Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nutritional deficiencies are believed to be instrumental in producing reduced immune responses in a variety of animal species. Malnutrition may result in an increase or a decrease in immune functions, depending upon its degree, and also the timing and severity of the nutritional protein deprivation. Our experimental data suggest that there is a significant impairment of cytotoxic activity against K-562 and of the ability of spleen cells to produce interferon in protein-deprived mice in comparison with control mice. Paradoxically accelerated tumor growth after administration of OK-432 or Lentinan was also noted in protein-deficient tumor-bearing mice. In addition, a clinical randomized study of advanced or recurrent gastric cancer patients treated with MMC and FT(MF) with or without lentinan was performed. We recognized excellent end-point results only in the lentinan-treated patients with normal protein levels, while no effect of this agent was seen in patients with low serum protein levels (below 5.9/dl). Aggressive postoperative chemotherapy for cases with distant lymph node metastasis was performed under active nutritional support without any depression of metabolic and immunological states, resulting in a good 5-year survival rate (36.9%).
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PMID:[Anti-cancer effects of BRMs associated with nutrition in cancer patients]. 338 33

Immuno-chemotherapeutic effects on the growth of MM-48 mammary tumor were studied in syngeneic C3H/He mice fed diets containing a low (D), normal (N) or arginine-supplemented (NA) protein content. The serum protein levels were 5.7 g/dl in N-mice and 3.7 g/dl in D-mice, respectively. On the other hand, no difference was seen between the two groups, with regard to intra-tumoral protein concentrations. The natural killer (NK) activity of spleen cells was significantly lower in D-mice than in N-or NA-mice. Augmentation of NK activity was detected following the i.p. injection of OK-432 or LENTINAN, while no augmentation was recognized in D-mice. Interferon production of cultured spleen cells was significantly reduced in D-mice, and significantly increased in NA-mice compared with N-mice. NK activity was markedly augmented at 7 days after bilateral oophorectomy in N-mice. Both NK and IFN titers were significantly reduced following administration of estradiol every 7 days. The growth of MM-48 tumor was inhibited by daily administration of OK-432 or LENTINAN in N-mice. However, the tumor growth was paradoxically accelerated after administration of the same drugs in D-mice. These findings indicated that the nutritional or endocrine environment of cancer-bearing mice plays an important role in the effect of some kinds of BRMs. A clinical randomized study of advanced and recurrent gastric cancer patients treated with MMC and FT (MF) with or without LENTINAN, was then performed. We recognized excellent end-point results only in LENTINAN-administered patients with normal protein levels, while no effect of LENTINAN was seen in patients with low protein levels (below 6.0 g/dl).
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PMID:[Modulation of the anti-tumor effect of BRM under various nutritional or endocrine conditions]. 372 50

Combined chemotherapy of 5-FU and CDDP is useful for advanced or recurrent gastric cancer. To evaluate the efficacy of this chemotherapy, using human gastric carcinoma (NSC-30) maintained in the subcutaneous (sc) space in nude mice, we designed the following four experimental groups: 1) control group, 2) 5-FU group, 3) CDDP group, and 4) combined therapy group of 5-FU and CDDP (FP group). 5-FU (150 mg/kg) was injected into the intraperitoneal space for seven days using AlZet osmotic pumps. CDDP (9 mg/kg) was injected into the intraperitoneal space at one time. The tumor growth of drug administered groups was inhibited compared with the control group, especially in the FP group. Body weight and general condition of nude mice did not differ between groups. We also measured tumor concentrations of 5-FU and thymidylate synthetase (TS) total, free, inhibition rate between 5-FU group and FP group. The tumor 5-FU concentration of FP group was slightly higher than in 5-FU group, but the TS inhibition rate was almost the same. In conclusion, this combined therapy using Alzet osmotic pump is a useful drug sensitivity test as a conventional system.
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PMID:[Evaluation of combination chemotherapy with 5-FU and CDDP for human gastric carcinoma transplanted into nude mice]. 902 Sep 44

Palliation of inoperable stenotic gastric and/or duodenal cancer remains an open problem due to high operative mortality and diffuse tumor growth. We describe here in 3 cases of stenotic recurrent gastric cancer in the elderly successful treated using self-expanding metal stents.
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PMID:Self-expanding metal stents as palliative treatment of stenotic relapsed gastric cancer after curative surgery in the elderly. 1649 51

The prognosis for patients with unresectable advanced or recurrent gastric cancer remains poor. The identification of additional oncogenes with influences similar to those of epidermal growth factor receptor gene mutations, upon which the growth of cancer cells is dependent, is needed. In this study, we evaluated sensitivity to MEK inhibitors (GSK1120212 and PD0325901) in several gastric cancer cell lines in vitro and found three poorly differentiated gastric cancer cell lines that were hypersensitive to the inhibitors. The sequence analyses in these three cell lines revealed that one cell line had a novel MEK1 mutation, while the other two had previously reported KRAS and MEK1 mutations, respectively; the gene statuses of the other resistant cell lines were all wild-type. Experiments using MEK1 expression vectors demonstrated that the MEK1 mutations induced the phosphorylation of ERK1/2 and had a transforming potential, enhancing the tumorigenicity. The MEK inhibitor dramatically reduced the phosphorylation of ERK1/2 and induced apoptosis in the cell lines with MEK1 mutations. In vivo, tumor growth was also dramatically decreased by an inhibitor. One of the 46 gastric cancer clinical samples that were examined had a MEK1 mutation; this tumor had a poorly differentiated histology. Considering the addiction of cancer cells to active MEK1 mutations for proliferation, gastric cancer with such oncogenic MEK1 mutations might be suitable for targeted therapy with MEK inhibitors.
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PMID:MEK inhibitor for gastric cancer with MEK1 gene mutations. 2525 79

This report describes a case of recurrent gastric cancer successfully treated with S-1 oral administration. A 77-year old female patient underwent distal gastrectomy for gastric cancer, followed by adjuvant chemotherapy with tegafur-uracil (UFT). However, 1 year after surgical resection, recurrence in the lymph node of the hepatic hilum was diagnosed by abdominal computed tomography. The patient was treated with S-1 alone after refusing in travenous infusion chemotherapy. Three months after treatment, the size of the target lesion decreased significantly, and a complete response was seen on imaging examination during the 2 years of chemotherapy treatment. One year and 5 months after the discontinuation of chemotherapy, recurrence was noted again. Although supportive care was eventually provided to the patient, S-1 oral administration was resumed that resulted in tumor growth control for>6 months. In this patient, S-1 treatment was effective in tumor growth suppression without deteriorating the patient's quality of life (QOL). Further studies are needed to identify patients for whom S-1 therapy is optimal treatment.
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PMID:[A case of recurrent gastric cancer successfully treated with S-1 oral administration]. 2559 86