Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bombesin (BBS) is proved to have a wide variety of the pharmacologic effects, including effects on the release of gastrointestinal hormones and control of gastrointestinal motility. More recently, the role of BBS in tumor growth, cellular proliferation and inflammation has attracted attention. There is evidence that increased BBS receptor expression may be considered as a specific marker for small-cell lung cancer, colorectal adenocarcinoma, gastric and pancreatic cancer, prostate, ovarian and breast cancer, neuroblastoma, renal cell carcinoma, malignant melanoma and thyroid carcinoma. BBS expression was found to be correlated with the histological grade of the tumor. Similarly, BBS treatment significantly improves the healing of chronic gastric ulcers and ameliorates the severity of burn- or colitis-induced gut injury. Although there is much complexity still to be elucidated to understand fully the physiologic and pathologic roles of BBS-like peptides several clinical or experimental trials have addressed that circulating or tissue levels of BBS-like peptides or their receptor expression may be used as diagnostic or prognostic markers of neoplastic disease, and incorporation of BBS receptor antagonists in the treatment of human cancer could provide substantial benefit to the cancer patients. Moreover, trophic, anti-ulcerogenic and anti-inflammatory actions of exogenous BBS make this peptide a potential supplement in minimizing or reversing tissue damage against several injurious challenges. In conclusion, based on the evidence summarized herein, related to the mitogenic and anti-inflammatory effects of BBS-like peptides, further investigations are needed to derive the benefit of BBS-like peptides in pharmacologic strategies.
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PMID:Bombesin-like peptides: candidates as diagnostic and therapeutic tools. 1267 68

Virulizin is a novel biological response modifier (BRM) approved for the treatment of melanoma and is currently in a phase III clinical trial against advanced pancreatic cancer. The purpose of this study was to define the anti-cancer activity of Virulizin against a number of solid human tumors. The therapeutic effect of Virulizin was evaluated in mouse xenograft models, and the results demonstrate that Virulizin has high efficacy against breast, ovarian and prostate tumor xenografts. Seventy-seven percent inhibition, with an optimal T/C value of 24.8%, was observed in human beast MDA-MB-231 xenografts treated with Virulizin as compared to saline-treated controls (p=0.0004). In human ovarian SK-OV-3 tumor xenografts, administration of Virulizin inhibited tumor growth by 77.6% compared to saline controls (p=0.0439). Furthermore, high anti-tumor activity was also demonstrated in DU145 and PC-3 prostate tumor xenografts, as indicated by 72.6 and 49.1% suppression of tumor growth (versus saline controls, p=0.0007 or p=0.0049), respectively. Direct comparisons with the anti-tumor activities of conventional drugs demonstrated that Virulizin has higher or equal efficacy against all four tumors tested. Finally, addition of Virulizin into co-cultures of tumor cells and macrophages stimulated the cytolytic activity of the macrophages against the tumor cells in a dose-dependent manner. This result suggests that stimulation of immune cells is at least part of the anti-tumor mechanism of action of Virulizin. These results clearly demonstrate that Virulizin inhibits the growth of human breast, ovarian and prostate tumors, indicating great potential for expansion of the clinical indications for this novel BRM.
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PMID:Preclinical efficacy of Virulizin in human breast, ovarian and prostate tumor models. 1267 33

FMNL (NM_005892.2) is a 5'-truncated partial cDNA encoding a Formin-homology protein related to DAAM1, DAAM2, DIAPH1 and DIAPH2. Here, we identified three members of FMNL gene family in the human genome by using bioinformatics. FMNL1 gene, corresponding to 5'-truncated KW-13 and FMNL cDNAs, was located within reference genomic contig NT_010748.9 (nucleotide position 100576-125849, forward orientation). FMNL2 gene, corresponding to KIAA1902 and FHOD2 cDNAs, was located within NT_005151.10 (nucleotide position 122465-436828, forward orientation). FMNL3 gene, corresponding to 5'-truncated DKFZp762B245 and KIAA2014 cDNAs, was located within NT_026397.10 (nucleotide position 209769-279037, reverse orientation). FMNL1, FMNL2 and FMNL3 genes encode A and B isoforms with the C-terminal divergence due to alternative splicing (cassette splicing of exon 26). FMNL1A (1100 aa), FMNL1B (1114 aa), FMNL2A (1087 aa), FMNL2B (1093 aa), FMNL3A (1028 aa) and FMNL3B (1027 aa) consist of FDD, FH1 and FH2 domains. Total amino-acid identity were as follows: FMNL1A vs. FMNL2A, 59.3%; FMNL1A vs. FMNL3A, 56.1%; FMNL2A vs. FMNL3A, 68.6%. FMNL1 gene was mapped to human chromosome 17q21. FMNL2 gene was linked to FNBP3/HYPA gene on chromosome 2q23.3, while FMNL3 gene was linked to FNBP3L/HYPC gene on chromosome 12q13. FMNL1 mRNA was expressed in natural killer cells, Burkitt lymphoma, pancreatic cancer, prostate cancer, and lung large cell carcinoma, FMNL2 mRNA in several normal tissues, diffuse-type gastric cancer, breast cancer, chondrosarcoma, melanoma, and glioblastoma, and FMNL3 mRNA in gastric cancer. FMNL1, FMNL2 and FMNL3 might be implicated in polarity control, invasion, migration, or metastasis through regulation of the Rho-related signaling pathway.
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PMID:Identification and characterization of human FMNL1, FMNL2 and FMNL3 genes in silico. 1268 86

Troxacitabine [BCH 4556; SPD 758; Troxatyl] is a DNA synthesis inhibitor. This profile has been selected from R&D Insight, a pharmaceutical intelligence database produced by Adis International Ltd. It is a member of a novel class of nucleoside analogues discovered by BioChem Pharma and is the first example of a synthetic L-nucleoside analogue to have shown anticancer activity in animal models. On 11 May 2001, BioChem Pharma was acquired by, and integrated into, Shire Pharmaceuticals Group. In February 2002 Shire announced that it intended to pursue development of troxacitabine as a treatment for solid tumours. In addition, Shire indicated that it would pursue the drug's development for acute myeloid leukaemia. In March 1999, phase II trials were initiated to investigate the efficacy and tolerability of troxacitabine in a variety of solid tumours including pancreas, prostate, colorectal, renal and non-small cell lung cancers and melanoma. The trials were conducted throughout North America and were closed to patient accrual in 2000. Two phase I combination chemotherapy trials in solid tumours (one with cisplatin and another with paclitaxel) have been initiated. One of these trials is in patients with pancreatic cancer. A phase III trial in patients with pancreatic cancer is expected to begin during the second or third quarter of 2003. In addition, further clinical development was initiated in May 2000, in the form of a combination chemotherapy trial in patients with acute leukaemia. A phase II trial in patients with acute myeloid leukaemia (AML) and chronic myeloid leukaemia-blast phase (CML-BP) has reported that troxacitabine demonstrated significant activity in these cancers. However, Shire indicated that no further development for CML-BP will be conducted. The company indicated that it would focus future development in the haematological malignancy area on AML and has initiated an exploratory phase III trial of troxacitabine in previously untreated patients with poor prognosis AML. The study will compare troxacitabine in combination with either cytarabine or idarubicin, with a control drug regimen. The aim is to identify the most promising treatment regimens in a relatively small number of patients before commencing the larger pivotal trial. A pivotal phase III trial is expected to begin in the first half of 2003. In September 2002, Shire Pharmaceuticals forecast Troxatyl to reach peak sales of $US100-200 million, for the indications of pancreatic cancer and myeloid leukaemia.
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PMID:Troxacitabine: BCH 4556, SPD 758, Troxatyl. 1284 94

The HCA587 gene, identified by serological analysis of recombinant cDNA expression library (SEREX) from a hepatocellular carcinoma (HCC) patient, encodes a new member of cancer-testis antigens. HCA587 mRNA expression in normal tissues and cancers has been previously reported. To estimate its immunogenicity to induce immune response, it is essential to analyze HCA587 expression at the protein level. In this study anti-HCA587 polyclonal antibody, termed "TC-1," was generated, and the expression of HCA587 protein was assessed by immunohistochemical staining in a panel of normal and tumor tissue sections. No HCA587 protein was shown in normal tissues except germ cells in testis and Purkinji cells in cerebellum. In HCC specimens the HCA587 protein was expressed in 37.1% (26 of 70) samples. The expressed protein was either located in the cytoplasm or nucleus depending on the individual samples. More importantly, there appears to be correlation between the tumor differentiation of HCC and HCA587 protein expression, ie, the lower differentiation, the higher percentage of protein expression. Coincidentally, seroreactivity showed that the Ab specific to recombinant HCA587 protein was detected only in the sera of three patients with poorly differentiated HCCs. HCA587 antigen was also expressed in different proportions in melanoma, lymphoma, pancreatic cancer, and lung cancer.
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PMID:HCA587 antigen expression in normal tissues and cancers: correlation with tumor differentiation in hepatocellular carcinoma. 1292 Feb 47

There are numerous risk factors for the development of malignant melanoma. It has been documented that genetic predisposition exists but exogenous factors are also very important. In familial melanomas it has been well established that mutation in the CDKN2A gene which is located at chromosome 9 leads to a marked risk for malignant melanoma. This tumor-suppressor gene is important for the regulation of the cell cycle and mutation in this gene is associated also with an increased rate of pancreas cancer. The penetrance of this mutation is influenced by UV-energy. In addition it has been shown that a second cluster for the familial atypical nevus syndrome is located at chromosome 1p36. Patients with the rare disease xeroderma pigmentosum have a defect in the DNA-repair mechanism inherited in an autosomal recessive trait and therefore develop within the first 20 years of life numerous malignant skin tumours including malignant melanomas. But also in non-syndromic patients a decrease of DNA-repair ability may occur. It has been shown recently that reduced DNA-repair ability is an independent risk factor for malignant melanoma and may contribute to susceptibility to sunlight-induced melanoma among the general population. Other constitutional risk factors for the development of malignant melanoma are fair skin, red hair and blue eyes. The most important exogenous risk factor is UV-exposition. Extensive and repetitive sunburns before the age of 15 years are especially predisposing to malignant melanoma. The most important preventive measures are continuous sun-protection including avoidance of sun in noon time on tropical and subtropical places, wearing a hut and sunglasses and application of sun-screens with high sun-protection factor. Furthermore a regular check for changing moles is indicated in persons with multiple atypical nevi or a familial melanoma syndrome. Nowadays molecular genetic screenings are available within research projects for members of melanoma-prone families. The controversy of such possibilities is discussed.
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PMID:[Genetic counseling and DNA testing in patients with increased risks for malignant melanoma]. 1450 54

The major utilization of clinical PET is in oncology, and oncologic PET utilizes FDG as the radiopharmaceutical. FDG imaging demonstrates the increased metabolism by malignant cells compared to normal cells. The initial clinical application of FDG-PET was demonstrated in brain tumors, and the gradation of accumulation of FDG related to the degree of malignancy. Subsequent studies have documented the accuracy of FDG-PET in detecting and staging several different malignancies. Whole-body imaging has made a major impact on the ability of PET to document the distribution of malignancy.FDG-PET imaging is very accurate in determining if an indeterminate solitary pulmonary nodule is malignant and in staging lung cancer. The cost-effectiveness of PET has been demonstrated for these indications. Third-party payers have policies for paying for PET scans performed in the evaluation of solitary pulmonary nodules and in staging lung cancer. The preliminary data on the use of FDG-PET imaging in other malignancies supports its use in detecting liver metastases from colorectal cancer and differentiating fibrosis from recurrent tumor after therapy for colorectal cancer; staging the axilla in primary breast cancer; staging melanoma and lymphoma; and staging and detecting recurrence of head and neck cancer. The initial reports on the use of FDG-PET are encouraging in its use in musculoskeletal malignancy, ovarian cancer, pancreatic cancer, and thyroid cancer.
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PMID:Clinical PET in Oncology. 1451 5

Virulizin, a novel biological response modifier (BRM), has been demonstrated to have a high level of anti-tumor activity against pancreatic cancer and melanoma in many clinical trials and preclinical studies. However, its anti-tumor mechanism has not been fully elucidated. The purpose of this study was to define the mechanism of Virulizin anti-tumor activity in cultures and in a murine xenograft model. The presence of Virulizin stimulated in a dose-dependent manner the cytolytic activity against tumor cells by splenocytes and macrophages, but not by non-adherent splenocytes. The cytotoxic activity of macrophages was significantly increased (approximately 5-fold) in cultures containing 2.5% of Virulizin compared to that of cultures without Virulizin (p<0.001). An increase of 21% in the protease secretion was observed in Virulizin (2.5%)-stimulated macrophages compared to PBS-treated cells (p<0.0001). Moreover, the anti-tumor efficacy of Virulizin observed in CD-1 nude mice was abrogated in mice that were depleted of macrophages, thus stimulation of macrophages may be one mechanism through which Virulizin acts. These results suggest that macrophages may play a critical role in the anti-tumor activity of Virulizin.
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PMID:Macrophages play a critical role in the anti-tumor activity of Virulizin. 1453 75

Familial atypical multiple mole melanoma (FAMMM) syndrome is an autosomal dominant disorder with variable incomplete penetrance of the clinical phenotypes. Pathogenesis of this syndrome has not been fully investigated. Across multiple studies, germline mutations in the INK4a antioncogene encoding p16 protein were found on average in approximately 40% of the FAMMM syndrome. Patients with the FAMMM syndrome are genetically loaded with an increased risk of developing melanoma and other malignant neoplasms, for example, a pancreatic cancer. Melanoma can develop from numerous atypical moles as well as de novo. A proper diagnosis of the syndrome and early application of prophylactics decreases the risk of neoplastic transformation of melanocytes.
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PMID:FAMMM syndrome: pathogenesis and management. 1487 Dec 23

Clinical hyperthermia with controlled alteration of temperature (40 to 44 degrees C) in the target area is used in interdisciplinary treatment concepts for tumor treatment in combination with radiation and/or radiotherapy. Besides the direct cytotoxic power of hyperthermia there is an immunomodulatory effect and a radiation and chemotherapy sensitizing effect in the heated tissue. Clinical hyperthermia is an invasive or non-invasive supply of energy to the body of the patient, which leads to an artificial heating of the tumor and the surrounded tissue. The clinical hyperthermic procedures should take into account the oncologic disease and its pattern of organ involvement. There are three different types of hyperthermia: local hyperthermia (LHT), regional hyperthermia (RHT) and part body hyperthermia (PBH). PBH is used to heat regions of the body in case of metastatic disease, e. g. to the abdomen. I and phase II trials could show that the effects of radiation and chemotherapy can be altered by the simultaneous addition of hyperthermia. Data of trials involving skin metastasis in malignant melanoma, local relapse in breast cancer, tumors of the head and neck with regional lymph node metastasis, as well as trials in colorectal tumors, bladder cancer, pancreatic cancer, cervical cancer and sarcoma are presented. The results shows, that response to treatment can be improved by hyperthermia.
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PMID:[Principles, technology and indication of hyperthermia and part body hyperthermia]. 1504 93


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