The association between interval from acceptance to first-time donation, missed first appointment and future donation behaviour.

BACKGROUND AND OBJECTIVES: We examined the association of the interval between the date an individual is accepted for blood donation and the date of first donation (IFD-interval, index-to-first-time donation interval) and missed first appointment with future donation behaviour among new donors. These two variables have not been analysed in previous studies of donation behaviour among new donors. METHODS: Categories were generated for age (18-29 vs 30-65 years), missed-appointment status (no-show vs same-day cancellation) and the IFD-interval [short (≤median time) vs long (>median time)]. Accepted donors (n = 807) were followed for 19 months. Outcome measures were first-appointment attendance rates, return rates among first-time donors and the proportion of experienced donors, defined as those who gave ≥5 donations. RESULTS: In logistic regression analyses, high no-show rates were significantly associated with decreased likelihood of first-time donation. Long IFD-intervals were significantly associated with decreased likelihood of returning for a second donation among first-time donors. Experienced donors, compared to novice donors, were more likely to be male than female, older than younger and with shorter vs longer IFD-intervals. CONCLUSIONS: No-show and long IFD-intervals may be behavioural markers of low levels of motivation for making the first donation and for returning for a second donation, respectively.

Poor appointment-keeping behaviour among repeat blood donors and its relationship to the intent to donate again.

BACKGROUND AND OBJECTIVES: Anecdotal evidence suggests that missed donation appointments among repeat whole-blood donors are associated with decreased likelihood of future blood donation. This study sought to examine the relationship between missed donation appointments and intention to donate again among repeat whole-blood donors and to examine whether demographic variables are related to appointment-keeping behaviour. METHODS: During the period February-June 2013, telephone interviews were conducted with repeat donors who either did not show up for or cancelled their donation appointments on the day of the appointment. We asked them whether or not they wanted to schedule appointments for subsequent donations. RESULTS: Rates of missed donation appointments varied by age, but not gender. Although a statistically significant difference between male and female donors was not found with regard to willingness to donate again, female donors were more likely than male donors to call and cancel their appointment. Finally, compared with repeat donors who called and cancelled their appointment, no-show donors were 2.5 times less likely to schedule appointments for subsequent donations (P < 0.001). CONCLUSION: The results demonstrate that poor appointment-keeping behaviour, and in particular no-show behaviour, is significantly associated with decreased likelihood of future blood donation among repeat whole-blood donors.

Association between short time in bed, health-risk behaviors and poor academic achievement among Norwegian adolescents.

OBJECTIVE: To investigate the prevalence of short time in bed (<8h/day) and to examine the association between time in bed, overweight/obesity, health-risk behaviors and academic achievement in adolescents. METHODS: This study included a sample of adolescents (n=2432) aged 15-17 years in the southern part of Norway (participation rate, 98.7%). A self-report questionnaire was used to assess time in bed, body mass index, dietary habits, physical activity habits, sedentary behavior, smoking and snuffing habits, and academic achievement. RESULTS: A total of 32.3% of the students reported short time in bed (<8h/day) on an average school night. Several health-risk behaviors were associated with short sleep duration, including not being physically active for > or =60 min for > or =5 days/week (adjusted odds ratio, 1.33; 95% confidence interval, 1.05-1.68); using television/computer >2 h/day (1.63; 1.23-2.17); being a current smoker (2.46; 1.80-3.35) or snuffer (2.11; 1.57-2.85); having an irregular meal pattern (1.33; 1.05-1.68); intake of sweets/candy > or =4 times/week (0.51; 0.32-0.83); and poor academic achievement (1.62; 1.26-2.09). All odds ratios were adjusted for sex, age and parental education. CONCLUSIONS: In Norwegian adolescents, short time in bed is associated with several health-risk behaviors and poor academic achievement.

Spectral karyotyping and fluorescence in situ hybridization detect novel chromosomal aberrations, a recurring involvement of chromosome 21 and amplification of the MYC oncogene in acute myeloid leukaemia M2.

Recurring chromosomal aberrations are of aetiological, diagnostic, prognostic and therapeutic importance in acute myeloid leukaemia (AML). However, aberrations are detected in only two thirds of AML cases at diagnosis and recurrent balanced translocations in only 50%. Spectral karyotyping (SKY) enables simultaneous visualization of all human chromosomes in different colours, facilitating the comprehensive evaluation of chromosomal abnormalities. Therefore, SKY was used to characterize 37 cases of newly diagnosed AML-M2, previously analysed using G-banding. In 15/23 patients it was possible to obtain metaphases from viably frozen cells; in 22 additional cases, fixed-cell suspensions were used. Of the 70 chromosomal aberrations identified by SKY, 30 aberrations were detected for the first time, 18 aberrations were redefined and 22 were confirmed. SKY detected two reciprocal translocations, t(X;3) and t(11;19). In five cases, eight structural aberrations resulted in partial gains of chromosome 21, six of which were undetected by G-banding. In 4/5 cases, these resulted in copy number increases for AML1. Amplification of MYC was detected in three cases. Using SKY and FISH, clonal aberrations were identified in 5/18 cases with a presumed normal karyotype; 3/5 aberrations were of known unfavourable prognostic significance. Karyotypes were entered into a custom-designed SKY database, which will be integrated with other cytogenetic and genomic databases.

Paclitaxel selects for mutant or pseudo-null p53 in drug resistance associated with tubulin mutations in human cancer.

The efficacy of anticancer therapy is limited by the development of drug resistance. While the role of p53 in the intrinsic sensitivity of human cancer cells to paclitaxel (PTX) remains controversial, its role in acquired paclitaxel resistance has never been addressed. In this study we examined the p53 status of three paclitaxel selected human ovarian carcinoma sublines, resistant to paclitaxel due to acquired beta-tubulin mutations which impair paclitaxel's interaction with tubulin. In contrast to parental cells which have wt p53, in all PTX-resistant sublines p53 was functionally inactive. Two of the resistant sublines expressed high levels of transcriptionally inactive p53 protein, each with a distinct point mutation in codons 236 and 239 of the DNA binding domain. The third subline presented a novel p53 pseudo-null phenotype as a result of markedly decreased wt p53 mRNA expression. Introduction of ectopic wt p53 had no effect on PTX sensitivity in both parental and resistant cells, while it induced p21WAF1/CIP1, demonstrating an intact p53 pathway. While PTX resistance is primarily conferred by the tubulin mutations, the loss of functional p53 observed in all clones, suggests that this loss may facilitate the development of resistance potentially by providing a clonal advantage which promotes the isolation of paclitaxel resistant cells.

Amplification of 4q21-q22 and the MXR gene in independently derived mitoxantrone-resistant cell lines.

Molecular cytogenetic studies were conducted on three multidrug-resistant cancer sublines which are highly resistant to the chemotherapeutic agent mitoxantrone, an anthracenedione. The three independently selected sublines were derived by exposure to mitoxantrone or Adriamycin and do not overexpress MDR1 or MRP. Two sublines, MCF-7 AdVp3000 and MCF-7 MX, showed an amplification peak at 4q21-q22, as demonstrated by comparative genomic hybridization (CGH), while the third, S1-M1-80, did not. FISH using a whole chromosome 4 paint demonstrated multiple rearrangements involving chromosome 4 in MCF-7 AdVp3000 and MCF-7 MX, while S1-M1-80 contained only a simple reciprocal translocation. The parental cell lines had no chromosome 4 rearrangements and no copy number gain or amplification of chromosome 4. Spectral karyotyping (SKY) analysis revealed a balanced translocation, t(4;17)(q21-q22;p13) in S1-M1-80 and multiple clonal translocations involving chromosome 4 in MCF-7 AdVp3000 and MCF-7 MX. A novel cDNA, designated MXR, which encodes an ABC half-transporter and is highly overexpressed in the three sublines, was localized to chromosome 4 by somatic cell hybrid analysis. Southern blot analysis demonstrated amplification of the MXR gene in MCF-7 AdVp3000 and MCF-7 MX, but not in S1-M1-80. FISH studies with a BAC probe for MXR localized the gene to 4q21-22 in the normal chromosome 4 and revealed in both MCF-7 AdVp3000 and MCF-7 MX amplification of MXR at one translocation juncture, shown by SKY to be t(4;5)(4qter-->4cen-->4q21-22::5q13-->5qter++ +) in MCF-7 AdVp3000 and t(6;4;6;3)(6pter-->6q15::4q21-q22::hsr::6q?::3q?27-->+ ++3qter) in MCF MX; neither of the breakpoints in the partner chromosomes showed amplification by CGH. The data are consistent with the hypothesis of a transporter, presumably that encoded by the MXR gene, mediating mitoxantrone resistance. The MXR gene encodes a half-transporter and the absence of cytogenetic evidence of coamplification of other regions suggests that a partner may not be overexpressed, and instead the MXR half-transporter homodimerizes to mediate drug transport. Genes Chromosomes Cancer 27:110-116, 2000. Published 2000 Wiley-Liss, Inc.

Cytogenetic and molecular characterization of random chromosomal rearrangements activating the drug resistance gene, MDR1/P-glycoprotein, in drug-selected cell lines and patients with drug refractory ALL.

Drug resistance, both primary and acquired, is a major obstacle to advances in cancer chemotherapy. In vitro, multidrug resistance can be mediated by P-glycoprotein (PGY1), a cell surface phosphoglycoprotein that acts to efflux natural products from cells. PGY1 is encoded by the MDR1 gene located at 7q21.1. Overexpression of MDR1 has been demonstrated in many cancers, both in patient tumors and in cell lines selected with a variety of chemotherapeutic agents. Recent studies in drug-selected cell lines and patients samples have identified hybrid mRNAs comprised of an active, but apparently random, gene fused 5' to MDR1. This observation indicates that random chromosomal rearrangements, such as translocations and inversions, leading to "capture" of MDR1 by constitutively expressed genes may be a mechanism for activation of this gene following drug exposure. In this study, fluorescence in situ hybridization (FISH) using whole chromosome paints (WCP) and bacterial artificial chromosome (BAC)-derived probes showed structural rearrangements involving 7q in metaphase and interphase cells, and comparative genomic hybridization (CGH) revealed high levels of amplification at chromosomal breakpoints. In an adriamycin-selected resistant colon cancer line (S48-3s/Adr), WCP4/WCP7 revealed t(4;7)(q31;q21) and BAC-derived probes demonstrated that the breakpoint lay between MDR1 and sequences 500-1000 KB telomeric to it. Similarly, in a subline isolated following exposure to actinomycin D (S48-3s/ActD), a hybrid MDR1 gene composed of heme oxygenase-2 sequences (at 16p13) fused to MDR1 was identified and a rearrangement confirmed with WCP7 and a subtelomeric 16p probe. Likewise, in a paclitaxel-selected MCF-7 subline where CASP sequences (at 7q22) were shown to be fused to MDR1, WCP7 showed an elongated chromosome 7 with a homogeneously staining regions (hsr); BAC-derived probes demonstrated that the hsr was composed of highly amplified MDR1 and CASP sequences. In all three selected cell lines, CGH demonstrated amplification at breakpoints involving MDR1 (at 7q21) and genes fused to MDR1 at 4q31, 7q22, and 16p13.3. Finally, in samples obtained from two patients with drug refractory ALL, BAC-derived probes applied to archived marrow cells demonstrated that a breakpoint occurred between MDR1 and sequences 500-1000 KB telomeric to MDR1, consistent with a random chromosomal rearrangement. These results support the proposal that random chromosomal rearrangement leading to capture and activation of MDR1 is a mechanism of acquired drug resistance.

Cytogenetic changes in the progression of lymphoma.

The study of chromosomal changes related to tumor progression in NHL is complicated by the various histologic classification systems and the lack of large serial studies comparing abnormalities at different disease stages. The T-cell lymphomas frequently involve rearrangements of the T-cell receptors and tumor progression is marked by a change from single cell aberrations and polyclonality in low grade disease to monoclonal formation, complex clones, polyploidy, and abnormalities of 1p, 6q, 7, and 13 in high grade T-NHL. In B-cell NHL, specific translocations and oncogene rearrangements are associated with specific NHL subtypes de novo; many of these translocations involve immunoglobulin genes, such as t(14;18) in follicular lymphoma, t(11;14) in MCL, t(3;14) in DLLC, and t(8;14) in Burkitt's lymphoma. Tumor progression is associated with secondary abnormalities which are generally not confined to a particular NHL subtype. Some abnormalities, such as those involving chromosomes 1, 6, and 17, >4-6 clonal markers/cell, and rearrangements of c-MYC and TP53, have prognostic significance while others, such as trisomies 7, 12, 18, and X, are associated with tumor progression but their influence on overall survival is uncertain.

Familial eosinophilia: clinical and laboratory results on a U.S. kindred.

We describe a five-generation kindred with familial eosinophilia (FE; MIM131400), characterized by the occurrence of sustained eosinophilia of unidentifiable cause in multiple relatives. The inheritance pattern is consistent with an autosomal dominant pattern. Among 52 related subjects studied, 19 were affected and 33 were unaffected. Ten unaffected spouses were also evaluated. Four subjects with sustained eosinophilia were diagnosed with cardiac abnormalities and two of them also had neurologic symptoms. In comparison with the unaffected or spouses, evaluation of complete blood counts showed that the affected relatives had, as expected, significantly higher white cell (P < 0.005) and absolute eosinophil counts (P < 0.001) and lower red cell counts (P < 0.05). Evaluation of serum cytokine levels (IL-5, IL-3, and granulocyte-macrophage colony-stimulating factor (GMCSF) and serology for parasitic helminth infection demonstrated no differences between the affected and unaffected individuals; no individuals studied had serologic evidence for parasitic infection. There were also no differences in anti-nuclear antibody, serum cobalamin (vitamin B12) level, immunoglobulin level, leukocyte alkaline phosphatase, rheumatoid factor, HLA analysis, and stool findings for ova and parasites. Among eight affected persons who had peripheral blood or bone marrow karyotype analysis, two carried the same chromosome abnormality, a pericentric inversion of chromosome 10, inv (10) (p11.2q21.2). A gene mapping study is currently underway to study the underlying genetic mechanism(s) of this syndrome.

Gene rearrangement: a novel mechanism for MDR-1 gene activation.

Drug resistance, a major obstacle to cancer chemotherapy, can be mediated by MDR-1/P-glycoprotein. Deletion of the first 68 residues of MDR-1 in an adriamycin-selected cell line after a 4;7 translocation, t(4q;7q), resulted in a hybrid mRNA containing sequences from both MDR-1 and a novel chromosome 4 gene. Further selection resulted in amplification of a hybrid gene. Expression of the hybrid mRNA was controlled by the chromosome 4 gene, providing a model for overexpression of MDR-1. Additional hybrid mRNAs in other drug-selected cell lines and in patients with refractory leukemia, with MDR-1 juxtaposed 3' to an active gene, establishes random chromosomal rearrangements with overexpression of hybrid MDR-1 mRNAs as a mechanism of acquired drug resistance.

Cytogenetic mechanisms in the pathogenesis and progression of follicular lymphoma.

A summary of the clinically significant cytogenetic markers in follicular lymphoma is presented in Table 3. It is clear that the use of cytogenetic analysis to evaluate progression and transformation in follicular lymphoma is complicated by the variety and complexity of the chromosomal aberrations present in this disease. Cytogenetic and molecular studies have indicated that the t(14;18) translocation is the prerequisite of a multistep process in the lymphomagenesis of follicular lymphoma; it is usually followed by a long quiescent period during which the B cell population expands and additional oncogenic mutations occur leading to eventual progression and transformation to a highly malignant form. This process can be accomplished by a variety of pathways: Activation of other oncogenes by additional chromosomal rearrangements (e.g. MYC, LAZ3) Deletion and mutation of tumour suppressive genes (e.g. TP53, proposed genes on 6q) Gain of whole or parts of chromosomes, leading to increased expression of important regulating factors (e.g. MDR and T cell receptor genes on chromosome 7) More studies are required to determine which of these pathways, if any, is most important for neoplastic transformation.

Metastatic human rhabdomyosarcoma: molecular, cellular and cytogenetic analysis of a novel cellular model.

A new human metastatic rhabdomyosarcoma (RMS) model was established and analyzed for a number of biologic, cytogenetic and molecular parameters. Consistent with previous studies, the metastatic capacity of different RMS cell variants did not correlate with their tumorigenic or proliferative capacities. Interestingly, a highly metastatic variant was diploid, while a nonmetastatic variant was tetraploid, which parallels previous clinical observations. Genes whose expression had been found to be associated with either low- or high-metastatic capacity in carcinoma or melanoma did not show a similar association with different metastatic variants of RMS, derived from a mesenchymal tumor. We also found, in transient reporter gene assays, that several promoters had higher transcriptional activity in highly metastatic than in nonmetastatic RMS cell variants. This novel human RMS metastatic model may be instrumental for a better understanding of the regulatory pathways that control the metastatic phenotype of tumors of mesenchymal origin.

Renal cell carcinoma. Cytogenetic analysis of tumors and cell lines.

Successful cytogenetic analysis was performed on 27 samples from 25 patients with RCC, including 7 of 11 tumors studied and 20 cell lines. Clonal chromosomal abnormalities were detected in all 27 samples. The most frequently involved chromosomes were 7, 1, 3, 9, and the Y (20, 17, 17, 14, and 10 cases, respectively). Polysomy 7 or rearrangement of 7q was seen in 80% (20/25) of the patients, and loss or rearrangement of 3p was seen in 48% (12/25); of the latter, four patients had loss of the whole chromosome and 10 patients had deletions or translocations involving 3p, with breakpoints at either 3p11-14 or 3p21-23 (5/7 translocation breakpoints were at 3p21-23). Loss of the sex chromosomes was seen in 15 patients, including -Y in 10/22 males. Other clonal changes included structural abnormalities of chromosome 1 centromere and the long arm, breakpoints at or near the centromere of chromosome 9 (10 patients), polysomy 16, monosomy 17, polysomy 20, and monosomy 22. With the exception of chromosome 3p loss, which was primarily confined to the nonpapillary cases, no specific clonal abnormality was noted for any particular subtype of RCC. Trisomy or tetrasomy 7 and -Y were seen in all subtypes of renal cell carcinoma.

Molecular genetic characterization of neuroendocrine lung cancer cell lines.

Small cell lung cancers express neuroendocrine (NE) cell features, while most non-SCLC tumors lack these features. We studied the cytogenetic and genetic alterations in cell lines derived from three unusual subtypes of lung cancer: including carcinoids, non-small cell lung cancers expressing NE properties (NSCLC-NE) and extrapulmonary small cell cancers (ExPuSC) and compared them with those of SCLC and NSCLC lines. Our studies included: cytogenetic studies, restriction fragment length polymorphism (RFLP) analyses with 8 probes spanning commonly deleted loci on chromosomes 3p, 13q and 17p, retinoblastoma gene product (RB) expression, and mutations in the ras and p53 genes. We also summarize previously published data on in vitro chemosensitivity patterns and MDRl gene expression. Our studies demonstrate that all three of the NE cell subtypes have their own distinctive genotypes and phenotypes, each having some similarities and dissimilarities with SCLC and NSCLC.

Sequential analysis of 43 patients with non-Hodgkin's lymphoma: clinical correlations with cytogenetic, histologic, immunophenotyping, and molecular studies.

Few reports correlating specific cytogenetic abnormalities with distinct subtypes of lymphoma have performed serial studies at diagnosis and at tumor recurrence or progression. In our file of 325 cytogenetically analyzed non-Hodgkin's lymphoma (NHL) patients studied over the past decade, 43 had serial biopsies, 39 of whom had at least two successful preparations; of the 43, nine had one and 32 had two or more cytogenetically abnormal specimens. In this study, we correlated cytogenetic, histopathologic, molecular, and clinical parameters. Patients with low-grade lymphomas were as likely as patients with intermediate- or high-grade lymphomas to acquire new chromosomal abnormalities with time (16 of 23 patients as compared with 7 of 16; P2 = .11, chi 2 test). In four patients, originally diagnosed indolent disease progressed to aggressive disease; all had t(14;18), all gained additional chromosomal abnormalities with disease progression, and three of the four expressed abnormalities associated with disease progression and/or short survival: der(18), +7, and/or +12. Cytogenetic results from early disease were compared with those obtained later in disease: in the t(14;18) group, the most common abnormalities were +7 (eight patients) and der(18) (five patients), both seen later in disease. The most common abnormalities in patients without t(14;18) were 6q deletions; they were seen in both early and late disease and were associated with significantly shorter survivals (P2 = .0014) compared with all patients without 6q deletions. Secondary chromosomal abnormalities, observed after at least one previous abnormal study, were seen in 19 of 22 t(14;18) patients and in 11 of 21 patients without t(14;18) and were associated with a poor survival (P2 = .13) compared with patients without any secondary chromosomal abnormalities. Chromosome 1 abnormalities were seen in almost half of the patients and were observed in initial specimens and early in disease as well as late in disease and as secondary abnormalities; 1q involvement was more frequent than 1p (15 versus eight patients) and was significantly associated with poor survival only in patients with intermediate-/high-grade disease; the most common breakpoints were 1q21-q22 (nine patients) and 1p36 (six patients). Breakpoints at 2q21 and 3q27-q29 were limited to patients with t(14;18) and were almost exclusively secondary in nature. Molecular studies in 24 of our patients showed discrepancies with the cytogenetic results in only three patients: two had t(14;18) but no molecular rearrangements while two patients had no visible t(14;18) but were positive for major breakpoint region (MBR) rearrangement. The presence of MBR or minor breakpoint cluster (MCR) rearrangement had no apparent effect on survival.(ABSTRACT TRUNCATED AT 400 WORDS)

Cytogenetic study of two cases with lymphoma of mucosa-associated lymphoid tissue.

Cytogenetic studies have been reported in fewer than 20 patients with lymphoma of mucosa associated lymphoid tissue (MALT). Two patients with this disease at the Clinical Center, National Institutes of health had numerical and structural chromosome abnormalities, including +12 in both cases. The clonal karyotypes observed were 48-49,XX,t(2;8)(q33;p23), +3, -10,del(10)(q23), +12, +18 [cp] and 47,X,-X,i(6p), +7, +inv(12)(p13q13). Review of cytogenetic studies from published data showed that all cases of MALT lymphoma reported to date also have both numerical and structural chromosome abnormalities, the most frequent being numerical involvement of chromosomes 3, 7, and 12. Identification of a clonal abnormality can help establish the diagnosis when differential diagnosis includes atypical hyperplasia. Although trisomy 12 has been associated with a poor prognosis in B-cell chronic lymphocytic lymphoma (B-CLL), both these patients with MALT lymphoma have had long survival: 8 and 11 years, respectively.

Examination of human tumors for rhoA mutations.

rhoA encodes a ras-related GTP-binding protein that is thought to play a role in cytoskeletal organization. Recent evidence has suggested both that rhoA could act either as a dominant oncogene, since transfection of both normal and activated rho genes confer a transformed phenotype on fibroblast cells in culture, or as a recessive tumor suppressor gene, by virtue, in part, of its chromosomal location at 3p21, a site deleted in many human malignancies. In either case, a role for rhoA in the oncogenesis of human tumors would be supported by the finding of rhoA mutations in tumors. We therefore examined human tumors and cell lines for mutations in the protein coding regions of rhoA by RNAase protection analysis. We first examined the expression of rhoA in renal cell carcinoma cell lines in which 3p21 was heterozygously deleted or retained. We found no evidence for rhoA mutations in these specimens. We also examined RNA from lung, breast, colon or ovarian tumors and also found no evidence of activating rhoA mutations. Furthermore, there was no relation between the level of rhoA mRNA expression and the presence or absence of 3p21 deletions in the renal cell carcinoma specimens. Thus, although rhoA has transforming potential in vitro, there is no evidence that it is activated by mutation in human malignancies, or that it could act as a tumor suppressor gene in tumors in which 3p21 is deleted.

Chromosome studies in HTLV-I, -II, and HIV-1, -2 cell lines infected in vivo and in vitro.

HTLV-I, II and HIV-1, 2 are T-cell tropic viruses, all belonging to the retrovirus family. These viruses are transmitted horizontally by intimate contact or through blood products. The study of chromosomal changes in these T cells may enhance our understanding of the nature and mechanism of these viral infections. However, because of the cytopathic effect of these viruses on T cells, the direct observation of abnormalities in these cells is sometimes difficult. We performed chromosomal analysis on six HTLV-I cell lines from patients with HTLV-I-positive leukemia/lymphoma, one HTLV-I variant cell line, and two HTLV-II-positive cell lines. The results of these studies were compared with the findings in an earlier (published) study of direct preparations and short-term cultures of cells from 11 HTLV-I-positive NIH patients. Our study also included cytogenetic analysis of seven established cell lines and six normal peripheral bloods infected in vitro with the HTLV-IIIB strain of HIV-1 (five cell lines and six bloods) or HIV-2 (two lines); all were studied both before and after viral infection. The results showed that all six HTLV-I cell lines and the variant cell line had multiple chromosomal changes: three lines had deletions of chromosome 6, with breakpoints between q21 and q25. Nine of the 11 NIH patients with HTLV-I had clonal abnormalities, and six of these nine had chromosome 6 deletions with breakpoints ranging from band q11 to band q23. The high incidence of 6q involvement may be of considerable significance in this clinical subgroup of HTLV-I patients. The two HTLV-II cell lines were established from patients suffering from HTLV-II infection. Both of these cell lines had translocations of chromosome 21 at p11, and both had extra copies of chromosome 20; no known oncogenes or receptors are located on these two chromosomes. Chromosome 17 was the chromosome most frequently involved (three lines) in the five HIV-1-infected cell lines, followed by chromosomes 3 and 21; it is of interest that NGL (also known as C-ERBB2 or NEU oncogene), CD7 (a lymphocyte antigen), HTLV-1 receptor, NGFR (nerve growth factor receptor), and MIC6 are all cell surface antigens coded by genes on chromosome 17q. No specific chromosome abnormalities were found in the normal blood samples infected with HIV-1, and no unique chromosome changes were noted in the two cell lines infected with HIV-2; however, the infected H9 line had a chromosome 17 abnormality, a translocation involving band 17p11.

[Transurethral microwave therapy of benign prostatic hyperplasia. Results after 1-year follow-up]. / Transurethral mikrobølgeterapi ved benign prostatahyperplasi. Resultater etter ett års oppfølging.

We describe the results after one year follow-up of the first 17 patients treated with transurethral microwave therapy at the University Hospital in Tromsø. We used the Prostatron (Technomed International), a microwave generator delivering heat to the prostate through a water-cooled transurethral catheter. After six weeks we recorded significant improvement in symptom score, residual urine and peak flow rate. There was continuous improvement in all recorded parameters until the last control 13 months after treatment, except in the case of symptom score, where the level was the same after 13 months as after six months. We found a high incidence of urinary tract infections after treatment, owing to liberal use of prophylactic transurethral catheters. In one patient we also recorded retrograde ejaculation as an adverse effect of treatment. To our knowledge this has not been reported earlier.

Cytogenetic studies in subgroups of rhabdomyosarcoma.

Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma of childhood and accounts for 10% of all solid tumors in children. There are three different histologic forms of this tumor: embryonal (RMS-E), alveolar (RMS-A), and primitive (RMS-P). Among these, the embryonal form has responded well to chemotherapy. Identification of the correct subtype is important for both the management and treatment of this malignancy. However, the histopathologic classification of RMS is sometimes difficult and distinguishing between the embryonic and primitive forms can present a diagnostic dilemma. Chromosomal abnormalities have been observed in all subtypes. We present the cytogenetic findings in six cases of RMS or related sarcoma. All four cases with RMS-A had both numerical and structural abnormalities in the tumor and involved bone marrow specimens. Three patients had a common marker, t(2;13)(q37;q14), and one patient had a variant marker involving 13q14, t(1;13) (p36;q14), and double minutes (dmin). The single embryonal RMS patient had modal chromosome numbers in the hypertriploid range and extensive structural abnormalities; the t(2;13) was not present, but translocation of 13q to both 1q and 2p was observed, der(1)t(1;13)(q21;q14) and der(2)t(2;13)(p25;q14). The patient with primitive type RMS had a hypodiploid line with several markers, including a complex translocation involving chromosomes 5 and 13 with a breakpoint at 13q14, and t(11;12)(q24;q12), a chromosome marker heretofore found only in Ewing's sarcoma and related tumors. This patient had atypical RMS with mixed neural and myogenic elements. The significance of these chromosomal markers and their importance in the characterization of childhood tumors are discussed, along with a review of the literature.