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At least 19 recordsLinked to original sources
PubMed1977

Degradation of carmustine in aqueous media.

The degradation rate of carmustine was investigated in buffered aqueous media at several pH values. The buffering agents studied were those with potential use in parenteral formulations of this drug: acetate, citrate, and phosphate. The apparent first-order degradation rate constants were calculated using a linear regression procedure. A pH range over which minimum degradation occurred was ascertained. General acid and specific base catalysis was demonstrated for the degradation of carmustine. From the data at 5, 22, and 37 degrees, the apparent activation energies for carmustine degradation in buffered aqueous media were computed and were strongly pH dependent.

Buffers↗
PubMed1979

Pulmonary toxicity from carmustine (BCNU): a case report.

A patient who had a pneumonectomy for lung carcinoma was treated with carmustine when brain metastases developed. His pulmonary function was mildly compromised prior to the pneumonectomy by many years of smoking. After six months of carmustine therapy [total dose: 2,250 mg (1,200 mg/m2)] he developed interstitial pulmonary fibrosis with histologic changes consistent with drug toxicity. With seven previously reported cases of this drug-effect and the addition of our case, carmustine must be added to the list of cancer chemotherapeutic agents that can cause pulmonary toxicity.

Autopsy↗
PubMed1979

[A prospective multi-centre study of the response of metastatic gastrointestinal tumours (author's transl)].

In a prospective, multi-centre, randomized study of 109 patients with metastatic gastro-intestinal adenocarcinomas the response rate, survival time and side-effects of two drug combinations, carmustin +5-fluorouracil and carmustin + ftorafur, were compared (same carmustin dosage in both groups). Response to the treatment was 32.7% in those receiving carmustin +5-fluorouracil, 26.3% in those on carmustin + ftorafur. This difference occurred among the 42 patients with gastric adenocarcinoma (33.3% compared with 25%), as well as in 11 with pancreatic adenocarcinoma, and in 56 with colorectal adenocarcinoma (32.1% and 28.6%). Median survival time for 5-fluorouracil + carmustin was 330 days, double that for ftorafur + carmustin (163 days). Bone-marrow toxicity (leukopenia, thrombopenia) was below 10% for both drug combinations. Alopecia occurred in only a few patients. Gastro-intestinal toxicity was common (20% and 18.5%, respectively), but there was no difference between the two groups. The somewhat lower effectiveness of ftorafur compared with 5-fluorouracil was probably due to the deliberately smaller dosage of the former.

Adenocarcinoma↗
PubMed1979

The chemotherapy of plasma-cell myeloma and the incidence of acute leukemia.

Previously untreated patients with myeloma were randomized to initial treatment with melphalan and prednisone (and to cyclophosphamide or carmustine if relapse or progression occurred)(Group A, 125 patients), melphalan, cyclophosphamide, carmustine and prednisone in alternating (Group B, 123 patients) or concurrent (Group C, 116 patients) schedules. The groups were similar with respect to known prognostic factors. Response rates and survival were also similar. We were unable to identify a subgroup of patients who responded or survived better on melphalan-cyclophosphamide-carmustine and prednisone than on melphalan and prednisone. We conclude that the combination of the four drugs is not better than melphalen and prednisone for inducing responses or prolonging the survival of patients with myeloma. Myelomas producing only gamma chains have a poorer prognosis (P greater than 0.001) than IgG, IgA, or kappa myeloma. Acute leukemia has developed in 14 patients. The actuarial risk of developing acute leukemia, has increased rapidly to 17.4 per cent at 50 months.

Acute Disease↗
PubMed1976

Single-agent chemotherapy of brain tumors. A five-year review.

Identification of effective single chemotherapeutic agents for brain tumors must precede the rational use of multiple drug combinations. In phase 2 trials beginning in 1968, 158 patients with intrinsic brain tumors (mostly recurrent malignant astrocytomas) were considered evaluable. The larger trials with more effective drugs produced these results: carmustine (BCNU) response rate, 47%, with median duration of nine months; lomustine (CCNU), 44%, with median duration of six months; procarbazine hydrochloride, 52%, with median duration six months; carmustine and vincristine sulfate combined, 44%, with median duration of only four months; and BIC (5-[3,3-bis(2-chloroethyl)-1-triazeno]imidazole-4-carboxamide), 38%, with median duration of five months. Administration of glucocorticoids was not found to bias the frequency of response. Forty-seven patients, 26 of whom had responded to the initial drug, received a second drug. Among 26 patients who were evaluable, only four responded to the second drug.

Astrocytoma↗
PubMed1976

Treatment of malignant glioma. A controlled study of chemotherapy and irradiation.

Thirty-three patients with malignant glioma were randomly divided into two groups after extensive tumor resection. Those in group A received, every five to eight weeks, a course of chemotherapy consisting of intravenously administered carmustine, 80 mg/sq m/day for three days, and vincristine sulfate, 1.4mg/sq m on days 1 and 8. Patients in group B were treated identically and received radiation therapy (RT) as well, 4,500 rads whole brain plus 1,500 rads to the side of the tumor. The median survival time of group A was 30 weeks, while that of group B was 44.5 weeks, but the overall survival curves were not significantly different. The median survival times exceeded the 17 weeks reported elsewhere in comparable patients not receiving postoperative therapy. Estimates of the quality of survival suggested (1) the two groups were not comparable following randomization, possibly influencing the results; and (2) postoperative radiation and chemotherapy do not increase morbidity and offer a longer period than other treatments during which patients' conditions remain stable or improve.

Brain Neoplasms↗
PubMed1979

Improved survival of increased-risk myeloma patients on combined triple-alkylating-agent therapy: a study of the CALGB.

Two hundred fifty-two previously untreated evaluable patients with multiple myeloma were entered into a study testing a regimen of three intravenous alkylating agents, melphalan, cyclophosphamide, and carmustine (BCNU), given in combination (BCMP) against a regimen employing oral melphalan (MP). Both regimens included a tapering course of prednisone. Objective responses based on the Myeloma Task Force criteria were significantly more frequent in the group receiving BCMP. Survival for the entire group of BCMP-treated patients was not significantly better than that for MP-treated patients (p = 0.62). However, when the survival of the poor-risk (high tumor cell load) group of patients treated with BCMP was compared with the survival of the poor-risk (high tumor cell load) group of patients treated with MP, an improvement in survival attributable to BCMP therapy was seen (p = 0.049 and 0.02, respectively). In the good-risk (low and intermediate tumor cell load) group, BCMP treatment resulted in a trend toward poorer survival, but this did not achieve statistical significance (p = 0.080 and 0.23, respectively). These results indicate that optimal therapy in myeloma may be dependent on the extent of disease at the time of first treatment. Additional studies to explore the effects of treatment intensity and duration are needed in order to design improved myeloma treatment based on the patient's extent of disease.

Alkylating Agents↗
PubMed1978

Effect of chemotherapeutic agents on metabolic and bactericidal activity of polymorphonuclear leukocytes.

Blood was obtained on 36 occasions from 12 healthy adult volunteers and the polymorphonuclear leukocytes (PMNL) were separated. PMNL hexose monophosphate shunt activity of whole blood and ability of separated cells to phagocytize and kill E. coli were evaluated when the PMNL were incubated with normal pooled sera and sera containing therapeutic concentrations of either 15 cancer chemotherapeutic drugs singly and in combination or 9 antibiotics. Resting and stimulated HMPS activity was significantly (p less than 0.025 to p less than 0.001) decreased by cyclophosphamide, carmustine (BCNU), high dose prednisone (pred), vinblastine (vinbl) and vincristine (vinc) and significantly (p less than 0.025 to p less than 0.01) increased by combinations of vinc-pred, vinc-predasparaginase, 6-mercaptopurine (6MP)-methotrexate (Mtx) and 6MP-Mtx-pred when compared to controls. No significant differences in HMPS activity of PMNL were found when exposed to various antimicrobial agents singly or in combination. The killing of E. coli by PMNL was significantly (p less than 0.001) decreased when exposed to BCNU, high concentration pred or combinations of 6MP-Mtx-pred, 6MP-Mtx and vinc-vinbl-pred but not when exposed to other chemotherapeutic agents. This study shows a disparity in results obtained when evaluating PMNL function by HMPS activity and bactericidal assay. In addition, a functional impairment in PMNL exposed to various antimetabolites occurred at a time when they exhibited normal morphology.

Anti-Bacterial Agents↗
PubMed2026

Multi-Omics Integration Identifies a Five-Gene Metabolic Signature With Experimental Validation in Clear Cell Renal Cell Carcinoma.

BACKGROUND: Clear cell renal cell carcinoma (ccRCC) is hallmarked by profound metabolic reprogramming; however, its intricate crosstalk with the tumor immune microenvironment (TIME) and its clinical ramifications remain inadequately elucidated. This study aims to systematically decipher the metabolic-immune interplay in ccRCC through multi-omics integration, with the goal of identifying robust prognostic biomarkers and actionable therapeutic vulnerabilities. AIMS: This study aims to systematically decipher the metabolic-immune interplay in clear cell renal cell carcinoma (ccRCC) through multi‑omics integration, and to identify robust prognostic biomarkers and actionable therapeutic vulnerabilities that can inform precision risk stratification and individualized treatment strategies. METHODS: We integrated bulk transcriptomic, genomic, and clinical data from multiple ccRCC cohorts. Differential expression and functional enrichment analyses were performed to characterize metabolic pathway alterations. Mendelian randomization (MR) was employed to infer causal relationships between metabolic disorders and ccRCC risk. A machine learning-based prognostic framework, incorporating SHAP (SHapley Additive exPlanations) for feature interpretability, was constructed and rigorously validated. TIME heterogeneity was dissected using deconvolution algorithms, while drug sensitivity, tumor mutation burden (TMB), and TIDE scores were utilized to assess therapeutic responses and immune evasion. Candidate gene function was evaluated through in vitro gain- and loss-of-function assays, with expression validated via TCGA, HPA, western blot, and qRT-PCR. RESULTS: Enrichment analysis identified coordinated dysregulation in lipid metabolism, energy homeostasis, and hypoxia response pathways. MR analysis confirmed lipid metabolism disorders as a causal risk factor for ccRCC. Our machine-learning model, centered on five core SHAP-identified features (SUCLA2, ACAT1, PC, SUCLG1, and HMGCS2), demonstrated superior predictive accuracy over conventional clinical staging. Immune profiling unveiled dichotomous TIME states: the low-risk group retained active immune surveillance, whereas the high-risk group was enriched with immunosuppressive subsets. Drug sensitivity screening pinpointed LY2109761 and carmustine as high-risk-specific candidate agents. Furthermore, TMB and TIDE analyses stratified high-risk patients displaying genomic instability and immune evasion phenotypes. Functionally, SUCLA2 knockdown significantly enhanced ccRCC cell proliferation and invasion, while its overexpression suppressed these malignant phenotypes, corroborating its tumor-suppressive role. Expression patterns of the hub genes were consistently validated across multi-level datasets and experimental assays. CONCLUSION: This study establishes a precision oncology framework for ccRCC by functionally linking metabolic biomarkers, immunophenotypes, and stratified therapeutic strategies. Importantly, we identify SUCLA2 as a potential functional tumor suppressor and a promising target for further mechanistic and translational investigation.

Humans↗
PubMed1975

Combined modality therapy for intracranial tumors.

Three types of tumor (supratentorial astrocytoma, medulloblastoma, and craniopharyngioma), each requiring a fundamentally different therapeutic approach, will be used to illustrate the principles and practice of combined treatment in this field. The role of radiotherapy and ways of enhancing the effect of irradiation will be considered. Attention will be given to adjuvant chemotherapy and to multiple drug regimes. Reference will be made to an early effort at immunotherapy following the initial reduction of tumor cell load by surgery and irradiation.

Antigens, Neoplasm↗
PubMed1975

Modification of radiation injury to normal tissues by chemotherapeutic agents.

The effects of several cancer chemotherapeutic agents on radiation damage to normal intestine, esophagus, and lung tissue were evaluated in LAF 1 mice using quantitative endpoints. In all tissues tested, actinomycin D increased injury and BCNU did not. In the intestine, adriamycin enhanced radiation damage more than any other agent. Bleomycin increased damage in the esophagus but not in the lung or intestine. Cyclophosphamide increased injury only in the lung, where vincristine caused minimal injury, and hydroxyurea, none. Only prednisolone caused significant radioprotection when given at the time of irradiation or at the time of expected death from pulmonary injury.

Animals↗
PubMed1975

Clinical management of advanced gastrointestinal cancer.

Although advanced gastrointestinal cancer is the most commonplace problem encountered by the medical oncologist, this group of diseases has proved exceedingly resistant to past chemotherapy efforts. 5-Fluorouracil (5-FU), accepted by some as standard treatment, had provided only infrequent, incomplete, and fleeting antitumor effects, which are probably more than counterbalanced by its gastrointestinal, mucocutaneous, and hematologic antihost effects. There is no evidence that any manipulation of route or schedule of administration provides any improvement in the therapeutic ratio of 5-FU. There is no evidence that this drug contributes to patient survival when used at any stage of any type of gastrointestinal carcinoma. The search for alternative single drugs to 5-FU has been disappointing. The nitrosoureas and Mitomycin C produce occasional regressions, but they do not match the meager effectiveness of 5-FU; and they, in addition, present the difficult problem of cumulative bone marrow suppression. Recent trials with combination regimens have given some indication that the long stalemate in chemotherapy of gastrointestinal cancer may be breaking. Substantial improvements in frequency of tumor regression have been recorded for gastric carcinoma with combinations of 5-FU and BCNU, 5-FU and methyl CCNU, and 5-FU, Mitomycin C, and cytosine arabinoside; for colorectal carcinoma, with the combination of 5-FU, methyl CCNU, and vincristine; and for carcinoid tumors and islet cell carcinomas, with the combination of 5-FU and Streptozotocin. There are also suggestion that such combination chemotherapy with response rates in the 30 to 50% range may produce increased survival when compared to the untreated patient and patients treated with single-drug regimens. While the accomplishments of chemotherapy for the gastrointestinal cancer patient remain less than spectacular there is nevertheless realistic hope that a respectable contribution can now be made to multidisciplinary efforts applied at a stage of disease with minimal tumor burden.

Adenoma, Islet Cell↗
PubMed1976

Effect of surgical and chemotherapeutic treatment on alpha-fetoprotein levels in patients with hepatocellular carcinoma.

Quantitative determinations of serum alpha-fetoprotein (AFP) by radioimmunoassay in 193 patients with hepatocellular carcinoma have demonstrated a wide variation in serum levels that appear to be relatively constant for each patient by the time that diagnosis is made. If there is no therapeutic intervention the serum AFP usually follows a gradual increase as the tumor progresses. A few patients have a fall in serum AFP as a preterminal event. Various forms of chemotherapy cause only minor and transient decrease in serum AFP. Surgical resection of tumor produces an immediate fall that parallels the catabolic decay rate for AFP. All AFP-positive patients treated with surgery had recurrence of their tumor with a rise in serum AFP preceeding clinical discovery. The correlation of serum AFP and effective treatment is demonstration of the usefulness of this oncofetal protein marker as an indicator of neoplastic activity for hepatocellular carcinoma and tumors with embryonal cell components and possibly for some other entodermally derived neoplasms.

Carmustine↗