Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We attempted a new regimen of low-dose CPT-11 and PSK against a high age man with liver metastasis from gastric cancer. CPT-11 was administered at 20 mg/m2/day x 2/week, and PSK was given orally 3.0 g/day daily, respectively. Serum CEA level decreased gradually and almost reached normal limits (130 to 3.0 ng/ml). The tumor was reduced more than 50% at 13 weeks after the start of chemotherapy, when it had been continued for more than 8 weeks. There were no adverse effects and this regimen has been continued for more than 20 weeks without missing a week. These results suggest that the combination of low-dose CPT-11 and PSK has fewer side effects even in an elderly patient and may induce not only tumor shrinkage but also a prolonged time to progression.
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PMID:[Chemotherapy by combination of low-dose CPT-11 and PSK in an elderly man with liver metastasis from gastric cancer]. 1132 90

Side effects due to administration of anti-cancer drugs often cause the treatment to be abandoned or a decrease in the amount of anti-cancer drugs. Recently, the anti-tumor effects of "low-dose CPT-11", which can be administered at the outpatient clinic, are reported. We performed "low-dose CPT-11 + CDDP" as a neoadjuvant chemotherapy to a patient with advanced gastric cancer. CPT-11 and CDDP combination chemotherapy caused very few side effects, so we could continue the treatment and achieve anti-tumor effects. Consequently, surgery could be performed, but disseminated metastasis was found so that the surgery ended as a non-curative operation. However, it was considered that this method of "low-dose CPT-11 + CDDP" was very effective as the neoadjuvant chemotherapy in a patient with advanced gastric cancer.
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PMID:[A case of advanced gastric cancer treated with neoadjuvant chemotherapy of low-dose CPT-11 + CDDP]. 1143 51

Levofolinate and fluorouracil regimen (l-leucovorin and 5 fluorouracil regimen) is a biochemical modulation of 5 fluorouracil (5FU) by leucovorin (LV). In the USA and Europe d,l-LV and 5FU regimen is frequently administered for colorectal cancer treatment and recognized as the standard regimen. In Japan, multi-institutional clinical trials of l-leucovorin (l-LV), a bioactive diastereomer of leucovorin, and 5FU combination were conducted for the treatment of advanced gastrointestinal cancer with comparable results to the US/Europe data. This l-LV and 5FU regimen was approved in August 1999 for the indications of advanced gastric cancer and colorectal cancer. The dosage and administration is referred to the weekly method developed at RPMI. Recently, the irinotecan (CPT-11) or oxariplatin plus LV and 5FU combination showed higher antitumor activities than the LV and 5FU combination with increased progression-free survival. These regimens, however, are not yet properly established because clinical trial results with Japanese patients are not completed for agreement of the dosage and administration schedule. For the l-LV and 5FU regimen diarrhea and leukocytopenia, including grade 3 and higher, were reported as the major adverse events. Administration for eligible patients with periodical monitoring of diagnostic data is necessary.
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PMID:[Levofolinate and fluorouracil combination therapy]. 1157 62

We studied the pharmacokinetics of the intraperitoneal administration of CPT-11 for four patients with peritoneal metastasis (2 gastric cancer cases, 2 colon cancer cases). CPT-11 was administrated in a dose of 40-60 mg and the intraperitoneal and serum levels of CPT-11, SN-38 and SN-38 glucuronized (SN-38 Glu) were measured periodically. Intraperitoneal therapy with CPT-11 was effective for the control of malignant ascites. No serious side effects were observed. The levels of CPT-11, SN-38 were no different 30 min afterwards the administration of CPT-11 either intraperitoneally or intravenously. The high concentration of CPT-11 was achieved with intraperitoneal therapy and a small fraction of CPT-11 changed into SN-38 in the abdominal cavity.
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PMID:[Pharmacokinetic study of the intraperitoneal administration of CPT-11 for patients with peritoneal seedings of gastric and colonic cancers]. 1170 65

We examined the role of neoadjuvant therapy in downstaging locally advanced gastric cancer. Preoperative staging was performed with a combination of CT scans, endoscopic ultrasonography and/or laparoscopy, and laparoscopic ultrasonography. Patients with T > or =3 tumors and/or node-positive disease by preoperative clinical staging were eligible for entry. Neoadjuvant therapy consisted of two cycles of CPT-11 (75 mg/m(2)) with cisplatin (25 mg/m(2)) weekly four times every 6 weeks. This was followed by resection with D2 lymph node dissection and two cycles of intraperitoneal chemotherapy with floxuridine and cisplatin. Twenty-two patients were entered into the study (4 with T3N0 disease and 18 with T3N1 disease). Induction chemotherapy was well tolerated with major toxicities being neutropenia and diarrhea. A median of 78%/75% of the planned dosage of CPT-11/cisplatin was delivered. Two patients withdrew consent during the first cycle and were lost to follow-up. One patient progressed to stage IV disease during induction chemotherapy and did not undergo surgery. Nineteen patients underwent surgery. One patient had undetected stage IV disease (liver) and underwent a palliative R2 resection. Of the 18 remaining patients, 17 had curative R0 resections and one had a palliative R1 resection. A median of 21 lymph nodes (range 1 to 121) were examined histologically. There was one postoperative death. Surgical morbidity did not appear to increase after the neoadjuvant regimen. The median postoperative length of hospital stay was 9 days (range 3 to 75 days). Postoperative pathologic staging yielded 16% T3 lesions compared to 85% before treatment based on clinical staging; postoperative American Joint Committee on Cancer staging yielded 37% stage IIIA disease compared to 70% stage IIIA before treatment. With a median follow-up of 15 months, median survival has not yet been reached. We conclude that CPT-11-based neoadjuvant therapy downstages locally advanced gastric cancer. Further follow-up is necessary to determine the ultimate impact of this combination therapy on recurrence and survival.
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PMID:Neoadjuvant chemotherapy with CPT-11 and cisplatin downstages locally advanced gastric cancer. 1199 7

Gastrointestinal tumors are among the most common cancers in the world. Palliative chemotherapy is widely used to treat patients with advanced or metastatic disease. The mainstay of chemotherapy for colorectal cancer is 5-fluorouracil (5-FU) modulated by leucovorin (LV), alone or in combination with oxaliplatin or irinotecan (CPT-11). Gemcitabine is currently the standard of care in patients with pancreatic cancer. There is no standard in gastric cancer, although cisplatin, 5-FU, and the anthracyclines are the most common drugs used. Pemetrexed, a new-generation antifolate antimetabolite, has demonstrated a 15% to 17% response rate in metastatic colorectal cancer, similar to those of other single agents in previously untreated patients. In patients with advanced pancreatic cancer, pemetrexed achieved a 6% response rate and a 28% 1-year survival rate, which is comparable to single-agent gemcitabine. Preliminary results in gastric cancer are encouraging. The generally mild side effect profile of pemetrexed, especially with folate supplementation and dexamethasone premedication, and the synergy between pemetrexed and drugs frequently used in gastrointestinal cancers, such as irinotecan, oxaliplatin, and gemcitabine, suggest that further clinical studies are indicated to determine the role of pemetrexed in the treatment of colorectal, pancreatic, and gastric cancers.
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PMID:Pemetrexed in patients with gastrointestinal carcinoma. 1202 92

Today, no effective chemotherapy regimen has been established for non-resectable or postoperative recurrent gastric cancer, and most such therapy seems to be palliative. Thus, a highly effective chemotherapy that allows good patient QOL is desired. We report three gastric cancer patients responding to chronomodulation chemotherapy (tegafur + cisplatin + Isovorin) based on circadian rhythms plus a new antitumor drug, CPT-11. The treatment protocol was tegafur 1,200 mg/body, days 1-12 (continuing 16 h, intravenously with 800 mg/body from 16 to 24 h, 400 mg/body from 24-8 h, for non-uniform administration), cisplatin 10 mg/body, days 1-5, 8-12, (16 h, one shot infusion), Isovorin 25 mg/body, days 1-5, 8-12 (16 h, one shot infusion), followed by CPT-11 100 mg/body, days 13 (one shot infusion). We performed 1 or 2 courses, and with 2 courses the CPT-11 dose was increased to 150 mg/body. The first patient was a 54-year-old female with advanced type 3 gastric cancer with liver metastasis (H3). After chemotherapy (2 courses), there was a 30% reduction in the advanced gastric cancer and a 95% reduction in the liver metastasis. The second patient was a 73-year-old male with recurrent type 1 gastric cancer in the remnant stomach 24 months after partial gastrectomy. After chemotherapy (1 course), there was a 45% reduction in advanced gastric recurrent cancer. The third patient was a 67-year-old male with advanced type 2 plus 3 gastric cancers with liver (H3) and abdominal lymph node metastases. After chemotherapy (1 course), there was a 70% reduction in the type 2 and 55% reduction in the type 3 advanced gastric cancer, and a 50% reduction in the liver metastasis and 35% reduction in the abdominal lymph node metastasis. The only adverse effect was grade 2 pancytopenia, gastrointestinal disorder, and alopecia. In conclusion, this regimen resulted in good intrachemotherapeutic QOL and was highly effective in advanced gastric cancer patients.
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PMID:[Three patients with advanced nonresectable and recurrent gastric cancer responding to chronomodulation chemotherapy with tegafur + cisplatin + isovorin followed by CPT-11 administration]. 1221 74

The anti-metastatic efficacy of MMI-166, which is a selective matrix metalloproteinase (MMP) inhibitor, in combination with CPT-11 was examined using two metastasis models of human gastrointestinal cancer cells. In the liver metastasis model, C-IH human colon cancer cells were injected into the spleen of athymic BALB/c nude mice. Daily oral (p.o.) dosing of MMI-166 at 200 mg/kg starting 1 day after tumor inoculation led to a significantly prolonged survival effect by inhibiting liver metastasis of C-1H tumor cells. CPT-11 (5 or 20 mg/kg) was administered intraperitoneally (i.p.) three times on day 3, day 7 and day 11 and also improved the survival of tumor-inoculated mice compared with the vehicle control. When MMI-166 was combined with CPT-11, the anti-metastatic efficacy was significantly augmented. Moreover, long tumor-free survival was noted in two of eight mice that were given the combination therapy but not either MMI-166 or CPT-11 monotherapy. In the peritoneal dissemination model, TMK-1 human gastric cancer cells were injected i.p. into nude mice. While both MMI-166, administered daily p.o. from day 1 at 200 mg/kg, and CPT-11, administered intravenously (i.v.) three times, inhibited the tumor dissemination and growth, the combination therapy of MMI-166 plus CPT-11 showed a greater inhibitory effect than each monotherapy. A hematotoxicity study demonstrated that CPT-11 alone significantly decreased the number of white blood cells (WBC) and bone marrow cells (BMC) in the mice during treatment, while the daily administration of MMI-166 alone had no such effect. More importantly, the combination therapy of MMI-166 with CPT-11 did not augment the hematotoxicity caused by CPT-11. An in vitro cytotoxicity study showed that MMI-166 itself neither has direct cytotoxicity in C-1H and TMK-1 tumor cells, nor does it augment the cytotoxicity of SN-38, an active form of CPT-11. The findings indicate that the augmented anti-metastatic efficacy in combination treatment was not simply due to the augmentation of direct cytotoxic activity, but was rather an additive or synergistic effect of anti-metastatic activities with different mechanisms. In conclusion, we demonstrated that the anti-metastatic efficacy against C-1H colon cancer and TMK-1 gastric cancer were augmented by the combination therapy of MMI-166, an orally active MMP inhibitor, with CPT-11. However, the hematotoxicity caused by CPT-11 was not augmented in the combination with MMI-166. Thus, the combination therapy of MMI-166 and CPT-11 exhibited potent anti-metastatic efficacy without increased hematotoxicity. These results point to the clinical advantage of using MMI-166 in combination with CPT-11.
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PMID:Augmented anti-metastatic efficacy of a selective matrix metalloproteinase inhibitor, MMI-166, in combination with CPT-11. 1240 89

A case of AFP-producing gastric cancer successfully treated with CPT-11 and cisplatin combined therapy is reported together with a review of the literature. A 52-year-old male was admitted with complaints of upper abdominal pain and body weight loss. Gastric cancer with multiple liver metastases was diagnosed based on endoscopy and computed tomography findings. The patient's serum AFP level was 697,100 ng/ml and a biopsy specimen showed AFP-positive tumor cells immunohistochemically. He was treated with a combination chemotherapy consisting of CPT-11 (70 mg/m2) on day 1 and 15, and cisplatin (80 mg/m2) on day 1, repeated every 4 weeks. The primary lesion of the stomach and the liver metastases were remarkably reduced, and the serum level of AFP decreased to 18 ng/ml after 5 cycles of this treatment. No severe side effects were seen during this treatment. This result suggests that combination chemotherapy consisting of CPT-11 and cisplatin may be effective and safe for patients with AFP-producing gastric cancer with multiple liver metastases.
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PMID:[A case of AFP-producing gastric cancer with multiple liver metastases responding to CPT-11 and cisplatin combination chemotherapy]. 1246 1

We studied the pharmacokinetics of CPT-11 with intraperitoneal administration in a patient with a PTCD tube. The patient had advanced gastric cancer with peritoneal metastasis. CPT-11 was administrated in a dose of 40 mg and the intraperitoneal, plasma and bile levels of CPT-11, SN-38 and SN-38 glucuronide (SN-38 GLU) were measured periodically. The results showed that the periodical concentration pattern of CPT-11, SN-38 and SN-38 GLU in the bile was closely related to that of CPT-11 in the abdominal cavity.
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PMID:[Pharmacokinetic study of CPT-11, SN-38 and SN-38 glucuronide in the ascites, plasma and bile after intraperitoneal administration of CPT-11]. 1248 33


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