PubMed Health⌕ Search

Biomedical subjects

C Ficorella

Publications and source records attributed to C Ficorella.

16 recordsLinked to original sources
PubMed1996

Molecular diagnosis of p53 mutations in gastric carcinoma by touch preparation.

Thirty-one tumor samples from selected cases of gastric carcinoma were analyzed for mutations of the p53 tumor suppressor gene. Template DNA was prepared according to the touch preparation procedure, which allowed us to isolate clusters of neoplastic cells out of a stromal cellular background to be used as a template in the amplification of target exons of the p53 locus. In our present study, by polymerase chain reaction/single strand conformation polymorphism analysis we give evidence of p53 mutations occurring in the DNA-binding core domain of the protein (exons 5 through 9), which are clustered in stages III and IV of the disease (six mutations out of seventeen samples; 35%). No p53 mutations were detected in fourteen gastric cancer samples at I and II stages. Beside the use of conventional molecular scanning procedures, our study proposes the application of the touch preparation method to increase the detection of genetic alterations in human solid tumors.

Base Sequence↗
PubMed1990

[Medical emergencies in oncology: hypercalcemia. II. Diagnosis and therapy].

The acute metabolic abnormalities associated with cancer may cause symptoms that require urgent medical treatment and may constitute a more dangerous threat to life than the cancer itself. Hypercalcaemia is probably the most common metabolic complication of neoplastic disease (occurring in up to 30% of cancer patients) and its timely treatment may often save the patient and may permit subsequent chemotherapy. In this communication we focused our attention on the pathogenetic mechanism (part 1), diagnosis and subsequent treatment of this metabolic disorder (part 2).

Diagnosis, Differential↗
PubMed1990

[Metabolic emergencies in oncology: hypercalcemia. I. Pathogenesis].

The acute metabolic abnormalities associated with cancer may cause symptoms that require urgent medical treatment and may constitute a more dangerous threat to life than the cancer itself. Hypercalcaemia is probably the most common metabolic complication of neoplastic disease (occurring in up to 30% of cancer patients) and its timely treatment may often save the patient and may permit subsequent chemotherapy. In this communication we focused our attention on the pathogenetic mechanism (part 1), diagnosis and subsequent treatment of this metabolic disorder (part 2).

Bone Neoplasms↗
PubMed1990

Efficacy and toxicity of 5-fluorouracil and folates in advanced colon cancer.

From February 1987 to December 1988, 34 patients with histologically confirmed advanced colorectal carcinoma were entered in a phase II trial with 5-fluorouracil (5-FU) and folinic acid, for evaluation of treatment effectiveness and toxicity. Our data confirmed that the association 5-FU and folates represents an effective and moderately tolerated palliative treatment, with diarrhea being the only dose-limiting toxicity.

Clinical Trials as Topic↗
PubMed1989

Familial ovarian cancer: a study of 11 families.

In a group of 152 ovarian cancer patients, 11 cases with familial recurrence were investigated (7.23%). Of the families evaluated we found 26 patients with ovarian cancer and twenty two with different cancers in other sites. In ovarian cancer the familial aspect, despite its relatively low frequency, is one of the few factors for identifying "high risk" patients, thus allowing effective secondary prevention.

Adult↗
PubMed1984

Studies on chemically induced neoplastic transformation and mutation in the BALB/3T3 Cl A31-1-1 cell line in relation to the quantitative evaluation of carcinogens.

Mutagenesis and neoplastic transformation assays on mammalian cells in culture have been extensively used for quantitative estimates of the activity of carcinogens, in spite of the limitations that such in vitro systems have when compared with in vivo systems for tumor induction. In order to assess the validity of these correlations, a series of studies was undertaken in our laboratory with the BALB/3T3 Cl A31-1-1 mouse embryo cell line. Different carcinogens were found to induce dose-dependent frequencies of transformation, including the direct-acting alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and carcinogens that were metabolically activated by these cells through different pathways (benzo[a]pyrene, 3-methylcholanthrene, aflatoxin B1, and benzidine). Their respective level of activity on a molar basis was different from that obtained in standard Salmonella + S9 mutagenesis tests. Studies currently underway indicate the possibility of lowering the serum content in the medium considerably, thereby reducing a major variable in the assay. Methods were established for the induction of ouabain-resistant (ouar) mutants in these cells. Studies were conducted by applying 30-min MNNG exposures to cells that were synchronized by serum deprivation followed by serum-induced release from growth block. While maximal induction of mutants occurred in the S phase, the transformation frequency remained constant for treatments in G1 and early or late S.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Temporal dissociation in the exposure times required for maximal induction of cytotoxicity, mutation, and transformation by N-methyl-N'-nitro-N-nitrosoguanidine in the BALB/3T3 ClA31-1-1 cell line.

Cytotoxicity, alkali-labile DNA lesions, ouabain resistance mutations, and neoplastic transformation were analyzed concurrently in the BALB/3T3 ClA31 -1-1 cell line treated with the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) for different exposure times (15, 30, 60, 90, 120, and 240 min; 24, 48, and 72 hr). The half-life of MNNG in complete medium was approximately 70 min, both without cells and with cell numbers as used in the assays for cytotoxicity (2 X 10(2) cells/60-mm dish), transformation (1 X 10(4) cells/dish), and mutation (1 X 10(5) cells/dish). The cytotoxic effect of MNNG (0.5 or 2 micrograms/ml) appeared to be completed after an exposure time between 100 and 200 min. Maximal frequency of ouabain resistance mutations, however, was reached after a much shorter treatment time (30 to 60 min). Detection of DNA damage by alkaline elution analysis showed maximal increase in single-strand breaks already after treatment for 30 min. Exposures for 30 min followed by posttreatment incubation for 30 or 90 min showed active repair of single-strand breaks during these periods, indicative of an even balance between the additional MNNG-induced damage and its repair. Morphological transformation assays, at the same treatment times and concentrations used in the mutation assays, yielded frequency curves that reached their maxima 1 to 3 hr later than did the mutation frequencies. The ratio of transformation to ouabain resistance mutation frequencies was 3.7 for short treatment times (30 to 60 min), while it increased to more than 20 for exposure times of 240 min or longer. The temporal dissociation in the exposure times for maximal induction of mutation and transformation, observed with MNNG in this cell line, supports the hypothesis that a single gene mutational event is not sufficient to account for the full expression of neoplastic transformation.

Animals↗