Small cell and anaplastic prostate cancer: correlation between CT findings and prostate-specific antigen level.

PURPOSE: To evaluate the computed tomographic (CT) findings in patients with the anaplastic clinical variant of prostate cancer and to correlate these with prostate-specific antigen (PSA) levels. MATERIALS AND METHODS: Twenty-seven men with the anaplastic clinical variant of prostate cancer, including 12 patients with small cell cancer of the prostate, underwent CT before platinum-based chemotherapy. CT findings were retrospectively reviewed for the extent of disease in the abdominal and pelvic lymph nodes, liver, bone, and prostate. CT findings were correlated with baseline PSA levels. RESULTS: The overall mean PSA level was 59.9 ng/ml +/- 23.3 (range, 0-583 ng/ml; median, 4 ng/ml), with a mean PSA level in the small cell cancer subgroup of 12.3 ng/ml +/- 9.0 (range, 0-110 ng/mL; median, 1.7 ng/mL). Twenty-six patients (96%) had metastatic disease evident at CT, but only nine (33%) had PSA levels greater than 10 ng/mL. The mean PSA level in patients with pelvic lymphadenopathy was 12.8 ng/mL +/- 7.9 (median, 1.6 ng/mL); that in the small cell cancer subgroup was only 2.8 ng/ml +/- 1.4 (median, 1.6 ng/ml). Whereas 19 (70%) of all patients had osseous metastases and an average PSA level of 73 ng/ml +/- 32(median, 9.1 ng/mL), the seven (58%) with small cell cancer and bone metastases had an average PSA level of 18 ng/mL +/- 13 (median, 4 ng/mL). CONCLUSION: Unlike patients with advanced typical adenocarcinoma of the prostate, patients with the anaplastic clinical variant of prostate cancer often have extensive metastatic disease at CT despite relatively low PSA levels.

Benign and malignant phyllodes tumors: mammographic and sonographic findings.

PURPOSE: To characterize imaging findings that suggest the benign or malignant histologic nature of phyllodes tumors. MATERIALS AND METHODS: Clinical and imaging findings were retrospectively reviewed in 46 women with 51 phyllodes tumors (32 benign, 19 malignant) identified at preoperative mammography. Thirty of these tumors were also evaluated with preoperative sonography. RESULTS: Mammography showed nonspiculated soft-tissue masses in 49 tumors. Four masses contained calcifications; three of these masses were benign. The tumors were 1-20 cm in diameter; tumors 3 cm or larger were statistically significantly more likely to be malignant (P < .004). Sonography showed solid, hypoechoic masses in 28 cases. At sonography, cystic areas were more often seen in malignant than in benign tumors, but the difference was not statistically significant. CONCLUSION: There is substantial overlap in the imaging characteristics of benign and malignant phyllodes tumors. A tumor diameter of 3 cm or greater appears to be associated with a higher likelihood of malignancy.

Impact of stereotaxic core breast biopsy on cost of diagnosis.

PURPOSE: To determine the frequency with which stereotaxic core biopsy of the breast obviated diagnostic surgical biopsy and to estimate the savings in cost of diagnosis with this procedure. MATERIALS AND METHODS: Stereotaxic core biopsy of 182 nonpalpable, mammographically evident lesions was performed, and data from clinical follow-up were obtained. Savings in cost were assessed by using national Medicare reimbursement data and a relative value system based on national physician reviews (Relative Values for Physicians [RVP]). RESULTS: Stereotaxic core biopsy replaced a surgical procedure in 140 of 182 patients. The mean adjusted direct savings in cost per stereotaxic core biopsy were $893 (Medicare) or $1,491 (RVP). Use of stereotaxic core biopsy decreased the cost of diagnosis by 52% (RVP) or 55% (Medicare). CONCLUSION: Stereotaxic core biopsy obviated surgical biopsy for most nonpalpable lesions sampled, resulting in a greater than 50% reduction in biopsy costs. If these results were generalizable to the national level, annual savings would approach $200 million.

Structure of the human CR1 gene. Molecular basis of the structural and quantitative polymorphisms and identification of a new CR1-like allele.

Structural and quantitative polymorphisms have been described in human CR1. In the former, the S allotype is larger than the F allotype by 40-50 kD, the size of a long homologous repeat (LHR). In the latter, homozygotes for a 7.4-kb Hind III fragment express fourfold more CR1 per erythrocyte than do homozygotes for the allelic 6.9-kb restriction fragment. The basis for these genomic polymorphisms has been determined by restriction mapping the entire S allele and part of the F allele. The S allele is 158 kb and contains 5 LHRs of 20-30 kb, designated -A, -B/A, -B, -C, and -D, respectively, 5' to 3'. Extensive homology was found among the LHRs in their restriction maps, exon organization, and the coding and noncoding sequences. The presence of LHR-B/A in the S allele but not in the F allele accounts for the longer transcripts and polypeptide associated with the former allotype. At least 42 exons are present in the S allele, with distinct exons for the leader sequence, the transmembrane and cytoplasmic regions and most of the SCRs comprising the extracellular portion of CR1. Consistent with the mapping of the ligand binding site to the first two SCRs in each LHR, the second SCRs in LHR-A, -B/A, -B, and -C are encoded by two exons, reflecting a specialized function for this unit. The allelic 7.4/6.9-kb Hind III fragments extend from the 3' region of LHR-C to LHR-D. The 6.9-kb restriction fragment is the result of a new Hind III site generated by a single base change in the intron between the exons encoding the second SCR of LHR-D. A second cluster of genomic clones has been identified by hybridization to CR1 probes. Although they contain regions of hybridization to the cDNA and genomic probes derived from CR1, these cannot be overlapped with the structural gene owing to their distinct restriction maps. Three genomic polymorphisms previously identified by CR1 cDNA probes map to this region. These additional clones may represent part of a duplicated allele located nearby within the CR1 locus.

Analysis of multiple restriction fragment length polymorphisms of the gene for the human complement receptor type I. Duplication of genomic sequences occurs in association with a high molecular mass receptor allotype.

Human CR1 exhibits an unusual form of polymorphism in which allotypic variants differ in the molecular weight of their respective polypeptide chains. To address mechanisms involved in the generation of the CR1 allotypes, DNA from individuals having the F allotype (250,000 Mr), the S allotype (290,000 Mr), and the F' allotype (210,000 Mr) was digested by restriction enzymes, and Southern blots were hybridized with CR1 cDNA and genomic probes. With the use of Bam HI and Sac I, an additional restriction fragment was observed in 20 of 21 individuals having the S allotype with no associated loss of other restriction fragments. Southern blot analysis with a noncoding genomic probe derived from the S allotype-specific Bam HI fragment showed hybridization to this fragment and to two other fragments that were also present in FF individuals. Thus, an intervening sequence may be repeated twice in the F allele and three times in the S allele. A restriction fragment length polymorphism (RFLP) unique to two individuals expressing the F' allotype was seen with Eco RV, but the absence of persons homozygous for this rare allotype prevented further comparisons with the F and S allotypes. Analysis of the CR1 transcripts associated with the three CR1 allotypes indicated that these differed by 1.3-1.5 kb and had the same rank order as the corresponding allotypes. Taken together, these findings suggest that the S allele was generated from the F allele by the acquisition of additional sequences, the coding portion of which may correspond to a long homologous repeat of approximately 1.4 kb that has been identified in CR1 cDNA. We saw two other RFLPs with Hind III and Pvu II that were in linkage dysequilibrium with the Bam HI-Sac I RFLPs associated with the S allotype, and a third polymorphism was seen with Eco RI that was not in linkage dysequilibrium with the other polymorphisms. Thus, 10 commonly occurring CR1 alleles can be defined, making this locus a useful marker for the long arm of chromosome 1 to which the CR1 gene maps.