia). As the tissue progressed from normal through premalignant stages to squamous cell carcinomas, we observed not only incremental increases in the labeling index, but also incremental increases in PCNA expression per labeled cells. CONCLUSIONS: These results indicate that PCNA could be a useful biomarker for multistep carcinogenesis in head and neck cancer and may serve as an intermediate end point in chemopreventive trials.

Antigens, Neoplasm↗
PubMed1993

Increased polysomies of chromosomes 7 and 17 during head and neck multistage tumorigenesis.

Head and neck cancer development has been proposed to represent a multistage process characterized by dysregulation of proliferation and differentiation and driven by an accumulation of genetic alterations in an anatomic field repeatedly exposed to carcinogens. To visualize the accumulation of genetic alterations during head and neck tumorigeneses and to determine the extent of the genetically altered field, we probed 25 squamous cell carcinomas of the head and neck and their adjacent premalignant lesions for numerical chromosome aberrations by nonisotopic, in situ hybridization using chromosome-specific centromeric DNA probes for chromosomes 7 and 17. Normal control oral epithelium from individuals free of cancer showed no chromosome polysomy (i.e., cells with > or = 3 chromosome copies), whereas histologically normal epithelium adjacent to the tumors showed squamous cells with polysomies for chromosomes 7 and 17. Moreover, the frequency of cells with polysomy increased as the tissues passed from histologically normal epithelium to hyperplasia to dysplasia to cancer. The finding of genotypic abnormalities in histologically normal and precancerous regions adjacent to the tumor supports the concept of field cancerization. The finding of progressive genetic changes as the tumor develops supports the concept of multistep carcinogenesis in the head and neck region. Such genotypic parameters could serve as biomarkers in the assessment of the risk of progression to malignancy and as intermediate end points in chemoprevention trials.

Adult↗
PubMed1993

Phase II study of taxol in patients with untreated advanced non-small-cell lung cancer.

BACKGROUND: Taxol, a complex plant product (a diterpene) extracted from the bark of Taxus brevifolia, has demonstrated substantial anticancer activity in ovarian and breast cancers, malignant melanoma, and acute myelogenous leukemia. Due to allergic reactions in phase I and early phase II studies, use of a 24-hour infusion of taxol with prophylactic dexamethasone, diphenhydramine, and cimetidine has been recommended. PURPOSE: In this phase II study, we attempted to determine the efficacy and toxicity of taxol in patients with advanced (stage IIIB or IV) non-small-cell lung cancer who had never received chemotherapy. METHODS: Patients were not excluded because of prior surgery or because of radiotherapy administered more than 4 weeks before study entry. Taxol was administered in the hospital at a dose of 200 mg/m2 as an intravenous infusion over 24 hours and repeated every 3 weeks, provided that patients had recovered from any toxic effects. Dexamethasone, cimetidine, and diphenhydramine were given before chemotherapy to prevent hypersensitivity reactions. Therapy was continued for at least two courses unless there was rapid disease progression and for at least three courses if no change was observed and no grade 3 or 4 toxic effects occurred. Treatment was continued for six more courses after maximum response or for two more courses after complete remission but was discontinued if disease progressed. RESULTS: Of the 27 patients entered in the study, 25 were assessable for toxic effects and response. One patient had an allergic reaction that was not life threatening. The overall response rate was 24% (one complete response and five partial responses). An additional seven patients (28%) had minor response. Granulocytopenia was the dose-limiting toxic effect, and neutropenic fever occurred in eight of 118 courses. One additional patient developed neutropenic sepsis with hypotension but recovered with intensive treatment. CONCLUSIONS: Taxol appears to have activity against non-small-cell carcinoma of the lung. IMPLICATIONS: A phase II study combining taxol, etoposide, and cisplatin and using hematopoietic stimulating factors is now proposed. The optimal dose for combination chemotherapy has yet to be determined. An important consideration is potential cardiac effects of taxol with other drugs.

Carcinoma, Non-Small-Cell Lung↗
PubMed1993

Early genetic changes during upper aerodigestive tract tumorigenesis.

Upper aerodigestive tract tumorigenesis has been hypothesized to represent a field cancerization process with multistep events based on its association with known carcinogens, its frequent associated premalignant lesions, and its multifocal clinical manifestation. To further explore this working hypothesis, we have examined normal tissue and premalignant lesions in the field of tumors for evidence of genetic change. Paraffin sections of head and neck tumors harboring neighboring premalignant lesions were explored for the presence of chromosome polysomies using in situ hybridization and chromosome-specific centromeric probes. Cells exhibiting random polysomy were observed in the premalignant regions near the tumors. The frequency of polysomy in the tumor field increased as the tissue progressed from normal morphology (33%), to hyperplasia (67%), to dysplasia (95%), and to squamous cell carcinoma (96%). These results support the notions of field cancerization and multistep tumorigenesis in the aerodigestive tract. To determine whether the degree of accumulated genetic alterations might serve as a biomarker for risk of developing malignancy, a set of biopsies of oral premalignant lesions (leukoplakia, erythroplakia) were retrospectively chosen for polysomy analysis from two groups of individuals: one group who subsequently developed oral cancer and one group who did not develop oral cancer. Three of the five individuals who showed significant chromosome polysomies in their biopsies subsequently developed oral cancer, whereas only one of eight individuals with little evidence of polysomy subsequently progressed to oral cancer. These results suggest that evidence of generalized genetic change or instability might be useful as a genetic biomarker for risk assessment.

Digestive System Neoplasms↗
PubMed1993

Activation of ribosomal protein S2 gene expression in a hamster model of chemically induced oral carcinogenesis.

7,12-Dimethylbenz[a]anthracene (DMBA)-induced carcinogenesis of the hamster buccal pouch has been an excellent model for the study of squamous cell carcinogenesis in human head and neck cancer. Using a differential hybridization of cDNA cloning technique, we isolated a cDNA clone that is expressed in N-ras-transformed PA-1 cells but poorly expressed in non-tumorigenic PA-1 cells; the cDNA codes for the human ribosomal S2 gene product. To define the involvement of S2 gene expression during carcinogenesis in this animal model, we used in situ hybridization technique with non-radioactive digoxigenin-11-dUTP-labeled cDNA. S2 gene was expressed at low levels in basal and suprabasal cell layers of the epidermis in the control, but showed marked elevation throughout the epidermis other than the keratin layer in samples treated for 4 or 8 weeks; S2 was highly expressed in all malignant squamous cell carcinoma cells resulting from DMBA treatment for 16 weeks. As tumors progress from normal epithelium to squamous cell carcinomas, mRNA of the S2 gene was not only elevated sequentially, but also demonstrated the marked heterogeneity among transformed populations, particularly in dysplastic lesions and squamous cell carcinomas. The S2 gene was expressed in a stage-specific manner in the hamster tumor model; S2 could be useful as a neoplastic marker for the detection of certain epithelial origin of tumors and premalignant lesions as well.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Elevated expression of the ribosomal protein S2 gene in human tumors.

Differential screening of a cDNA library was used to isolate genes differentially expressed in a nontumorigenic clone and a ras-transformed variant of the human teratocarcinoma cell line PA-1. The RNA transcript for one of the cDNA clones that we identified was expressed at a 25-fold higher level in the ras-transformed PA-1 cells than in the nontumorigenic PA-1 cells. DNA sequence analysis of this clone showed that it had 86% nucleic acid homology to the mouse LLRep3 gene and only differed at a single amino acid codon (codon 198), which is changed from serine in LLRep3 to threonine in this cDNA clone. The rat ribosomal S2 protein is closely related to the yeast omnipotent informational suppressor SUP44, which encodes the yeast ribosomal protein S4; to the mouse protein LLRep3; and to the human cDNA clone we describe in this report. We therefore concluded that this clone codes for the human ribosomal S2 protein. In situ hybridization experiments revealed that expression of this gene was elevated in cultured human head and neck squamous cell carcinomas compared with normal keratinocytes. In situ hybridization experiments also demonstrated that expression of this gene was elevated in histological sections of human premalignant leukoplakia, head and neck squamous cell carcinomas, and colon and breast cancers compared with the adjacent normal tissues. S2 expression may be a useful diagnostic or prognostic marker for grading human tumors.

Amino Acid Sequence↗
PubMed1992

Thymoma: treatment and prognosis.

Thirty-six patients with pathologically confirmed thymoma were treated at M.D. Anderson Cancer Center from 1962 to 1987. The tumors were staged based on invasion and intrathoracic dissemination. Twenty-one patients had total resection, five had subtotal resection, and 10 had biopsy alone. Twenty-two patients had definitive megavoltage radiation therapy with a median dose of 50 Gy. The 5-year, disease-free survival by stage was 74% for Stage I (n = 11), 71% for Stage II (n = 8), 50% for Stage III (n = 10), and 29% for Stage IVA (n = 7) (p less than 0.03). The 5-year, disease-free survival by extent of surgery was 74% for total resection, 60% for subtotal resection and 20% for biopsy only (p = 0.001). There were 15 patients with recurrences: two in Stage I, two in Stage II, five in Stage III, and six in Stage IVA. The median months to relapse, for those who failed treatment, were 46, 36, 2, and 13 for Stages I, II, III, and IVA respectively. Of the patients with recurrences four had a total resection, two subtotal resection, and nine biopsy only. Only one patient had distant metastases as the first site of relapse without intrathoracic relapse. For the eight patients who relapsed following radiation therapy, four were in the radiotherapy field. All four of the in-field failures were in patients who had a partial response. There were insufficient numbers of patients to determine a dose response to radiotherapy. For patients with invasive, incompletely resected disease, a multimodality approach may be necessary for long term, disease-free survival.

Adolescent↗
PubMed1992

Phase II study of combination therapy with high-dose cisplatin, etoposide, and mitomycin in patients with advanced non-small-cell lung cancer.

Forty-six patients with metastatic non-small-cell lung cancer (NSCLC) were treated with a combination of high-dose cisplatin, etoposide, and mitomycin. Thirty-four patients (74%) had a performance status of 1, and 39 patients (85%) had adenocarcinoma. Of the 42 patients evaluable for response and toxicity, four achieved a partial response (10%); no patient achieved a complete response. Seven patients who had received prior chemotherapy showed no major response. The median survival of all 42 patients was 23 weeks. Myelosuppression was the major dose-limiting toxicity for this regimen, and 12 of 46 patients (26%) developed neutropenic fever requiring hospitalization and parenteral antibiotics. Of the 12 patients with severe neutropenic fever, one patient died because of toxicity. Nonhematologic toxicities, including azotemia, peripheral neuropathy, nausea, vomiting, and hearing loss were transient and modest. We conclude that high-dose cisplatin combined with etoposide and mitomycin is a relatively toxic regimen with a low response rate. Further evaluation of the combination as given in this trial is not warranted.

Adult↗
PubMed1992

Implantation metastasis of carcinoma after percutaneous fine-needle aspiration biopsy.

Implantation of malignant cells along the needle tract is an extremely rare but potential complication following percutaneous needle aspiration biopsy of malignant lesions. Percutaneous fine-needle aspiration biopsy (FNAB) has recently received more attention for cytologic diagnosis of bronchogenic carcinoma because of its high diagnostic yield, simplicity, and low morbidity. On the other hand, dissemination of cancer cells by needle aspiration biopsy can change a potentially resectable localized lung cancer to an unresectable one. We report two cases: one patient underwent FNAB of a metastatic left adrenal mass that seeded a paraspinal muscle implantation of malignant cells that subsequently developed a tumor mass, and the second patient had tumor cell implantation in the chest wall after FNAB of a pleural-based adenocarcinoma of the lung. The theoretical and practical importance of tumor cell spread along the needle tract is discussed. Because of its rare incidence, however, this complication should not affect the use of needle aspiration biopsy in bronchogenic carcinoma, although care should be undertaken during the procedure.

Adenocarcinoma↗
PubMed1992

Renal salt wasting in patients treated with high-dose cisplatin, etoposide, and mitomycin in patients with advanced non-small cell lung cancer.

Cisplatin has many toxic effects; emesis, impairment of renal function, myelosuppression, peripheral neuropathy, ototoxicity and renal tubular wasting. We used MVP regimen (Mitomycin C, Vp-16, and Cisplatin) in advanced Non-Small Cell Lung Cancer (NSCLC). Using hydration and prophylactic supplementation of sodium and potassium before and during chemotherapy, we have observed the development of hyponatremia in 48 courses (43%), hypokalemia in 23 courses and hypomagnesemia in 11 courses. Some patients showed abnormalities of renal function in 16 courses. All the electrolyte depletion and renal problem was corrected before next courses by hydration and replacement of the wasting. Frequent measurement of serum cation and appropriate replacement are recommended when high dose Cisplatin containing regimen is used in chemotherapy of neoplasms.

Adult↗