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 883 records · Page 49Linked to original sources
PubMed2002

Vascular tumor growth and treatment: consequences of polyclonality, competition and dynamic vascular support.

A mathematical model is presented to describe the evolution of a vascular tumor in response to traditional chemotherapeutic treatment. Particular attention is paid to the effects of a dynamic vascular support system in a tumor comprised of competing cell populations that differ in proliferation rates and drug susceptibility. The model consists of a system of partial differential equations governing intratumoral drug concentration, cancer cell density, and blood vessel density. The balance between cell proliferation and death along with vessel production and destruction within the tumor generates a velocity field which drives the expansion or regression of the neoplasm. Radially symmetric solutions are obtained for the case when only one cell type is present and when the proportion of the tumor occupied by blood vessels remains constant. The stability of these solutions to asymmetric perturbations and to a small semi-drug resistant cell population is then investigated. The analysis shows that drug concentrations which are sufficient to insure eradication of a spherical tumor may be inadequate for the successful treatment of non-spherical tumors. When the drug is continuously infused, linear analysis predicts that whether or not a cure is possible is crucially dependent on the proliferation rate of the semi-resistant cells and on the competitive effect of the sensitive cells on the resistant population. When the blood vessel density is allowed to change dynamically, the model predicts a dramatic increase in the tumor's growth and decrease in its response to therapy.

Animals↗
PubMed1991

[T1 bladder tumors. Can they be considered superficial?].

The authors report about a series of 60 cases of superficial (Ta and T1) bladder tumors and study their evolution towards infiltration according to the grade, size and number. 16% of the T1 tumors evolved towards infiltration and/or metastatic spread after a period of 42 months. In our opinion, T1 tumors can be regarded as superficial tumors. However, our therapeutic attitude is cautious because of pejorative factors of prognosis: high grade, multiple foci, and size exceeding 5 cm.

Follow-Up Studies↗
PubMed1993

[Spontaneous hemorrhage of the parathyroid disclosed by an extensive cervical hematoma].

Extra capsular bleeding occupies a particular place within the evolutional complications of parathyroid tumors. Its rarity, the difficulty of the pre-operative diagnosis and its potential evolution towards airway obstruction by compression underline its singular character. A case is presented where an evolutive cervico-thoracic hematoma, evolving without functional symptoms, has led to the diagnosis of parathyroid hyperplasia. The diagnostic and therapeutic characteristics of this pathology are detailed and confronted to the similar cases found in the literature.

Aged↗
PubMed2001

Genetic predisposition and somatic diversification in tumor development and progression.

Studies on human cancer predisposition syndromes have contributed significantly to our understanding on tumor initiation and progression. Work performed on hereditary colon cancer has been particularly fruitful. Much of the molecular background of the various intestinal polyposis syndromes, such as familial adenomatous polyposis (FAP), juvenile polyposis, and Peutz-Jeghers syndrome, has been revealed, pinpointing several key cancer-associated genes. Studies on hereditary nonpolyposis colorectal cancer (HNPCC) have revealed a novel mechanism of tumorigenesis; genomic instability caused by defective DNA mismatch repair (MMR). Understanding the molecular background of these diseases helps us to understand tumor initiation in the affected individuals. Relatively little is known about the details of tumor progression in hereditary and sporadic neoplasia. Certain additional gene mutations can be associated with advancing stages of the disease, but the pace and tempo of the process have remained obscure. A high mutation rate in MMR-deficient tumors has provided a new approach in the analysis of human tumor dynamics. Microsatellite (MS) sequences are frequently mutated in MMR deficient tumors. The high mutation rate allows the use of microsatellite mutations as a tool for analyzing the past patterns of tumor progression. This approach is similar to the use of MS mutations in studying human evolution and migrations. Such tumor studies have revealed progression pathways that differ from the classic adenoma-cancer sequence. The reasons why and how molecular clocks may reveal something new about a well-studied problem are discussed.

Animals↗
PubMed1999

Humoral immune responses of cancer patients against "Cancer-Testis" antigen NY-ESO-1: correlation with clinical events.

Humoral immune responses against the "Cancer-Testis" (CT) antigen NY-ESO-1 are frequently observed in patients with NY-ESO-1 expressing tumors. This is in contrast to other known tumor antigens (TA) defined by antibody or cytotoxic T cell (CTL) reactivity, i.e., MAGE-1, MAGE-3, SSX2, Melan A, and tyrosinase. No NY-ESO-1 antibody has been detected in healthy controls and patients with NY-ESO-1 negative tumors. In this study, we have assessed the NY-ESO-1 serum antibody response in patients with NY-ESO-1 positive tumors of different histological types and stages using Western blotting and an ELISA. Of the 12 patients analyzed, 10 had demonstrable NY-ESO-1 antibodies at the start of the study. All patients were followed for changes in NY-ESO-1 antibody titers during the course of tumor treatment and clinical evolution. In 4 patients, an increase of NY-ESO-1 antibody titer was observed with progression of disease or extensive tumor necrosis under treatment. One patient showed a stable NY-ESO-1 antibody titer over 3 years along with gradual regression of a large tumor mass. In 5 patients, a decrease of NY-ESO-1 antibody was detected: in 1 patient after curative tumor resection, in 3 patients with partial regression of metastatic disease under chemo- and immunotherapy, and in another patient with a NY-ESO-1 negative tumor relapse. Our results indicate that the induction and maintenance of NY-ESO-1 antibody is dependent on the presence of NY-ESO-1 expressing tumors. Furthermore, changes in NY-ESO-1 antibody titers correlate with the evolution of NY-ESO-1 positive disease.

Adult↗
PubMed2006

Successful therapy must eradicate cancer stem cells.

Despite significant improvements in cancer therapy, tumor recurrence is frequent and can be due to a variety of mechanisms, including the evolution of resistance and tumor progression. Cancer stem cells have been postulated to maintain tumor growth similar to normal stem cells maintaining tissue homeostasis. Recently, the existence of these malignant stem cells has been proven for hematological as well as some solid tumors. Tumor stem cells are not targeted by standard therapy and might be responsible for treatment failure and tumor recurrence in many patients. We designed a simple mathematical model to demonstrate the importance of eliminating tumor stem cells. We explored different therapeutic scenarios to illustrate the properties required from novel therapeutic agents for successful tumor treatment. We show that successful therapy must eradicate tumor stem cells.

Animals↗
PubMedDate not supplied

Immediate and late results in the surgical treatment of gastric cancer.

The study of 248 patients mostly males, aged over 50 years, operated on for gastric cancer (GC) has shown that the majority were in stages III and IV of disease. The antral localization of the tumor was the most frequent. In 6.45% of the cases acute complications occurred during the evolution of gastric cancer. Association with other diseases was found in proportion of 5.64%. The surgical treatment was differentiated according to the site and evolutive stage of the tumor but the most frequent was radical subtotal gastrectomy. The postoperative complications were either general or local. Postoperative mortality was higher in cancers situated in the upper third of the stomach, after total gastrectomy, and in stage IV of disease. The 5-year survival was 66.66% for stage II and 10.18% for stage III and the 10-year survival decreased to 40 and respectively 1.85%.

Adenocarcinoma↗
PubMedDate not supplied

[Reactive lymph-node hyperplasia and pseudolymphomas with hypergammaglobulinemia. II. Pseudolymphoma and prelymphoma].

In this second part, the dysimmunitary conditions which associate a polyclonal hypergammapathy and adenopathy are studied. The latter simulate a malignant lymphoma both clinically and histologically, hence the term sometimes used: "pseudo-lymphoma". Above all, these dysimmunitary states should be considered as real pretumoral states, and a malignant lymphoma or Kaposi sarcoma can arise at any time during the evolution of the illness. Finally, all these illnesses, even apart from the appearance of malignant tumors, have a severe evolution and death can occur due to consequences of immune disorders and particularly to infection. The different histopathological and evolutive aspects of the following are successively studied: angio-immunoblastic lymphadenopathy; the association of adenopathy with Kaposi's sarcoma; the syndrome of epidemic immune deficiency of T cells (acquired immune deficiency syndrome; frequent in homosexuals; the Gougerot-Sjögren syndrome; adenopathy due to medicaments; and the lymphomatoid granulomatosis of Liebow. The similarity of the histopathological lymph node lesions observed in these different dysimmunitary states suggests an identical physiopathology. Also, the existence of frequent associations between these different diseases suggests a common triggering mechanism. The role of virus on a favourable hereditary ground is discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Malignant pleural tumor in a child mimicking a mesothelioma.

Malignant tumors of pleural origin are rare in childhood and difficult to diagnose. We report a case in a white 11 1/2-year-old girl who presented with a bulky tumour in the basal left lung field. There was an area of osteolysis at the ventral extremity of the 9th left rib allowing excision of the tumor by lateral thoracotomy. Macroscopically the operation was satisfactory. Despite two complementary excisions, chemotherapy with Vin-Caepi and consolidation chemotherapy followed by bone-marrow autograft, left pleural metastases appeared two years later. A second operation, a new course of chemotherapy with stage IV SIOP MMT, followed by a second bone-marrow graft and mediastinal radio-therapy, resulted in remission. At the time of this report, after three and a half years of evolution, the child's condition is satisfactory and she leads a normal life without treatment. A probable diagnosis of pleural mesothelioma was arrived at by elimination. This kind of tumour, without specific markers, is difficult to distinguish from small-round-cell tumors. Evolution is unpredictable and often rapidly fatal. Although these tumors generally have a weak response to chemo- and radiotherapy, we think that close follow-up and active therapy, rapidly initiated at the slightest sign, can improve the quality of life of the patients and increase their survival.

Child↗
PubMedDate not supplied

[Cutaneous histiocytosarcoma: clinical, immunohistochemical and ultrastructural aspects; difficulties of study and problems of nosology (author's transl)].

Reporting a case of cutaneous tumor of the back of recent occurrence and rapid increase in a 79-years-old woman, according to Crosti's "reticulosis", the authors discuss the following points:--the histiocytic nature of the tumor cells particularly based on immunohistochemical studies (peroxidase activity, anti-HTLA serum) and on electron microscopy with special reference to the multivesicular bodies found in their cytoplasm;--the tests for correct identification of the histiocyte (including electron microscopy, tests for HTLA and HBLA antigens, peroxidatic reaction, acid phosphatase activity, and in vivo or in vitro phagocytosis);--the out of date character of the concept of malignant "reticulosis" in the hematologica and dermatologic classifications, the recent advances in the knowledge of the nature of the so-called "reticulum" (or "reticular") cell which seems to be a distinct entity derived from the mesenchymal cell (as the fibroblast);--the clinical and evolutive characteristics of histiocytic tumors (no hematologic involvement, slow evolution, high radiosensitivity), the difficulties in defining their malignancy and, above all, in finding comparable references in the literature with complete cellular study;--the nosologic place of this affection among the group of haematodermas and in the pathology of the mononuclear phagocyte system. The generic term of cutaneous histiocytosarcoma (stage I or II) is suggested, including the whole malignant and isolated tumoral proliferations developing from the dermic histiocyte.

Aged↗
PubMed2026

Evolution of Precision Oncology, Personalized Medicine, and Molecular Tumor Boards.

With multiple molecular targeted therapies available for patients with cancer that correspond to a specific genetic alteration, the selection of the best treatment is essential to ensure therapeutic efficacy. Molecular tumor boards (MTBs) play a key role in this process to deliver personalized medicine to patients with cancer in a multidisciplinary manner. Historically, personalized medicine has been offered to patients with advanced cancer, but the incorporation of molecular targeted therapies and immunotherapy into the perioperative setting requires clinicians to understand the role of the MTB. Evidence is accumulating to support feasibility and survival benefit in patients treated with matched therapy.

Humans↗
PubMed1986

Evolution of a case of multicentric giant cell tumor over a 23-year period.

A 17-year-old girl had a multicentric giant cell tumor originating in the sphenoid and sella turcica that was observed for 23 years. During the first 12 years, the same lesion also appeared in the right proximal tibia and left distal radius. Curettage of the tibial lesion and packing with processed bovine bone were followed by a chronic osteomyelitis with continued intermittent wound drainage. Curettage of the radial lesion and packing it initially with autogenous iliac bone graft and subsequently with methylmethacrylate bone cement were followed by local recurrences. The radial lesion eventually was eradicated by a segmental resection of the distal radius. The resulting bony defect was bridged with a bicortical autogenous iliac graft and stabilized with a bone plate to produce a painless solid wrist fusion. No further tumor recurrence has been noted for the past two years.

Adolescent↗
PubMed2000

Loss-of-heterozygosity analysis of small-cell lung carcinomas using single-nucleotide polymorphism arrays.

Human cancers arise by a combination of discrete mutations and chromosomal alterations. Loss of heterozygosity (LOH) of chromosomal regions bearing mutated tumor suppressor genes is a key event in the evolution of epithelial and mesenchymal tumors. Global patterns of LOH can be understood through allelotyping of tumors with polymorphic genetic markers. Simple sequence length polymorphisms (SSLPs, or microsatellites) are reliable genetic markers for studying LOH, but only a modest number of SSLPs are used in LOH studies because the genotyping procedure is rather tedious. Here, we report the use of a highly parallel approach to genotype large numbers of single-nucleotide polymorphisms (SNPs) for LOH, in which samples are genotyped for nearly 1,500 loci by performing 24 polymerase chain reactions (PCR), pooling the resulting amplification products and hybridizing the mixture to a high-density oligonucleotide array. We characterize the results of LOH analyses on human small-cell lung cancer (SCLC) and control DNA samples by hybridization. We show that the patterns of LOH are consistent with those obtained by analysis with both SSLPs and comparative genomic hybridization (CGH), whereas amplifications rarely are detected by the SNP array. The results validate the use of SNP array hybridization for tumor studies.

Alleles↗