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PubMed1979

Delta-9-tetrahydrocannabinol as an antiemetic for patients receiving cancer chemotherapy. A comparison with prochlorperazine and a placebo.

The antiemetic activity and side-effects of delta-9-tetrahydrocannabinol (THC) were evaluated in 116 patients (median age 61 years) receiving combined 5-fluorouracil and semustine (methyl CCNU) therapy for gastrointestinal carcinoma. In a double-blind study, patients were randomized to receive THC, 15 mg orally three times a day, prochlorperazine, 10 mg orally three times a day, or placebo. The THC had superior antiemetic activity in comparison to placebo, but it showed no advantage over prochlorperazine. Central nervous system side-effects, however, were significantly more frequent and more severe with THC. With the dosage and schedule we used, and in our patient population of largely elderly adults, THC therapy resulted in an overall more unpleasant treatment experience than that noted with prochlorperazine or placebo. Although THC may have a role in preventing nausea and vomiting associated with cancer chemotherapy, this role must be more clearly defined before THC can be recommended for general use.

Adult↗

PubMed1991

[Brain metastases of malignant melanomas].

Cerebral metastases of malignant melanoma are correlated with a very poor prognosis. Surgery of an isolated metastase can lead to a long survival but the brain lesions are frequently numerous and associated with an extracerebral diffusion. Dacarbazine (DTIC) gives a mean response rate of 21% on visceral localisations but doesn't cross the blood brain barrier (BBB). Neither do the biological response modifiers like Interleukin 2 (Il2) that leads to 25% response rate in disseminated melanoma. Nitrosoureas like carmustine (BCNU) and semustine (CCNU) have been investigated in different non randomised studies and the clinical results didn't illustrate their theorical ability to cross the BBB. Radiotherapy is also used as a palliative therapy with 7 to 16 weeks survival. Fotemustine (muphoran), a new amino acid linked nitrosourea, can give a response rate up to 28.2% in patients with cerebral metastases and the increased survival of responding patients is significant. The availability of this new drug may suggest associations with surgery and radiotherapy in the future to improve the survival of such patients.

Antineoplastic Agents↗

PubMed1985

Intensive induction chemotherapy for small cell anaplastic carcinoma of the lung.

The role of intensive induction chemotherapy in small cell cancer of the lung remains unclear. Twenty-eight newly diagnosed patients with small cell lung cancer were randomized to receive either high-dose or standard-dose cyclophosphamide, vincristine, and semustine in a trial where the dose of induction chemotherapy was the sole treatment variable. Complete responses (CR) were achieved in 57% of patients receiving high-dose therapy as compared to 21% of patients receiving standard-dose therapy (P less than 0.05). There was a higher rate of severe toxicity in the high-dose group (P less than 0.01). The overall median survival was not improved (36 weeks for the high-dose group vs 43 weeks for the standard-dose group); however, the median survival in patients achieving CR was prolonged (92 weeks for the high-dose group vs 50 weeks for the standard-dose group). These effects were most pronounced in patients with extensive disease; a CR after induction was achieved in five of nine patients treated with high doses but not in any of those treated with standard doses (P less than 0.05). A small group of patients appear to benefit by achieving a long-term remission with intensive induction chemotherapy, but this effect may be offset by increased morbidity.

Aged↗

PubMed1984

Metabolic studies of delta-9-tetrahydrocannabinol in cancer patients.

The metabolism of oral delta-9-tetrahydrocannabinol (THC) was studied in nine patients with gastrointestinal neoplasms receiving chemotherapy regimens containing 5-FU and semustine. Plasma levels of THC and its metabolites 11-OH-delta-9-THC (11-OH-THC) and 11-nor-9-carboxy-delta-9-THC (C-THC) were measured. Plasma levels of THC and its metabolites were quite variable among the patients studied. Plasma levels of THC and 11-OH-THC tended to peak at the same time; the C-THC levels peaked later and lasted much longer than the others. Mean half-lives of THC, 11-OH-THC, and C-THC were estimated to be 1.5, 2.1, and 4.4 hours, respectively. Multiple doses of THC did not produce a significant additive effect on the plasma concentrations of the biologically active metabolites THC and 11-OH-THC. No correlation between antiemetic effect or cannabinoid toxicity and plasma levels of the three metabolites could be made in this small number of patients.

Adult↗

PubMed1983

Randomized phase II studies in advanced colorectal carcinoma: a North Central Cancer Treatment Group study.

5-FU, semustine (MeCCNU), triazinate (TZT), and razoxane (ICRF-159) have each shown activity against advanced colorectal cancer in studies by at least two investigative groups. Objective response rates, however, have been low, without evidence of increased patient survival. The hope of this study was that enhanced activity might result from giving these agents in two-drug combinations. There were 167 eligible and evaluable patients randomized among the programs: 5-FU at a dose of 500 mg/m2/day by iv push X 5 (F); 5-FU at a dose of 400 mg/m2/day iv X 5 plus TZT at a dose of 175 mg/m2/day iv X 3 (FT); 5-FU at a dose of 400 mg/m2/day plus ICRF-159 at a dose of 600 mg/m2/day orally X 3 (FI); MeCCNU at a dose of 150 mg/m2/day orally plus TZT at a dose of 200 mg/m2/day iv X 3 (MT); MeCCNU at a dose of 150 mg/m2 orally plus ICRF-159 at a dose of 500 mg/m2/day orally X 3 (MI); and ICRF-159 at a dose of 425 mg/m2/day orally X 3 plus TZT at a dose of 125 mg/m2/day iv X 3 (IT). Patients with limiting conditions (serum creatinine greater than 1.5 mg/dl or elevated bilirubin) were randomized among programs F, FI, and MI. Objective response rates by treatment arm were: F--13% (four of 31 patients); FT--13% (four of 31); FI--15% (four of 27); MT--11% (three of 28); MI--13% (four of 32); and IT--6% (one of 17). Response rates of combination arms were not significantly larger than those of 5-FU alone. With regard to survival, patients initially treated with 5-FU alone had the most favorable experience (median, 10.8 mos). Multivariate analysis showed the following factors to have a significant and independent influence on survival: Eastern Cooperative Oncology Group performance score, grade, site of indicator lesion, and the presence of 5-FU in the treatment regimen. Toxic effects most frequently seen were nausea, vomiting, thrombocytopenia, leukopenia, diarrhea, stomatitis, alopecia, and dermatitis. The incidence and severity of toxicity were roughly comparable among the six treatment arms.

Adult↗

PubMed1983

In vivo drug sensitivity assay of clonogenic human melanoma cells and correlation with treatment outcome.

In vitro tests of tumor cell drug sensitivity have been suggested as a means of selecting more appropriate clinical strategies against human cancer and improving preclinical drug development. The lack of biotransformation in these in vitro assays precludes the meaningful assessment of several major chemotherapeutic agents, including dacarbazine and cyclophosphamide. In vivo drug exposure of tumor cells in agar diffusion chambers placed in mice offers a possible solution to problems of drug biotransformation and pharmacokinetics. We have prospectively used this system as an assay for sensitivity of clonogenic human melanoma cells. Tumor cells were tested fresh, cryopreserved, and/or cultured in vitro before or after clinical use of dacarbazine, semustine, and mitolactol in 41 patient-drug combinations in which a clinical correlation could be made. Tumor cell drug sensitivity in the assay using fresh or cryopreserved tumor cells was highly correlated with clinical response and resistance with clinical nonresponse. Cultured melanoma cells exhibited enhanced plating efficiency in comparison to both fresh and cryopreserved cells of the same tumor. Cultured cells also showed increased drug sensitivity which did not correlate with drug sensitivity of the same fresh or cryopreserved tumor or with clinical response. Tumor cell drug sensitivity assays carried out in vivo provide a possible basis for preclinical evaluation of drugs which are unsuitable for in vitro testing.

Animals↗

PubMed1992

Chemotherapy for metastatic colorectal cancer.

The systemic management of patients with colorectal cancer continues to focus on the use of 5-fluorouracil (5-FU). In the setting of metastatic disease, parenteral 5-FU has been shown to be superior to oral 5-FU; however, survival duration seems similar whether such parenteral 5-FU is administered in a "loading," weekly, or continuous infusion manner. The addition of other cytotoxic agents such as semustine, mitomycin C, or cisplatin to 5-FU does not appear to increase the response rate or prolong survival. The results of five randomized trials assessing the value of intraarterial hepatic infusions of 5-FU or floxuridine show that such regional chemotherapy increases the likelihood of hepatic response compared with systemic treatment but has little effect on survival and is associated with significant toxicity. Recent efforts in the management of patients with advanced disease have been directed at optimizing the activity of 5-FU by (1) enhancing the inhibition of DNA synthesis through the concomitant administration of folinic acid; (2) increasing drug incorporation into RNA through pretreatment with methotrexate or phosphonacetyl-L-aspartate; and (3) improving the drug's activity through the synergistic action of alpha-2a-interferon. Although the results of some of these investigations have been promising, only the 5-FU and folinic acid combination consistently has appeared to be superior to single-agent 5-FU. These different approaches to biochemical modulation are being compared in ongoing cooperative group trials.

Antineoplastic Agents↗

PubMed1980

Cytotoxic drug-induced pulmonary disease: update 1980.

Administration of a number of cytotoxic agents has been associated with interstitial pneumonitis, alveolitis and pulmonary fibrosis. Some (bleomycin, busulfan, methotrexate) are well known to cause this problem, and others (carmustine, semustine, zinostatin, mitomycin, and chlorambucil) have only recently been recognized to do so. We review and update the available information about this form of drug toxicity. Interaction between these drugs and thoracic radiation or high oxygen fractions in inspired air has produced pneumonitis at doses lower than when the drug is used alone. Synergism between the drugs themselves when given concurrently also produces pulmonary toxicity at lower doses. With some drugs and in some patients steroids will diminish the pulmonary abnormalities, but death from hypoxia is a frequent outcome. Since early recognition of the problem and withdrawal of the injurious agent is the best treatment, physician awareness of and alertness to this toxicity and its relative risk is most important. The discovery of analogs of bleomycin with a better therapeutic index, specifically reducing pulmonary damage, is one of the goals of current cancer drug development.

Alkylating Agents↗

PubMed1989

Postoperative adjuvant therapy of rectal cancer: an analysis of disease control, survival, and prognostic factors.

Between 1976 and 1984, 139 patients with rectal cancer were treated with complete surgical resection and postoperative adjuvant pelvic radiation therapy with or without chemotherapy. In this group, tumor extended beyond the bowel wall or involved lymph nodes or both. Irradiation was begun between 15 and 182 days postoperatively (median delay, 42 days). The radiation was delivered with 4-, 6-, or 10-MV photons given 5 days per week at 1.8 to 2.0 Gy per fraction. Total doses ranged from 3.8 to 64.4 Gy (median, 50 Gy). The fields were AP:PA in 49 and AP:PA plus laterals in 90. Forty-four received concurrent chemotherapy: 5-fluorouracil and semustine in 37, and 5-fluorouracil alone in seven. Follow-up in survivors ranged from 2 to 10 years (median, 4.2 years). This analysis includes all failures, both initial and subsequent sites of failure. Local failure occurred in 30 (22%) of the 139 patients overall, 6 (18%) of 33 in Stage B-2, 1 of 3 in Stage B-3, 2 (10%) of 20 in Stage C-1, 20 (26%) of 76 in Stage C-2, and 1 (14%) of 7 in Stage C-3. Five-year actuarial survival was 59% overall, 82% in Stage B-2, 79% in Stages B-2 and B-3, 89% in Stage C-1, 41% in Stage C-2, and 42% in Stages C-2 C-3. The following prognostic factors were independently associated with poorer survival and increasing distant failure: lymph node involvement, tumor extension beyond the bowel wall, and high histologic grade. Use of chemotherapy was associated with a significant improvement in survival and decrease in distant failure. No single factor was significantly associated with local failure. Adequate perineal coverage after combined abdominoperineal resection yielded significantly fewer perineal failures. Overall, serious complications developed in 7%, but none was fatal. Treatment recommendations and optimal treatment techniques are discussed.

Adult↗

PubMed1986

Nephrotoxicity induced by cancer chemotherapy with special emphasis on cisplatin toxicity.

Renal failure in cancer patients is a common problem in oncology; this complication is frequently multifactorial in origin. Several antineoplastic agents are potentially nephrotoxic; previous renal impairment as well as combinations with other nephrotoxic drugs may increase the risk of nephrotoxicity during administration of chemotherapy. Methotrexate-related renal damage most frequently occurs with high-dose therapy and can be avoided by forced alkaline diuresis and administration of folinic acid. Renal dysfunction secondary to semustine (CH3-CCNU) is clearly related to cumulative doses in excess to 1,200 mg/m2; the onset may be delayed and renal failure progress despite drug discontinuation. Streptozotocin is also nephrotoxic and may cause proteinuria and renal tubular acidosis; progressive renal failure can be predicted by a close monitoring of proteinuria and prevented by drug discontinuance. Mitomycin-associated renal failure frequently presents with signs of microangiopathic hemolytic anemia; renal failure is usually delayed but occasionally, it may be rapidly progressive despite drug discontinuance. Cisplatin nephrotoxicity is clearly dose-related and used to be considered dose limiting. Renal insufficiency can be prevented by hydration and forced diuresis; in addition, hyperhydration with mannitol-induced saline diuresis may allow administration of high doses and thus circumvent the dose-limiting effect of cisplatin-induced renal toxicity. Cisplatin-induced renal magnesium wasting occurs frequently and should be supplemented. Other approaches to reduce cisplatin nephrotoxicity are currently under investigation and are discussed.

Animals↗

PubMed1988

Triazinate and platinum efficacy in combination with 5-fluorouracil and doxorubicin: results of a three-arm randomized trial in metastatic gastric cancer. Gastrointestinal Tumor Study Group.

The Gastrointestinal Tumor Study Group compared three regimens in a controlled prospectively randomized trial for the treatment of patients with advanced gastric cancer. All regimens contained 5-fluorouracil and doxorubicin (FA) but differed in the third drug: semustine (Me), triazinate (T), or cisplatin (P). FAT produced significantly superior overall survival (P less than .01) compared to FAMe. One-year survival rate for the FAT regimen was 30% compared to 15% for the FAMe regimen, and median survival times were 30 versus 24 weeks, respectively. The FAP regimen demonstrated a similar survival advantage compared to the FAMe regimen. The improved survival was observed despite decreased 5-fluorouracil and doxorubicin dosages for patients on the FAT and FAP arms. Severe toxicity rates were 42% for FAT, 69% for FAP, and 62% for FAMe. The FAT regimen produced significantly less hematologic toxicity than either FAP or FAMe, while mild neurotoxicity was the limiting toxicity of cisplatin in this study. Two classes of drugs, without known risks of potentially fatal long-term toxic effects, appear to be effective substitutes for long-acting alkylating agents such as Me or mitomycin in the treatment of advanced gastric cancer. These findings identify new approaches to therapy for this common disease.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2005

Research on the anti-tumour effect of steroid lactam alkylator (NSC-294859) in comparison with conventional chemotherapeutics in malignant melanoma.

Evidence indicating that hybrid steroid compounds of anti-cancer agents produce reduced toxicity, significantly lower than the cytotoxic components alone, and increased anti-cancer activity has prompted the design and development of such steroids, mostly alkylating esters. We investigated the in-vitro and in-vivo activity of a homo-aza-steroidal alkylating ester (HASE), in comparison with dacarbazine (DTIC), cisplatin (CPDD), carmustine (BCNU) and semustine (MeCCNU), in the treatment of malignant melanoma. Cytotoxicity was assessed in vitro by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay using a panel of six human malignant melanoma cell lines, with or without the presence of rat liver microsome assay. B16 melanoma-bearing mice were used to evaluate in vivo the anti-tumour activity of the tested compounds. In all cases of in-vitro screening, HASE displayed a significantly higher (P<0.0001) cytostatic and cytotoxic effect than DTIC, BCNU and MeCCNU, but produced significantly lower (P<0.0001) activity than CPDD. HASE exhibited a significantly smaller range than CPDD between concentration levels that produced growth arrest and those that induced a cytotoxic effect against melanoma cells in vitro. The anti-tumour activity of HASE in B16 melanoma-bearing mice, as determined by tumour growth rate inhibition (<42%) and percentage survival prolongation (treated versus control, 167%), was significantly superior (P<0.001) to that achieved by DTIC, BCNU and MeCCNU and was equal to that of CPDD. HASE exhibited a toxicity similar to that of DTIC, BCNU and MeCCNU, but significantly lower than that of CPDD. It can be concluded that HASE displays significant in-vitro and in-vivo activity in the treatment of melanoma.

Animals↗

PubMed1993

Mitomycin therapy in gastric cancer.

Adenocarcinoma of the stomach remains a significant cause of mortality worldwide. The majority of patients present with stage III or IV disease, negating surgery as a curative option. Numerous drugs have been tested over the past 2 decades in single-agent and combination chemotherapy trials. Given by intravenous bolus, mitomycin has induced responses as high as 63% and as low as 24% in patients with various gastrointestinal malignancies. Mitomycin has also demonstrated efficacy when given in combination with doxorubicin and in the three-drug regimen FAM (5-fluorouracil/doxorubicin/mitomycin). FAM has been explored in multiple phase II and III trials and has become the standard with which many new combinations are compared. Compared with other doxorubicin-containing regimens, it has demonstrated the longest median survival (29.5 weeks) and the lowest incidence of severe toxicity. The addition of semustine or leucovorin to FAM has yielded responses comparable with those attained by FAM alone. In Japan, where treatment of gastric cancer has been more successful, possibly due to earlier diagnosis and more aggressive surgical approaches, mitomycin has been given intraperitoneally during surgery and postoperatively in combination with fluorinated pyrimidines or other agents. Mitomycin will undoubtedly play a role in the development of new approaches to the treatment of gastric cancer.

Adenocarcinoma↗

PubMed2004

Impact of T and N stage and treatment on survival and relapse in adjuvant rectal cancer: a pooled analysis.

PURPOSE: To determine survival and relapse rates by T and N stage and treatment method in five randomized phase III North American rectal adjuvant studies. PATIENTS AND METHODS: Data were pooled from 3,791 eligible patients enrolled onto North Central Cancer Treatment Group (NCCTG) 79-47-51, NCCTG 86-47-51, US Gastrointestinal Intergroup 0114, National Surgical Adjuvant Breast and Bowel Project (NSABP) R01, and NSABP R02. Surgery alone (S) was the treatment arm in 179 patients. The remaining patients received adjuvant treatment as follows: irradiation (RT) alone (n = 281), RT + fluorouracil (FU) +/- semustine bolus chemotherapy (CT; n = 779), RT + protracted venous infusion CT (n = 325), RT + FU +/- leucovorin or levamisole bolus CT (n = 1,695), or CT alone (n = 532). Five-year follow-up was available in 94% of surviving patients, and 8-year follow-up, in 62%. RESULTS: Overall (OS) and disease-free survival were dependent on TN stage, NT stage, and treatment method. Even among N2 patients, T substage influenced 5-year OS (T1-2, 67%; T3, 44%; T4, 37%; P <.001). Three risk groups of patients were defined: (1) intermediate (T1-2/N1, T3/N0), (2) moderately high (T1-2/N2, T3/N1, T4/N0), and (3) high (T3/N2, T4/N1, T4/N2). For intermediate-risk patients, those receiving S plus CT had 5-year OS rates of 85% (T1-2/N1) and 84% (T3/N0), which was similar to results with S plus RT plus CT (T1-2/N1, 78% to 83%; T3/N0, 74% to 80%). For moderately high-risk lesions, 5-year OS ranged from 43% to 70% with S plus CT, and 44% to 80% with S plus RT plus CT. For high-risk lesions, 5-year OS ranged from 25% to 45% with S plus CT, and 29% to 57% with S plus RT plus CT. CONCLUSION: Different treatment strategies may be indicated for intermediate-risk versus moderately high- or high-risk patients based on differential survival rates and rates of relapse. Use of trimodality treatment for all patients with intermediate-risk lesions may be excessive, since S plus CT resulted in 5-year OS of approximately 85%; however, 5-year disease-free survival rates with S plus CT were 78% (T1-2/N1) and 69%(T3/N0), indicating room for improvement.

Adult↗

PubMed2001

Anticancer drug-induced kidney disorders.

Nephrotoxicity is an inherent adverse effect of certain anticancer drugs. Renal dysfunction can be categorised as prerenal uraemia, intrinsic damage or postrenal uraemia according to the underlying pathophysiological process. Renal hypoperfusion promulgates prerenal uraemia. Intrinsic renal damage results from prolonged hypoperfusion, exposure to exogenous or endogenous nephrotoxins, renotubular precipitation of xenobiotics or endogenous compounds, renovascular obstruction, glomerular disease, renal microvascular damage or disease, and tubulointerstitial damage or disease. Postrenal uraemia is a consequence of clinically significant urinary tract obstruction. Clinical signs of nephrotoxicity and methods used to assess renal function are discussed. Mechanisms of chemotherapy-induced renal dysfunction generally include damage to vasculature or structures of the kidneys, haemolytic uraemic syndrome and prerenal perfusion deficits. Patients with cancer are frequently at risk of renal impairment secondary to disease-related and iatrogenic causes. This article reviews the incidence, presentation, prevention and management of anticancer drug-induced renal dysfunction. Dose-related nephrotoxicity subsequent to administration of certain chloroethylnitrosourea compounds (carmustine, semustine and streptozocin) is commonly heralded by increased serum creatinine levels, uraemia and proteinuria. Additional signs of streptozocin-induced nephrotoxicity include hypophosphataemia, hypokalaemia, hypouricaemia, renal tubular acidosis, glucosuria, aceturia and aminoaciduria. Cisplatin and carboplatin cause dose-related renal dysfunction. In addition to increased serum creatinine levels and uraemia, electrolyte abnormalities, such as hypomagnesaemia and hypokalaemia, are commonly reported adverse effects. Rarely, cisplatin has been implicated as the underlying cause of haemolytic uraemic syndrome. Pharmaceutical antidotes to cisplatin-induced nephrotoxicity include amifostine, sodium thiosulfate and diethyldithiocarbamate. Dose- and age-related proximal tubular damage is an adverse effect of ifosfamide. In addition to renal wasting of electrolytes, glucose and amino acids, Fanconi syndrome, rickets and osteomalacia have occurred with ifosfamide treatment. High dose azacitidine causes renal dysfunction manifested by tubular acidosis, polyuria and increased urinary excretion of electrolytes, glucose and amino acids. Haemolytic uraemia is a rare adverse effect of gemcitabine. Methotrexate can cause increased serum creatinine levels, uraemia and haematuria. Acute renal failure is reported following administration of high dose methotrexate. Urinary alkalisation and hydration confer protection against methotrexate-induced renal dysfunction. Dose-related nephrotoxicity, including acute renal failure, are reported subsequent to treatment with pentostatin and diaziquone. Acute renal failure is a rare adverse effect of treatment with interferon-alpha. Haemolytic uraemic syndrome occurs with mitomycin administration. A mortality rate of 50 to 100% is reported in patients developing mitomycin-induced haemolytic uraemic syndrome. Capillary leak syndrome occurring with aldesleukin therapy can cause renal dysfunction. Infusion-related hypotension during infusion of high dose carmustine can precipitate renal dysfunction.

Antimetabolites, Antineoplastic↗

PubMed2003

[Whole-brain radiotherapy combined with COAPC regimen in patients with non-small cell lung cancer].

BACKGROUND & OBJECTIVE: The main treatment strategy of cancer patients with brain metastases was irradiation; while so far there were few researches concerning chemotherapy combined with radiotherapy for these patients. This study was designed to observe the therapeutic effect, toxicity, and survival of concurrent whole-brain radiotherapy (WBRT) combined chemotherapy with COAPC regimen in non-small cell lung cancer (NSCLC) patients with brain metastases. METHODS: A total of 45 NSCLC patients with brain metastasis received a course of COAPC regimen [cyclophosphamide 0.3 mg/m(2) i.v. d(1), vincristine 1.4 mg/m(2) i.v. d(1), doxorubicin 50 mg/m(2) i.v. d(1), cisplatin 20 mg/m(2) i.v. d(1-5), semustine 80 mg/m(2) PO d(1)] every 3-4 weeks. Whole-brain radiotherapy was administered on day 6 of the first course of chemotherapy using (60)Co at a dose of 2 Gy given in 5 fractions per week. Patients with brain lesions of 1-3 received WBRT at a dose of 40 Gy and then small field to a total dose of 60 Gy. Patients with brain lesions of more than 3 received WBRT at a total dose of 40 Gy. RESULTS: The treatment improved neurological symptoms in 80% of the patients. The response rates to brain lesions and primary lesions were 64.4% and 40.0%, respectively. The median survival time (MST) was 10 months. The 1-year and 5-year survival rates were 44.1% and 6.7%, respectively. The MST in the patients with brain metastasis was only 14 months,which was longer than the MST of 9 months in the patients with other metastasis sites(P=0.012). CONCLUSION: Concurrent WBRT and chemotherapy can be safely preformed for the patients with brain metastasis from NSCLC with a remarkable response rate and encouraging survival duration.

Adult↗

PubMed2005

Gateways to clinical trials.

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables have been retrieved from the Clinical Trials Knowledge Area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: (-)-Epigallocatechin gallate, (Z)-4-hydroxytamoxifen; Ad.muIFN-beta AD-237, adalimumab, adefovir dipivoxil, agalsidase alfa, alemtuzumab, almotriptan, ALVAC vCP1452, alvimopan hydrate, ambrisentan, anakinra, anti-IFN-gamma MAb; Bimatoprost, BMS-188797, BMS-214662, bortezomib, bosentan, bovine lactoferrin; Caffeine, canertinib dihydrochloride, canfosfamide hydrochloride, cannabidiol, caspofungin acetate, cetuximab, cH36, ChimeriVax-JE, ciclesonide, cilansetron, cinacalcet hydrochloride, clopidogrel, CpG-7909, Cypher; Daptomycin, darbepoetin alfa, darifenacin hydrobromide, decitabine, denufosol tetrasodium, Dexamet, diindolemethane, drotrecogin alfa (activated), duloxetine hydrochloride, DX-9065a; E-7010, edaravone, efalizumab, eicosapentaenoic acid/docosahexaenoic acid, elacridar, eletriptan, emtricitabine, epratuzumab, erlotinib hydrochloride, ertapenem sodium, eszopiclone, everolimus, ezetimibe; Fludarabine, fondaparinux sodium; gamma-Hydroxybutyrate sodium, gavestinel sodium, gefitinib, granisetron-Biochronomer; Human Albumin, human insulin; Imatinib mesylate, indiplon, interleukin-2 XL, isatoribine, ISS-1018, i.v. gamma-globulin, ivabradine hydrochloride, ixabepilone; Lanthanum carbonate, L-arginine hydrochloride, liposomal doxorubicin, LY-450139; Magnesium sulfate, melatonin, motexafin gadolinium, mycophenolic acid sodium salt; Natalizumab, nesiritide, niacin/lovastatin; OGX-011, olmesartan medoxomil, omalizumab, ospemifene; PACAP38, panitumumab, parathyroid hormone (human recombinant), parecoxib sodium, patupilone, pegfilgrastim, peginterferon alfa-2a, peginterferon alfa-2b, peginterferon alfa-2b/ribavirin, pemetrexed disodium, pimecrolimus, pirfenidone, posaconazole, prasterone, pregabalin; R-112, ramelteon, ranolazine, rasagiline mesilate, rebimastat, roflumilast, rosuvastatin calcium, rotigotine hydrochloride, rupatadine fumarate; S-3013, S-3304, semustine, sitaxsentan sodium, St. John's Wort extract; Tadalafil, tamoxifen, Taxus, Tc-99m-EDDA-HYNIC-TOC, TH-9507, tiotropium bromide, tipifarnib, tocilizumab, tolvaptan, torcetrapib, TR-14035, tramadol hydrochloride/acetaminophen, treprostinil diethanolamine, troglitazone, troxacitabine; Valdecoxib, valganciclovir hydrochloride, vandetanib, vardenafil hydrochloride hydrate, VAS-991, veglin, vinflunine, voriconazole; White sweet potato extract; Ximelagatran.

Clinical Trials as Topic↗

PubMed1991

Systemic therapy for colorectal cancer: an overview.

The systemic management of patients with colorectal cancer continues to center on the use of 5-fluorouracil (5-FU). In the setting of metastatic disease, parenteral 5-FU has been shown to be superior to oral 5-FU; however, survival duration seems similar regardless of whether parenteral 5-FU is administered in a "loading schedule," weekly, or in a continuous-infusion regimen. The addition of other cytotoxic agents, such as semustine (methyl-CCNU) and/or mitomycin C, to 5-FU does not appear to be beneficial. Recent efforts have been directed toward enhancing the activity of 5-FU by (1) increasing its incorporation into RNA through pretreatment with methotrexate or phosphonoacetyl-L-aspartate (PALA), (2) enhancing DNA synthesis inhibition via the concomitant administration of folinic acid, and (3) an undetermined modulatory action by the addition of alpha-interferon. These pharmacologic approaches are being compared in ongoing cooperative group trials. The results of five randomized trials assessing the value of intra-arterial, hepatic infusions of 5-FU or 5-fluorodeoxyuridine have demonstrated that regional chemotherapy increases the likelihood of a hepatic response when compared with systemic treatment, but has little effect on survival and is associated with significant toxicity. Recent adjuvant chemotherapy trials have indicated both a decrease in recurrence and a prolongation in survival when chemotherapy (5-FU + levamisole) is administered to patients with stage C colon cancer; and combined radiation therapy and chemotherapy is given to patients with stages B2 and C rectal cancer.

Chemotherapy, Adjuvant↗