Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “tumor evolution”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1977

Comparative investigation of DNA from mouse and Ehrlich ascites tumor cells.

Mouse DNA and DNA of Ehrlich ascites tumor have been comparatively studied in the search for changes in DNA during tumor progression. No differences were found in kinetics of homologous (mouse X mouse) and heterologous (mouse X tumor) DNA reassociation; in thermal stability of homologous and heterologous duplexes of repeated, unique and satellite DNA; in percentage of hybridization with mouse liver heterogenous nuclear RNA; in thermal stability of the RNA.DNA hybrids. The negative results suggest that the considerable evolution of transplantable tumors (both in biological properties and in karyotype) has not been accompanied by alterations of the genome which could be detected by the now available methods of molecular hybridization for studying DNA divergence. In the light of the results obtained the functions ascribed to the mouse satellite DNA are discussed.

Animals↗
PubMed1977

The evolution of mature teratoma from malignant testicular tumors.

During the period of 1969--1976, twelve cases of malignant germ cell tumor of the testis were seen in which the diagnosis was associated with the subsequent development of one or more metastases composed histologically of fully mature teratoma. These patients had a variety of primary germ cell tumors in the testis and were treated with radiation therapy and/or chemotherapy in addition to surgery, prior to the development of mature teratomas in different anatomic sites. The development of mature teratoma in this clinical setting seems to be a favorable prognostic sign, inasmuch as only one of the 12 patients has died with known persistent cancer. Since the incidence of this phenomenon seems to be increasing, the mechanism is probably related, directly or indirectly, to therapy.

Adolescent↗
PubMed1987

Polyclonal chromosomal evolution in a benign mixed salivary gland tumor.

Banding analyses of a human benign pleomorphic adenoma in the parotid gland revealed a polyclonal pattern where structural rearrangements predominated. These deviations were different from the anomalies previously observed in 100 mixed tumors. The reason found for the differences in all likelihood was x-ray treatment of tuberculous lymphadenitis in the neck during childhood. Implications regarding origin and development of pleomorphic adenomas are discussed.

Adenoma, Pleomorphic↗
PubMed1986

Continuous pyruvate carbon flux to newly synthesized cholesterol and the suppressed evolution of pyruvate-generated CO2 in tumors: further evidence for a persistent truncated Krebs cycle in hepatomas.

Viable tissue slices from rat liver and Morris hepatoma 3924A were compared as to their ability to incorporate carbons from [U-14 C]pyruvate into newly synthesized cholesterol versus CO2. By 4 h, the tumor slice incubation had incorporated over 6-fold more pyruvate carbons into the sterol than into CO2, relative to the normal liver slice incubation, per g tissue protein. However, the presence of the mitochondrial citrate exchange carrier inhibitor 1,2,3-benzenetricarboxylate in the incubation inhibited the formation of [14C]cholesterol, while simultaneously leading to an increase in the rate of 14CO2 production in the tumor. In the normal liver system by contrast, benzenetricarboxylate also inhibited [14C]cholesterol formation, but had hardly any effect on the already high rate of 14CO2 production. The ability of benzenetricarboxylate to inhibit the rapid carbon flux from pyruvate to cholesterol, and to steer the metabolic flow of carbons toward oxidative decarboxylation via the Krebs cycle in whole, viable tumor tissue, indirectly emphasizes the importance of the mitochondrial citrate exchange carrier in supporting the decontrol of cholesterogenesis de novo in tumors by accelerating the supply of lipogenic precursor carbons to the tumor cytosol. These studies may be therefore interpreted as extensions, to the level of whole-cell metabolism, of the concept of a persistent 'truncated' Krebs cycle in the mitochondria of metastatic cancer tissue. This concept states, in part, that a rapid efflux of mitochondrially generated citrate would operate preferentially in tumors, and thus provide carbons continuously to the cytoplasmic compartment where the well-established deregulated pathway of cholesterogenesis occurs (Parlo, R.A. and Coleman, P.S. (1984) J. Biol. Chem. 259, 9997-10003; Coleman, P.S. and Lavietes, B.B. (1981) CRC Crit. Rev. Biochem. 11, 341-393).

Animals↗
PubMed2007

Four hypotheses on mitochondria's role in the development and regulation of oxidative stress in the normal state, cell pathology and reversion of tumor cells.

The biological evolution has resulted in adaptation of both unicellular and multicellular organisms to negative effect of excessive O2 in reply to gradual increase of free oxygen (O2) contents in the earth atmosphere. This adaptation has led to formation of various antioxidant systems in the organism. Such system within the cell has hierarchic structure and is represented by at least than three levels of protection: antioxygene, antiradical and antiperoxide. The first and most effective antioxidant level is represented as mitochondrial respiration able to perform several functions. One of these functions is antioxygene since the very the mitochondria's capability to be a main O2 consumer in the cell provides for low but sufficient for respiration and energy supply levels of O2 partial pressure and dependent concentrations of active O2 forms. The latters, being signal molecules at certain values, modify regular and synthetic processes in the cells either directly or indirectly. This is the possibility for mitochondria to more extensively affect the intracellular processes than simply produce ATP. In case of defective of the cell first protection line the hyperoxia starts due to poor utilization of the incoming O2. Change in mitochondria's "capacity" (quantity, size and maturity level of mitochondria) anyway occurring in the cells are an efficient way of regulation of the oxy-peroxide condition (oxidative stress) and related signal channels. The relationship between changes in the condition of cells, i.e. from their normal state to different pathologic forms, and growing disbalance Delta(PO-AO) between its pro-oxygen (PO) and anti-oxygen (AO) components has been assumed. It is expected that during the evolution the cell could have supposedly acquired a sequence of "specialized" Delta(PO-AO) disbalances. Each sequence needs to implement a certain set of biochemical processes. The probability of Delta(PO-AO) disbalance gradation with specification of their value ranges has been determined. These ranges identify or impact certain cell state, namely proliferation of normal cell (oxidative mitogenesis), ageing, A1 apoptosis, carcinogenesis, A2 apoptosis, and oxidative cytolysis. The cited assumption allows us to: (1) explain reverse dependence of cell proliferation due to the level of their differentiation, increase in the amount and activity of mitochondria as an indispensable condition for the disbalance shift towards differentiation, (2) bring up the idea that regress of the cells, and in particular tumour cells, directly results from the Delta(PO-AO) disbalance decrease to certain levels under the influence of reverse inductors, (3) explain relatively easy and frequent embryonic and stem cells malignancy, and also their reversal normalization. These phenomena occur due to small number and/or size of mitochondria in the designated cells. To verify the above mentioned hypotheses it is primarily necessary to be able to stimulate and slow down the mitochondria biogenesis in the embryonic, stem, ageing, cancer and other cells.

Animals↗
PubMed2003

Cytogenetic and morphologic typing of 58 papillary renal cell carcinomas: evidence for a cytogenetic evolution of type 2 from type 1 tumors.

We evaluated clinical characteristics, patient outcome (mean follow-up, 47 months), and cytogenetic abnormalities in the largest as yet reported cytogenetic series of 47 primary and 11 secondary papillary renal cell carcinomas for differences between the recently proposed type 1 and type 2 subtypes. Secondary tumors were more often of type 2 morphology (P = 0.02), whereas primary type 2 tumors were associated with higher clinical stage (P = 0.001) and worse patient outcome (P = 0.02). Although both subtypes had at least one of the primary chromosomal gains at 17q, 7, and 16q, type 2 tumors had moderately lower frequencies of primary gains at 17p (61 versus 94%; P = 0.007) and 17q (72 versus 97%; P = 0.02). On the other hand, type 2 tumors overall had more chromosomal alterations than type 1 tumors (P = 0.01), particularly gains of 1q (28 versus 3%; P = 0.02) and losses of 8p (33 versus 0%; P = 0.001), 11 (28 versus 3%; P = 0.02), and 18 (44 versus 9%; P = 0.01). Hierarchical clustering suggested cytogenetic patterns common but not restricted to type 2 morphology, one characterized by multiple additional gains, and another predominantly showing additional losses. These findings provide genetic evidence that type 1 and type 2 tumors arise from common cytogenetic pathways and that type 2 tumors evolve from type 1 tumors. Independently of type, losses of 9p were statistically correlated with advanced disease (P = 0.0008) and may serve as a potential adverse prognostic marker in papillary renal cell carcinomas.

Adult↗
PubMed1975

Evolution and modes of transmission of RNA tumor viruses. Parke-Davis Award lecture.

Most vertebrates contain sets of gene sequences (virogenes) which are an integral part of the chromosomal DNA and which can code, in some instances, for the production of Type C RNA tumor viruses. These genes are transmitted from parent to progeny along with other cellular genes, and their activation from a normally reressed state may be part of the mechanism by which RNA tumor viruses produce cancer. Isolates of endogenous genetically transmitted baboon Type C viruses are morphologically and biochemically related to other mammalian Type C viruses but can clearly be distinguished from the other groups (mouse, rat, cat, etc.) by immunologic and nucleic acid hybridization criteria. Within the primates, Type C viral gene sequences have evolved as the species have evolved, with virogenes from the most closely related genera and families showing the most sequence homology; all higher primate, including man, however, do have detectable virogene sequences in their normal tissues. Type C viruses have also been transferred under natural conditions between species only remotely related phylogenetically. The results show three clear examples where viral genes from one group of animals have become incorporated into the germ line of genetically distant groups of animals (inheritance of acquired genes). Infectious Type C viruses of primates, distinct from the endogenous primate virus group, have also been isolated (woolly monkey and gibbon isolates) and can be shown to produce tumors in other primates. Related viral information (nucleic acid sequences, enzymes, and antigens) have been reported in human tumors. The significance of infectious and/or genetically transmitted viruses in naturally occurring cancer is a major focus of current research. The presence of genetically transmitted viral genes in so many vertebrate species and the evidence that they have been conserved in several distinct vertebrate lineages suggests that they may provide some normal function(s) advantageous to the species carrying them and that their potential to cause cancers is a pathologic manifestation of normal, as yet undefined, physiologic processes.

Animals↗
PubMed1977

Evolution of surgical treatment of bilateral Wilms' tumor.

Bilateral Wilms' tumor (stage V) accounts for 10 to 15% of patients with nephroblastoma. Heretofore, surgical resection in many of these children presented insoluble technical problems. Ex vivo renal perfusion with "bench" surgical excision and revascularization has been applied in the management of a child with bilateral Wilms' tumor unresectable by conventional techniques. Complete extirpation of tumor was accomplished. Furthermore, the autotransplanted kidney was removed from the field of radiation therapy given after operation. By selective application of this technique, the child with bilateral Wilms's tumor can be approached with a greater expectation of cure.

Child, Preschool↗