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At least 19 recordsLinked to original sources
PubMedDate not supplied

[Transdiaphragmatic shunt with a Roux loop in non-resectable neoplastic processes of the cardia].

On the basis of 26 cases with non-operable primary or secondary neoplastic obstructions of the cardia the authors express the opinion that the best solution is the transdiaphragmatic pontage with a jejunal loop mounted in Y. Enlargement of this indication should not be made on behalf of radical or palleative resections, but on the contrary internal derivations should increase the range of surgical solutions in cancer of the cardia. Making an analysis of the major aspects (death-rate, indications and some technical details) in connection with the by-pass with a Roux loop the authors stress the benignity of this type of surgery and the chances it has to take the place of external derivations, compared with which it provides both nutritional and moral advantages.

Cardia↗
PubMed1975

Paget's disease of the breast.

Criteria of the morphological diagnosis as well as the histogenesis of the lesions in Paget's disease are presented; the authors claim that the initial lesion occurs in the lactiferous ducts, the skin being secondarily involved. Likewise, the dyskeratotic lesions are considered as secondary to the neoplastic process, either by neoplastic induction or by mobilization and proliferation of cancerous cells from lactiferous ducts. The utility of biopsies in all cases of nipple eczema, and of the histologic investigation of the profound tissues is pointed out. In this way the canalicular starting point in the vicinity of the nipple can be noticed.

Breast↗
PubMed1976

Editorial: Chromosomes and human neoplasms. Achievements using new staining techniques.

Numerical and structural chromosome aberrations are frequently found in neoplastic cells. As demonstrated by the new chromosome banding techniques these aberrations are not random, but tend to show a specific occurrence. A model example is the leukemias where many cytogenetical investigations have been done to date. In leukemia chromosome analysis serves the following purposes: to identify a neoplastic process, to confirm and strengthen the hematological diagnosis, for the early diagnosis of transformation from a chronic leukemia into its blastic phase and for following up the clonal evolution of a leukemic cell line. In the discussion of chromosomes and neoplasms it must be mentioned that individuals demonstrating chromosomal instability and some trisomic patients show a greater tendency toward the development of a malignancy. Malignancy is primarily a cellular phenomenon caused by a disturbance in cellular regulation, whose fine events are not known. Therefore the exact role of the chromosomes in neoplastic processes cannot be stated. From experimental investigations it appears that the affected chromosomes carry cell growth regulating factors and also that a specific aberration is the result of the action of a specific agent.

Acute Disease↗
PubMed1977

Zinc biochemistry in normal and neoplastic growth processes.

Zinc is essential for the growth of all species. Growth arrest results from its deficiency and presumably reflects important roles for this metal at critical points of metabolism. Studies of zinc metalloenzymes show that zinc serves as a coenzyme to more than 80 enzymes, among which are the reverse transcriptases which cause leukemia in many species. Its role in nucleic acid metabolism is emphasized.

DNA-Directed DNA Polymerase↗
PubMedDate not supplied

Spontaneous mutation of RNA tumour viruses.

There are 2 categories of spontaneously occurring avian and mammalian RNA tumour virus mutants: conditional and non-conditional. 1) Conditional mutants are able to replicate in or transform cells only under certain physiological conditions or in certain cells. RNA tumour virus temperature-sensitive mutants, focus-morphology mutants, and host range mutants are spontaneously formed. Some of these conditional mutants probably arise by point mutations in the viral genome. 2) Non-conditional mutants have genetic lesions that render them inactive under all conditions. There are non-conditional spontaneous RNA tumour virus mutants that are missing either the virion envelope glycoprotein or both the envelope glycoprotein and the virion DNA polymerase. These mutants cannot replicate or transform cells. Other spontaneous non-conditional mutants can replicate but are defective in their ability to transform fibroblastoid cells. These spontaneous transformation-defective mutants can have deletions in 10-20% of the genomic RNA. Conditional mutants with an altered host range occur at a high rate of approximately 1 mutation/50 infected cell generations during DNA-to-DNA information transfer. This type of conditional mutation requires cell replication but does not occur frequently either during the original synthesis of viral DNA (RNA-to-DNA information transfer) or during the transcription of progeny viral RNA from the (RNA-to-DNA information transfer) or during the transcription of progeny viral RNA from the DNA (DNA-to-RNA information transfer). Temperature-sensitive and focus-morphology mutants also have a high rate of spontaneous formation. Non-conditional mutants missing the viral envelope glycoprotein, DNA polymerase, or transformation gene, also appear to be spontaneously formed at a high rate. Normal avian and mammalian cells contain RNA tumour virus-related genes in their DNA. It is hypothesized that these endogenous RNA tumour virus-related genes in normal cells also have a high rate of spontaneous mutation and are involved in neoplastic processes.

Animals↗
PubMed1977

Persistently abnormal brain scintigraphy after cerebral infarction.

The current literature indicates nuclear brain images typically return to normal within two to three months following an episode of cerebral infarction. In this report, two patients are described who demonstrated no significant change in their brain scan abnormalities 11 and 17 months following their strokes. Computed tomography confirmed the clinical impression that the persistent brain scan abnormalities were due to cerebral infarction rather than to neoplastic process.

Aged↗
PubMedDate not supplied

Persistence of nucleolar RNA-rich structures and Ph1 duplication in the blastic crisis of chronic myeloid leukaemia.

Nucleolar persistence in metaphase plates is a feature observed in most of the cells in neoplastic processes. Pathological persistence or fragmentation of the nucleoli is thought to be the cause of some numerical chromosomal aberrations due to non-disjunction of the chromatids, with particular involvement of the satellite chromosomes. Thus, a combined selective staining of both the nucleoli (amido black 10B according to Mundkur and Brauer's cytochemical technique) and the chromosomes (neutral red) was applied to the metaphase plates of patients with chronic myeloid leukaemia in the blastic crisis. Duplicated Ph1 was associated with amido black-stained areas at a very high rate in some cases. Since the blastic crisis in chronic myeloid leukaemia is characterized by the appearance of an increased number of immature, highly nucleolated cells, these findings lend support to the hypothesis that the duplication of the Ph1 represents a feature possibly favoured by the pathological persistence of nucleolar RNA-rich structures in the metaphase.

Adult↗
PubMed1977

Treatment of Paget's disease of bone with mithramycin.

The hypothesis that Paget's disease of bone is a low grade neoplastic process led us to use the cytotoxic antibiotic mithramycin in its treatment. The dramatic effects observed on the serum calcium and alkaline phosphatase, and urinary hydroxyproline are compatible with the concept that mithramycin is primarily toxic to osteoclasts. Subjective and objective clinical effects establish this agent as useful in the treatment of Paget's disease despite its observed toxicity to other organ systems.

Chemical and Drug Induced Liver Injury↗
PubMed1975

Influence of carbon tetrachloride or riboflavin on liver carcinogenesis with a single dose of aflatoxin b1.

Liver carcinogenesis with a single dose of aflatoxin B1 (7 mg/kg body weight) has been investigated in a group of female Wistar strain rats by repeated biopsies and necropsies. Another group received a subsequent intoxication with carbon tetrachloride by inhalation (approximately 200 doses) and another one was overloaded with riboflavin (25 parts/10(6) in drinking water). The frequency of hepatomata was almost equal in the aflatoxin and aflatoxin-carbon tetrachloride group. It was lowere in the riboflavin-aflatoxin group. In these 3 groups cirrhosis was never present in neoplastic livers. Megalocytosis was the first lesion observed. All tumoral livers had previous or concomitant megalocytosis. This modification was about as frequent, intense and widespread in aflatoxin-CCl4 and aflatoxin groups but appeared much earlier, as did the first hepatoma, in the aflatoxin-CCl4 group. It was less frequent, less intense and less widespread in the riboflavin-aflatoxin group than in the aflatoxin group. There was also a lower frequency of hepatomata in the riboflavin-aflatoxin group, but the difference was not significant due to the too small number of animals involved. The facts are not a proof of the existence of an obligatory link between megalocytosis and carcinogenesis since a slight megalocytosis was observed in the riboflavin group not affected by the neoplastic process. However, the simplest explanation of our results would be to consider that the potential tumour cells are located among the megalocytic cells, without admitting that every megalocyte is obligatorily a precancerous cell. CCl4 seems to act in shortening the time of appearance of megalocytosis. The protective effect of riboflavine should be regarded with more caution.

Aflatoxins↗
PubMed1975

[Progressive multifocal encephalitis (PML)].

In four cases of progressive multifocal leucoencephalitis the basic disease was always a malignant lymphogranuloma. Changes in the brain were multifocal, however the frontoparietal area of the white matter was affected most frequently and foci in this part were oldest. In these foci demyelination with atypical astrogliosis predominated, and there was a very small number of scavenger cells. At the periphery of foci always proliferation and enlargement of homogenous oligodendroglia nuclei were found sometimes with inclusions which in immunoassay sometimes had a common antigen with papovirus SV 40 and on electronoptic examination always contained many virions of the papovirus. No direct relationship was found between the duration of the neoplastic process, its type and changes in the CNS.

Adult↗
PubMed1976

Serological and epidemiological considerations of the role of herpes simplex virus type 2 in cervical cancer.

To assess the possible biological significance of the observations that women with cervical cancer tend to be younger at first intercourse than control women, data from 1823 women were analyzed for the relationship between age at 1st intercourse and number of sex partners. Women who were younger at first intercourse had more sex partners than did women who were older at first intercourse. The interdependence of age at first intercourse and number of sex partners does not exlude the possibility that intercourse at an early age represents a biologically significant event in which the neoplastic process is initiated. However, it is equally possible that younger women at first intercourse may have multiple sex partners and be at greater risk of coming in contact with a putative oncogenic agent later in life. In addition, sera from patients with herpesvirus infections were assayed for cross-reacting and type-specific antibodies. Approximately 80% of the total antibody activity was to the cross-reacting antigen and only 20% was to the type-specific antigens in the sera of patients infected with either type 1 or type 2 virus. Among patients infected with both types of virus, less antibody activity to the type-specific antigens and more antibody activity to the cross-reacting antigens were found. These observations are discussed with respect to case-control seroepidemiological studies.

Age Factors↗
PubMed1976

A general concept for molecular biology of cancer.

The demonstrations that "fetal" isozymes and other fetal or "oncodevelopmental" antigens are present in tumor cells has led to the general concept that genes normally silent in adult tissues are activated during the neoplastic process. Recent evidence that some chromatin proteins of tumor cells are fetal antigens has suggested that some of the "switches" involved in gene activation for tumor growth may also be fetal or oncodevelopmental. These results have led to current theoretical concept that fetal gene derepressors interact with the genome to produce messenger RNA for the protein products involved for growth, invasiveness, and metastasis. These processes may not be controllable in adult cells because of the lack of inhibitors, which were present during embryonic development but are not produced in adult tissues.

Animals↗
PubMed1978

Angio-immunoblastic lymphadenopathy. Report of a case with pleural effusion.

A 78-year old man is presented with a characteristic case history and physical and laboratory findings typical of angio-immunoblastic lymphadenopathy with dysproteinemia (AILD). The disease had an acute onset with constitutional symptoms, generalized lymphadenopathy and hepato-splenomegaly. The presence of a large pleural effusion was of particular interest. Histologically the distinctive feature was a pronounced proliferation of small blood vessels and immunoblasts in the lymph nodes. Management of patient with AILD is problematic. Since AILD is a non-neoplastic process, symptomatic treatment with small doses of steroids, if necessary, would seem to be the best therapeutic approach. However, in our patient, as well as in other cases reported in the literature, a rapid and long standing (18 months so far in our case) complete remission was obtained with a short cycle of chemiotherapy.

Aged↗
PubMed1979

Cytochemistry of nucleoproteids and some cathionic proteins in the peripheral blood leukocytes of patients with lung cancer.

In 40 patients with untreated lung cancer cytochemical studies of the peripheral blood leukocytes were conducted by means of a cytological method for the simultaneous staining of nucleoproteids (RNP and DNP) and some cathionic proteins (after Zvetkova and Zvetkov [60]). Changes were detected in the RNP cytoplasmic contents of lymphocytes, of which the most outstanding were the reduction and uneven distribution of RNP granules, their frequent extracellular expulsion by means of microclasmatoses, as well as changes in the staining of cathionic proteins of RNP accompanied by an increased nuclear chromatin condensation in the small and medium-sized lymphocytes. Parellel to reducing of the percentage of these cells in the peripheral blood of patients with advanced neoplastic disease an increased number of lymphoblastoid and monoblastoid cells is established with RNP diffusely stained, but reduced in quantity and localized in the cytoplasmic periphery and projections (compared to Downey type II atypical cells). By means of one of the variants of the method (modified type of Feulgen's reaction) a characteristic distribution and structuring of the nuclear chromatin is established in mono- and polymorphonuclear cells, most clearly expressed in the nuclei of monocytes and monoblastoid cells, as well as in nuclei of neutrophil granulocytes. In these cellular types a more specific nuclear modelling (microhypersegmentation) is observed resulting in multiple irregular nuclear projections on the nuclear surface, probably caused by subkaryolemal distribution of uneven chromatin thickenings. The changes are also recorded in the cathionic protein containing secondary cytoplasmic granules in granulocytes-neutrophils and eosinophils, probably associated with changes in the lysosomal and phagocytic functions of these cells in neoplastic diseases. The authors discuss the importance of the obtained results in connection with data on the participation of lymphocytes and neutrophils in the immune response to tumour antigenic stimuli during the course of the neoplastic process, as well as with data on the suppressive effect of antigenic (serum, viral) factors, possibly affecting the synthesis and the transport of cellular nucleoproteids (RNP and DNP) in leukocytes of cancer patients.

Blood Proteins↗
PubMed2026

Mapping micrometastatic seeds of relapse.

In this issue of Cancer Cell, Liu et al. apply spatial multi-omics to map colorectal cancer micrometastases across primary tumors and matched liver and lung metastases, revealing liver micrometastases as an early evolved, stem-like, immune-suppressed residual disease state linked to a six-gene recurrence signature.

Colorectal Neoplasms↗
PubMed2010

Mouse Prkar1a haploinsufficiency leads to an increase in tumors in the Trp53+/- or Rb1+/- backgrounds and chemically induced skin papillomas by dysregulation of the cell cycle and Wnt signaling.

PRKAR1A inactivation leads to dysregulated cAMP signaling and Carney complex (CNC) in humans, a syndrome associated with skin, endocrine and other tumors. The CNC phenotype is not easily explained by the ubiquitous cAMP signaling defect; furthermore, Prkar1a(+/-) mice did not develop skin and other CNC tumors. To identify whether a Prkar1a defect is truly a generic but weak tumorigenic signal that depends on tissue-specific or other factors, we investigated Prkar1a(+/-) mice when bred within the Rb1(+/-) or Trp53(+/-) backgrounds, or treated with a two-step skin carcinogenesis protocol. Prkar1a(+/-) Trp53(+/-) mice developed more sarcomas than Trp53(+/-) mice (P < 0.05) and Prkar1a(+/-) Rb1(+/-) mice grew more (and larger) pituitary and thyroid tumors than Rb1(+/-) mice. All mice with double heterozygosity had significantly reduced life-spans compared with their single-heterozygous counterparts. Prkar1a(+/-) mice also developed more papillomas than wild-type animals. A whole-genome transcriptome profiling of tumors produced by all three models identified Wnt signaling as the main pathway activated by abnormal cAMP signaling, along with cell cycle abnormalities; all changes were confirmed by qRT-PCR array and immunohistochemistry. siRNA down-regulation of Ctnnb1, E2f1 or Cdk4 inhibited proliferation of human adrenal cells bearing a PRKAR1A-inactivating mutation and Prkar1a(+/-) mouse embryonic fibroblasts and arrested both cell lines at the G0/G1 phase of the cell cycle. In conclusion, Prkar1a haploinsufficiency is a relatively weak tumorigenic signal that can act synergistically with other tumor suppressor gene defects or chemicals to induce tumors, mostly through Wnt-signaling activation and cell cycle dysregulation, consistent with studies in human neoplasms carrying PRKAR1A defects.

Animals↗