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PubMed1991

Cytogenetic evidence of involvement of an early progenitor myeloid cell in 4;11 translocation-associated acute leukemia.

The t(4;11)(q21;q23)-associated acute leukemia may show both lymphoid and myelomonocytic features, which suggests a pluripotent progenitor stem cell as the hematopoietic cell involved in this neoplastic process. However, there is no cytogenetic evidence to support this contention. We present a case of acute myelomonocytic leukemia (M4, FAB subtype) with t(4;11)(q21;q23), which was also found in several hypertetraploid metaphases probably corresponding to megakaryocytes. This confirms the cellular origin in an early progenitor myeloid cell of this type of acute leukemia.

Bone Marrow↗
PubMed1995

Chromosome analysis of uterine adenomyosis. Detection of the leiomyoma-associated del(7q) in three cases.

Adenomyosis is a uterine disease whose defining characteristic is the presence deep in the myometrium of endometrial glands and stroma. The condition is believed to arise from inordinate downward growth by contiguity from the endometrium rather than from in situ metaplasia or neoplasia. No acquired chromosome abnormalities have been associated with adenomyosis before. We analyzed short-term cultures from three cases and detected in all of them a del(7) (q21.2q31.2), a karyotypic anomaly that has hitherto been found repeatedly only in uterine leiomyomas. The cytogenetic similarity to leiomyoma suggests that the del(7q) was present in the mesenchymal or, more precisely, smooth muscle cells of the adenomyosis lesions. The very fact that clonal chromosome abnormalities were present questions whether the prevailing understanding of adenomyosis pathogenesis is adequate; the cytogenetic data would better fit a model of the disease envisioning the intramyometrial endometrial foci as having arisen through a neoplastic process.

Adult↗
PubMed1995

Cytogenetics of malignant gliomas. II. The sex chromosomes with reference to X isodisomy and the role of numerical X/Y changes.

Sex chromosomal monosomy with total loss of an X or Y is frequently observed in malignant gliomas. Beyond that, not much is known about the behavior of the sex chromosomes in these tumors. We noted loss of the X from 3 of 13 gliomas from women (23%) compared to loss of the Y from 16 of 28 gliomas from men (57%). There were two structural rearrangements of the Y (an inversion and a translocation with chromosome 4). Most unexpectedly, clones with sex chromosome reversal were encountered in 3 cases. These XX clones in gliomas from men are perforce the consequence of Y loss coupled with X isodisomy, a nonrandom sequence of sex chromosome changes. We examined the company kept by numerical X and Y changes in clones and found that clones with numerical sex chromosome changes had fewer autosomal abnormalities, reflecting a distinct tendency to clonal separation of sex chromosome from autosomal abnormalities. We conclude that the sex chromosome changes are not a necessary part of the neoplastic process in malignant gliomas but that they must be of biologic significance to the brain since they are highly nonrandom in frequency, type, and sequence in brain cells.

Adult↗
PubMed1990

Modulation of P-450 IIC7 and IIIA1,2 mRNA in pre-neoplastic liver. Effect of promotion by phenobarbital.

P-450 IIC7 and IIIA2 mRNAs are constitutively expressed in the hepatic tissue under developmental control. Both forms--as well as IIIA1, 90% homologous to IIIA2 mRNA--display positive modulation by phenobarbital a prototype inducer of the liver monooxygenases and a strong promoter of experimental chemical hepatocarcinogenesis. In the present work the variations in the concentration of these P-450 mRNA were studied in rats submitted to the hepatocarcinogenic protocol of Solt and Farber. We demonstrate that a decrease in the relative concentrations of P-450 IIC7 and IIIA1, 2 mRNA is set up along the tumor promotion stage. Animals--starting the experimental carcinogenic protocol at pubertal age--show a partial inhibition of the physiological expression of P-450 IIIA1,2 mRNA associated to male sex maturation. Administration of phenobarbital results in an acceleration of the pre-neoplastic process which is concomitant with an induction of P-450 IIC7 as well as IIIA1,2 at the earlier promotion stages. P-450 mRNA concentration markedly decreases as the preneoplastic process develops. While an impaired P-450 IIIA1,2 mRNA relative abundance is observed, an inversion of the modulation of P-450 IIC7 as well as of the male phenotype marker alpha-2u-globulin mRNA arises as the tumor promotion stage progresses, both mRNA becoming repressed in response to phenobarbital.

Alpha-Globulins↗
PubMedDate not supplied

Costal osteomyelitis after pectoralis major myocutaneous flap use in head and neck reconstruction.

Costal osteomyelitis and chondritis are rare complications of PMMF usage. They probably represent a secondary complication of a donor-site infection. This diagnosis must be considered in cases of PMMF donor-site infections, which fail to resolve with local wound care and antibiotics. Antibiotic coverage in these cases should be taylored to culture results, while having broad gram-positive activity. Workup of these patients should include CT and biopsy to rule out a neoplastic process.

Aged↗
PubMed1983

Influence of cholera toxin on the growth and development of N-methyl-N-nitrosourea-induced rat mammary carcinomas.

Daily injections of cholera toxin (2.0 micrograms/rat/day) for 4 weeks to female Sprague-Dawley rats did not significantly affect the growth of palpable N-methyl-N-nitrosourea (MNU)-induced rat mammary carcinomas. Percent increase in tumor volume was + 78.8% for control animals and +72.8% for cholera toxin treated animals. Daily treatment for 16 weeks of female Sprague-Dawley rats with cholera toxin (1.0 micrograms/rat/day), commencing 3 days after MNU treatment, resulted in a significant (P less than 0.05) increase in mean mammary carcinoma weight per rat at the termination of the study; mammary carcinoma incidence was not significantly affected by cholera toxin treatment. Retinyl acetate feeding (1.0 mM/kg diet) for 16 weeks significantly (P less than 0.05) reduced mammary carcinoma incidence and weight of mammary carcinoma per rat at the termination of study; feeding of retinyl acetate to cholera toxin treated rats blocked the stimulatory effect of cholera toxin on mammary carcinoma development. Thus, the reported striking inhibitory effect of cholera toxin on the growth of dimethylbenzanthracene (DMBA)-induced rat mammary carcinomas was not duplicated in our study, using the MNU-induced rat mammary carcinoma; indeed the toxin appeared to enhance the early developmental stage of this neoplastic process.

Animals↗
PubMed1986

The influence of subsequent dehydroepiandrosterone, diaminopropane, phenobarbital, butylated hydroxyanisole and butylated hydroxytoluene treatment on the development of preneoplastic and neoplastic lesions in the rat initiated with di-hydroxy-di-n-propyl nitrosamine.

The comparative modifying potential of dehydroepiandrosterone (DHEA), diaminopropane (DAP), phenobarbital (PB), butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) on the development of lesions initiated by dihydroxy-di-n-propyl nitrosamine (DHPN) in F344 rats were investigated. DHEA, BHA and BHT were all associated with significant reduction in numbers of glutathione-S-transferase P form (GST-P) positive foci in the liver whereas PB brought about their enhanced development. BHT and PB exerted promoting activity on the incidence of thyroid adenomas while DAP similarly increased lung adenoma formation. The results illustrate the advantages to be gained from two stage experiments using broad spectrum carcinogen initiation for comparative analysis of 'modifiers' of the neoplastic process and suggest that studies of enzyme alteration within putative preneoplastic lesions may be directly relevant to elucidation of mechanisms underlying such modification.

Animals↗
PubMed1989

Oxidative metabolism of 4-hydroxy-2,3-nonenal during diethyl-nitrosamine-induced carcinogenesis in rat liver.

In some chemically-induced hepatomas and in cultured transformed cells the aldehyde dehydrogenase activity was found increased in the presence of aromatic aldehyde as substrate. We studied this enzyme during diethyl-nitrosamine carcinogenesis in rat liver by using an aliphatic aldehyde, 4-hydroxynonenal, as substrate. 4-Hydroxynonenal is an important product of lipid peroxidation. The NAD- and NADP-dependent aldehyde dehydrogenase of the cytosolic fraction and the NADP-dependent aldehyde dehydrogenase of the microsomes show higher values in nodules and hepatoma than in normal liver. These results suggest that increased aldehyde dehydrogenase, when 4-hydroxynonenal is used, can be considered a marker of the neoplastic process, in the same way as the level of aldehyde dehydrogenase increased in presence of aromatic aldehyde.

Aldehyde Dehydrogenase↗
PubMed1995

Melatonin enhances junctional transfer in normal C3H/10T1/2 cells.

Gap junctional intercellular communication is known to be involved in controlling cell proliferation and differentiation, and seems to play a crucial role in suppression of tumor promotion. The pineal gland and its hormone, melatonin, are believed to intervene in the control of neoplastic processes. Several possible mechanisms have been suggested to be potentially responsible for melatonin's oncostatic action; however, the actual mechanisms involved in melatonin's effects at the cellular level remain unidentified. In the present study low-density cultures of C3H/10T1/2 mouse embryo fibroblasts were incubated until relatively quiescent monolayers were established (17-18 days). Gap junctional intercellular communication in control samples and in cells treated with 10(-12) to 10(-8) M melatonin was determined by the scrape-loading assay using the fluorescent dye Lucifer yellow. The results showed that concentrations of melatonin considered physiological (10(-11) and 10(-10) M) induced a significant increase in the transfer of the dye to adjacent cells through gap junctions; both higher and lower concentrations were ineffective. These results suggest that melatonin could exert its putative oncostatic action, in part, by modulating the levels of gap junctional intercellular communication.

Animals↗
PubMed1980

Neoplasia of the arterial wall: role in atherosclerosis.

An alternative means of investigating atherosclerosis is suggested in the hope that this will lead to preventative and therapeutic measures more successful than current approaches. A putative link between arterial atherosclerotic lesions and neoplasia, suggesting that arterial plaques are monoclonal in origin, is discussed. If plaques do minic a neoplastic process, it is possible to look at many conventially accepted aspects of arterial disease in a new light. This is particularly the case with the role of diet, smoking and how the disease might be prevented or treated at an early stage or how the process might be reversed.

Arteriosclerosis↗
PubMed1991

A reinterpretation of the events in gastric carcinogenesis.

It is proposed here that the initial events in gastric carcinogenesis occur at the junction of the oxyntic and antral mucosae. Intestinal metaplasia represents an adaptive counter-response to early neoplastic change at this site. Chronic gastric ulceration may arise due to the elimination of overtly dedifferentiated cells at a later stage in the evolution of the neoplastic process. Intestinal type gastric carcinoma possibly represents breakthrough past these mechanisms.

Animals↗
PubMed1996

Papillomaviruses and potential copathogens.

An in vitro multistage genital epithelial cell model for cervical cancer that parallels the in vivo neoplastic process has been developed using recombinant human papillomavirus (HPV) DNA and genital cells. HPV-16-immortalized genital cells are responsive to the genotoxic action of known chemical carcinogens (polycyclic hydrocarbons, alkylating agents or cigarette smoke condensate), but are not converted to malignancy. Ras oncogene and human herpes virus-2 did convert HPV immortalized cells to malignancy, whereas human herpes virus-6 infection only increased HPV expression. Human immunodeficiency virus did not infect genital cells.

Carcinogens↗
PubMedDate not supplied

The inguinal hernia: not always straightforward, not always a hernia.

Swelling in the groin may represent much more than an inguinal hernia and an inguinal hernia may be much more complicated than it seems upon superficial consideration. Intraperitoneal or retroperitoneal hemorrhage as well as many other congenital, inflammatory, infectious, or neoplastic processes occurring either locally or at distance from the groin may present in the groin, simulating a hernia, or within an inguinal hernia sac itself. Delayed and spontaneous rupture of the spleen are not rare occurrences. The case discussed, an episode of delayed rupture of the spleen presenting as blood within an inguinal hernia sac, serves to emphasize that following a complete clinical evaluation many entities other than simple inguinal hernia must be considered if a thorough differential diagnosis of a groin mass is to be developed.

Adult↗
PubMed1991

Muscle cramps in the cancer patient: causes and treatment.

Muscle cramps may occur in healthy individuals without any apparent cause; these are regarded as benign cramps. Cramps may also develop as a symptom of a systemic disease, such as uremia. Cramps probably originate in the distal portion of the motor nerve. It is unclear whether the nerve terminals are hyperexcitable or prone to repetitive activity in the various related conditions. In the cancer patient, muscle cramps may not be a benign complaint because they often represent an unsuspected underlying pathologic condition associated either with the neoplastic process or the undesirable side effects of therapy. Initial evaluation with a detailed neurologic examination, a complete biochemical profile with magnesium levels and muscle enzymes, and electrodiagnostic examination will lead to the diagnosis in the majority of these patients. Recognized etiologies of cramps may be related to neurologic abnormalities or to nonneurologic causes. Treatment decisions should be oriented according to the following classification: (1) reversible causes; (2) potentially reversible causes and (3) irreversible causes. Whereas the remedy in the first category is to attack the underlying process, if possible, pharmacologic suppression of cramps is the primary approach in the others. Membrane-stabilizing agents, such as quinine, phenytoin or carbamazepine, may be selected according to either nocturnal or daytime predominant occurrence of cramps.

Clinical Protocols↗
PubMed1991

On radical production by PMA-stimulated neutrophils as monitored by luminol-amplified chemiluminescence.

The means by which neutrophils within the body ward off infectious and neoplastic processes by the activation of molecular oxygen, as well as how such mechanisms dysfunction, is the subject of extensive ongoing research. Most previous studies of neutrophil activation indicate that there is a transient production of reactive oxygen species. Luminol-amplified chemiluminescence surveillance of O2-. and H2O2 supported these general findings. Yet, recent studies showed that production of reactive oxygen species by PMA-stimulated neutrophils is not transient but persistent; however, luminol-dependent methods do not corroborate such findings. The kinetics of O2-. production by human neutrophils were studied using luminol-amplified chemiluminescence (CL), spin trapping combined with electron spin resonance detection, and ferricytochrome c reduction. The effects of pH and O2 level on luminol-amplified CL were determined using hypoxanthine/xanthine oxidase to produce O2-. and H2O2 in cell-free systems. As we have found by electron spin resonance and ferricytochrome c reduction, stimulated neutrophils continued to generate O2-. for several hours, yet when luminol-amplified CL was used to continuously follow radical production, CL was shortly lost. Similar loss of CL was observed with continuous enzymatic formation of O2-. and H2O2. The failure of the CL assay to report O2-. and H2O2 formation results from some luminol reaction product which interferes with the light reaction. Our results show that the cells are operative for long periods indicating that cell exposure to prolonged O2-. fluxes does not terminate radical production, and even when pH, [O2], and reagents are optimized, the use of luminol-amplified CL is not a valid assay for continuous monitoring of O2-. and H2O2 generated by either stimulated neutrophils or in cell-free systems.

Cell-Free System↗
PubMedDate not supplied

CT demonstration of ascending colon varices.

The radiographic appearance of intestinal edema, including colonic edema, has been well described in the literature. Severe wall circumferential thickening can occur within the colon in a number of conditions. This includes edema secondary to colitis, allergy, ischemia, and infiltrative neoplastic processes. Edema may be secondary to low protein levels, as from protein losing enteropathy, nephrotic syndrome, and hepatic cirrhosis. The following case, in which there was severe ascending colonic wall thickening due to edema, is unusual in two respects: it had well-developed demonstrated "protective" right colonic varices and a normal protein level.

Blood Proteins↗
PubMed1994

Expression of c-fos proto-oncogene mRNA in non-melanoma skin cancer.

c-fos is a member of the proto-oncogene family and is implicated in the modulation of cell proliferation and differentiation. Previous studies have shown that the c-fos gene expression is regulated in a tissue specific manner. In order to clarify the role of the c-fos gene in human epidermis, we have investigated c-fos mRNA expression in both normal skin and non-melanoma skin cancer. In normal skin the intensity of the c-fos mRNA expression in spinous cells was found to be stronger than that observed in basal cells. In lesions of solar keratosis and Bowen's disease the spinous cells also showed stronger c-fos mRNA expression than in basal cells. In two of four cases of Bowen's disease some upper spinous cells showed very strong mRNA expression of the c-fos gene. In squamous cell carcinomas studied there was considerable variation in the intensity of c-fos mRNA expression. Our findings indicate that the degree of c-fos mRNA expression is related to the degree of dysplasia present. In all cases of basal cell carcinoma examined the c-fos mRNA expression was markedly decreased. These results suggest that c-fos expression may be involved in the differentiation of human keratinocytes in vivo rather than in the neoplastic process itself.

3T3 Cells↗
PubMed1988

Liver tumours.

Humans are remarkably resistant to many carcinogens that readily produce liver tumours in rodents, particularly the rat. The neoplastic process has been extensively studied in animal experiments, but little is known so far of how it evolves in humans. Few drugs have been shown to cause liver tumours in humans, and the risk appears to be low. The best-known examples are C17-alkylated or ethinylated gonadal sex steroids. Oral contraceptives have now been in use by millions for thirty years, but only a few hundred cases at most of liver cell adenoma have been observed. The role of these substances in liver cell carcinoma remains controversial, and the evidence is weaker still in relation to focal nodular hyperplasia and other tumour-like conditions. Anabolic-androgenic steroids stand out as the major cause of peliosis, but liver cell tumours induced by them seem to be adenomas and not carcinomas as originally suggested. The effect that both oral contraceptives and anabolic-androgenic steroids have on liver vasculature is of great clinical importance as the most important complication of liver tumours is rupture, leading to life-threatening haemorrhage. For this reason, liver tumours arising in users of these drugs should be removed whenever feasible. Thorium dioxide will remain a risk factor for the development of angiosarcoma, liver cell carcinoma and bile duct carcinoma for some time yet, and the number of patients who have been exposed is high--tens of thousands at least. The evidence of a carcinogenic role for many other drugs is anecdotal or weak. Neoplasia in the liver seems to be the least important side-effect of drugs in clinical use.

Anabolic Agents↗