SEARCH · PubMed Health

Results for “CP: Cancer”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 37 records · Page 2Linked to original sources

PubMed2000

[Diagnostic significance of cancer procoagulant activity in colorectal cancer].

This study aimed at evaluating diagnostic significance of cancer procoagulant (CP) activity in the homogenates of colon cancer tissues and in blood serum of patients with this neoplasm. Procoagulant activity, depending of specific cancer procoagulant, has been found in all examined tissues as well as in blood serum of cancer patients. CP activity in homogenates of colon cancer tissues as well as in blood serum of the examined cancer patients has been markedly higher than in the normal subjects. These data indicate that CP activity in the neoplastic tissue homogenates and in blood serum may be of value in the diagnosis of cancer.

Adult↗

PubMed2026

Whole-Exome Sequencing Identifies Candidate Genomic Features Associated with Response to Platinum-Based Chemotherapy and Ixabepilone-Based Treatment in Ovarian Cancer.

Carboplatin/paclitaxel (CP) chemotherapy is the cornerstone of therapy for advanced stage ovarian cancer (OC). However, despite initial sensitivity, this regimen cannot avoid the emergence of resistance. Ixabepilone ± bevacizumab (IB) is a combination recently added to NCCN guidelines for the treatment of platinum-resistant OC. It would be desirable to identify biomarkers able to differentiate patients who are resistant to CP and IB, and biomarkers that identify which patients may benefit from IB treatment. We analyzed whole-exome-sequencing (WES) data from 49 OC patients exposed to CP, including 28 platinum-sensitive vs. 21 platinum-resistant, and 31 additional platinum-resistant patients, including 16 responders (i.e., CR/PR) vs. 15 non-responders (SD/PD) to ixabepilone ± bevacizumab. Comprehensive genetic analyses were performed to identify alterations correlated with resistance to CP and IB. WES analysis of CP responders vs. non-responders revealed differences in HRD-signatures (p < 0.05), OS (p < 0.005) and gain/loss-of-function in multiple genes associated with tumor growth/progression including but not limited to ACVR2A, INHBA, MAP3K7, ATG5, SGK1, FYN, RSPO3, NOD1 and LRRK2. WES analysis of platinum-resistant IB-treated patients revealed additional nominally significant genes and deranged pathways including gains in the DROSHA and SDHA genes in responders vs. non-responders (p < 0.05). Patients harboring HRD-signatures showed significantly higher sensitivity to CP and prolonged survival compared to HRD-negative patients. Alterations in genes associated with tumor growth/progression correlated with resistance to CP regimen and may represent novel "druggable" candidate biomarkers for the targeted treatment of CP/IB-resistant patients. Further validation in independent cohorts and preclinical experiments in CP/IB-resistant models are warranted to establish the clinical utility of these findings.

Humans↗

PubMed2003

[Evaluation of diagnostic values of neoplastic procoagulant in pancreatic, hepatic and ovary cancers].

The cancer procoagulant (CP) activity has been evaluated in serum of patients with pancreas, liver and ovarian cancer and in homogenates of these cancer tissues. CP activity in examined cancer tissues as well as in blood serum was significantly higher than in the control. The obtained results indicate that estimation of CP activity may be useful in oncological diagnosis of pancreas, liver and ovarian cancer.

Aged↗

PubMedDate not supplied

Usefulness of examination of some tumor markers in diagnostics of liver cancer.

BACKGROUND/AIMS: Diagnostics of liver cancer is mainly based on imaging methods: which are ultrasound and computer tomography. Determination of tumor markers is an accessory investigation enabling us to detect cancer, to evaluate the effectiveness of its operative and postoperative treatment and to diagnose early cancer relapse or distant metastases. Alpha-fetoprotein (AFP) is a basic well-known marker in diagnostics of liver cancer. Carcinoembryonic antigen (CEA) and cancer procoagulant (CP) are also important in case of metastases to this organ, especially from the colon. The purpose of this study was to evaluate the usefulness of AFP, CEA and CP in detection of liver cancer. METHODOLOGY: The material of the study was the blood serum from 25 patients with liver cancer diagnosed histopathologically and 12 healthy individuals as a control group. The concentrations of AFP and CEP were assessed by immunoenzymatic method (MEIA) in the Axsym analyzer of Abbott and expressed in ng/mL. CP activity was determined by coagulation method worked out by Gordon and Benson and expressed as coagulation time in seconds (s). RESULTS: Based on the results obtained in our study, the concentrations of AFP and CEP were several fold higher in the serum of patients with liver cancer than the relevant values of these markers. CP activity was higher in the serum of patients with liver cancer than the mean values of patients in the control group. The differences found in the study between the groups examined and the control group were statistically significant atp<0.001. CONCLUSIONS: The results confirmed a high diagnostic value of AFP and CEA testing and suggest the possibility of using CP activity to detect liver cancer.

Adult↗

PubMed1995

Improved prediction of carcinogenic potencies from mutagenic potencies for chemicals positive in rodents and the Ames test.

Most studies of correlation between logs of mutagenic potency (MP) and cancer potency (CP) have obtained relatively small but statistically significant estimates of correlation (r) and corresponding log-log slope (b, in Log[CP] = a + b Log[MP]). But for mutagenic carcinogens, multistage cancer theory predicts that b and r should be highest when MP values best estimate mutation yields per unit dose at concentrations at least as high as those observed to cause cancer in bioassay animals. To test this hypothesis, the correlation of Ames test and rodent cancer potencies was examined for a total number n of 134 chemicals reported as positive in both assays. Values of maximum significant cancer potency (CP, in [mmol/kg-day]-1) were obtained from a published carcinogenic potency database. Values of maximum mutagenic potency (MP, as revertants per mmol/L-plate) were estimated from 2,347 sets of Ames test data reported by the NTP mutagenicity testing program, supplemented by similar data newly obtained for ten heterocyclic amines. For compounds with one or more significantly positive MP estimates based on approximately linear Ames test dose-response data, linear regression of maximum values of Log(CP) on Log(MP) yielded b = 0.27 +/- 0.065 and r = 0.39 (P = 0.0001, n = 105), similar to previously reported results for relatively large n. As predicted, when MP values were additionally restricted to include only values estimated from Ames test data approximately linear at corresponding lowest-TD50 concentrations, similar regressions yielded significantly improved fits (e.g,. b and r approximately 0.6, P < 10(-7), n = 68). Implications of these findings are discussed concerning the quantitative role that mutations like those measured in the Ames test may have in explaining observed cancer-bioassay results.

Animals↗

PubMed1999

Angiogenesis, angiogenic growth factors, and cell adhesion molecules are upregulated in chronic pancreatic diseases: angiogenesis in chronic pancreatitis and in pancreatic cancer.

Recent epidemiologic evidence suggests that patients with chronic pancreatitis (CP) have an increased risk of developing pancreatic carcinoma (PCA). In spite of numerous similarities in both diseases, mechanisms for progression from CP to PCA are poorly understood. We hypothesized that enhanced angiogenesis might play a pivotal role in the etiology and histopathology of both CP and PCA, and thus form a possible link between precancer and carcinoma. In surgical specimens of 18 patients with CP, 10 with PCA, and 18 controls, absolute numbers of blood vessels and relative blood vessel density were assessed after immunostaining of endothelial cells for von Willebrand factor and PECAM-1 (platelet/ endothelial cell adhesion molecule-1). Furthermore, the expression of cell adhesion molecules ICAM-1 (intercellular adhesion molecule-1) and VCAM-1 (vascular cell adhesion molecule-1) and of VEGF (vascular endothelial growth factor) was investigated in all specimens. Both CP and PCA exhibited areas of high vascular density ("hot spots"). The mean number of blood vessels in these areas in PCA was 132.2+/-16.8 per mm2, and in CP, 99.2+/-7.4 per mm2. The mean vessel count in controls was 25.1+/-5.1. Relative vessel density was increased in both PCA (41.3+/-3.5%) and CP (30.6+/-2.6%) versus controls (8.0+/-0.8%). Both absolute vessel count and relative vessel density were significantly higher (p<0.05) in PCA than in CP. Enhanced expression of ICAM-1 in CP and PCA was seen in ductal cells in CP and cancer cells. In controls, ICAM-1 and VCAM-1 were expressed only at low levels in endothelial cells. VCAM-1 was strongly expressed in acinar cells as well as in ductal cells. In CP and PCA, VEGF was strongly expressed in ductal cells in CP as well as in cancer cells. We show for the first time that angiogenic activity is increased in both CP and PCA. Based on this study, we suggest that antiangiogenesis might be a novel target for prevention or therapy in chronic pancreatic diseases.

Adenocarcinoma↗

PubMed2004

Efficacy and safety of transdermal fentanyl and sustained-release oral morphine in patients with cancer and chronic non-cancer pain.

PURPOSE: To evaluate effectiveness and safety information of transdermal fentanyl (TDF) (Duragesic/Durogesic) and sustained-release oral morphine (SRM) in cancer pain (CP) and chronic non-cancer pain (NCP), a pooled analysis was conducted on datasets of published, open label, uncontrolled (no comparator group) and randomised controlled (with SRM as comparator) studies of TDF. PATIENTS AND METHODS: Eight trials with treatment durations of at least 28 days met the inclusion criteria. The effectiveness analysis assessed changes in average pain and pain 'right now' scores between baseline and Day 28. The safety analysis evaluated the incidence of adverse events (AEs) reported within the first 28 days of treatment with TDF or SRM. Subgroup analyses included pain type, gender, age, weight, and body mass index. RESULTS: Pooled efficacy data were available from 1220 patients; these showed that both TDF and SRM were effective in improving pain 'right now' scores (0-100 scale) from baseline to Day 28. The improvement was significantly more pronounced in the TDF treatment group (-26.7 +/- 31.3 for TDF, -18.7 +/- 30.9 for SRM, p = 0.002). This favourable effect of TDF was most apparent amongst patients with NCP. Data concerning AEs were available from over 2500 patients with CP (3 out of 10 patients) or chronic NCP (7 out of 10 patients). Significantly fewer patients in the TDF than in the SRM group reported any AE (72% vs. 87% respectively; p < 0.001), or an AE leading to the study drug being permanently discontinued (16% vs. 23% respectively; p < 0.001). Constipation and somnolence occurred considerably less frequently in the TDF than in the SRM treatment group. This difference was statistically significant in both the CP and NCP subgroups. CONCLUSION: This pooled data analysis provides expanded insight into the safety and effectiveness profile of transdermal fentanyl in patients with chronic pain. It shows significantly improved pain relief with transdermal fentanyl compared with sustained-release oral morphine, and supports current evidence of favourable tolerability of transdermal fentanyl, particularly with regard to reduced constipation and somnolence.

Administration, Cutaneous↗

PubMed2025

Integrating mutation, copy number, and gene expression data to identify driver genes of recurrent chromosome-arm losses.

Aneuploidy is a hallmark of cancer, yet the genes driving recurrent chromosome-arm losses remain largely unknown. We present a systematic framework integrating mutation, copy number, and gene expression data to identify candidate driver genes of cancer type-specific recurrent chromosome-arm losses across 20 cancer types, using ∼7,500 tumors from The Cancer Genome Atlas. By analyzing focal deletions and point mutations that co-occur, or are mutually exclusive, with chromosome-arm losses, we pinpoint 322 candidate drivers associated with 159 recurring events. Our approach identifies known aneuploidy drivers such as TP53 and PTEN, while revealing multiple additional candidates, including tumor suppressors not previously linked to aneuploidy. We leverage expression changes associated with chromosome-arm losses to propose cancer-promoting pathway-level alterations. Integrating these findings highlights key candidate drivers that underlie the observed expression alterations, reinforcing their biological relevance. We provide a comprehensive catalog of candidate driver genes for recurrently lost chromosome-arms in human cancer.

Humans↗

PubMed2005

Cancer procoagulant in patients with adenocarcinomas.

Cancer procoagulant (CP) is a cysteine proteinase that may be produced by malignant and foetal tissue. The possible role of CP in the pathogenesis of cancer-related thrombosis has been suggested recently. The purpose of the study was to evaluate coagulation prothrombotic markers and their relation to CP concentration in the blood of patients with gastrointestinal adenocarcinomas (GIAC). The study group consisted of 45 patients with confirmed diagnosis of adenocarcinoma (stomach, 18 patients; colon, 27 patients) and without evident metastatic disease. In 24 patients further observation showed metastases. The control group for CP was composed of 10 healthy subjects. Blood samples were drawn on the admission day, before any treatment. Among 45 patients with GIAC, deep venous thrombosis was observed in two (4.4%). In all patients the CP activity in the serum was found, and the mean CP activity shortened the coagulation time almost three times compared with the healthy control group. Also, the mean thrombin-antithrombin complex concentration was above the normal range. A significant elevation of the mean prothrombin fragment 1+2 plasma content in this group of patients was noticed. Despite these observations, CP remained within the normal range and did not correlate with thrombin-antithrombin complex or prothrombin fragment 1+2 plasma concentrations. A positive correlation was observed between serum CP and fibrinogen concentration, and a negative correlation between CP and free protein S plasma content (P = 0.04 and P = 0.025, respectively). A negative correlation between activated protein C resistance ratio and protein C activity in the plasma was confirmed. Protein C activity in the plasma showed a correlation with free protein S plasma content. Analysis of factors influencing the activated partial thromboplastin time revealed the presence of antiphospholipid antibodies in seven persons from the study group (in three cases of IgG and in four cases of IgM class). Our data suggest that CP is a minor risk factor for deep venous thrombosis in GIAC patients. To confirm this, however, the number of patients and controls should be larger. After 3 years of observation, the follow-up in 10 living GIAC patients showed nobody with thromboembolic disease.

Adenocarcinoma↗

PubMed1994

Application of cancer procoagulant as an early detection tumor marker.

BACKGROUND: In spite of many advances in the analytical reagents (antibodies), analytical systems, and the clinical application of tumor markers, the present markers do not detect early stage cancer. Preliminary data with an antigen specific to tumor tissue, cancer procoagulant (CP), suggest its possible role in the detection of early stage cancer. This study was aimed at determining the clinical use of CP as an early stage tumor marker. METHODS: An improved enzyme-linked immunosorbent assay (ELISA) was developed to measure CP concentration in serum. A panel of 817 blinded serum samples were examined from three groups of people: 573 cancer, 106 benign, and 139 normal. RESULTS: The sensitivity of all samples analyzed from cancer patients was 80%. The CP ELISA was able to detect ovarian, colon, and kidney cancer at a sensitivity greater than 85%; breast, prostate and small cell lung cancer was detected at a sensitivity of 80-85%. Particularly interesting was the observation that early stage cancers, regardless of site, were detected effectively. In some groups, the CP assay correctly identified 100% of the patients with stage I and II cancer. The assay was able to identify correctly noncancer patient sera at a specificity of 83% for those with benign disease and 82% for the normal individuals. CONCLUSIONS: The CP assay has potential as an aid in diagnosing early stage malignancies and thereby may significantly improve the survival rate of cancer patients.

Adenocarcinoma↗

PubMed1989

Inhibition of cancer procoagulant by peptidyl diazomethyl ketones and peptidyl sulfonium salts.

Cancer procoagulant (CP) is a cysteine proteinase from cancer cells that initiates blood coagulation. Members of two classes of unique and highly specific cysteine proteinase inhibitors, peptidyl diazomethyl ketones (PDK) and peptidyl sulfonium salts (PSS), were studied to determine whether or not they inhibited CP. The inhibitors did not impair the activity of the coagulation system. There was a differential inhibitory effect of the 6 PDK and 2 PSS inhibitors, influenced by the amino acid composition or sequence of the peptide moiety, that suggests differences in structural features of the active site of CP and papain. CP was inhibited by both classes of inhibitors.

Animals↗

PubMed2001

[Diagnostic value of testing the procoagulant activity of neoplasms in cases of stomach and esophageal neoplasms].

The cancer procoagulant (CP) activity has been evaluated in homogenates of stomach and esophagus cancer tissues and in patients serum. Activity of CP in homogenates of stomach and esophagus cancer tissues as well as in serum of examined cancer patients were statistically higher than in the control group. The data indicate that estimation of CP activity in the neoplasmic tissues homogenates and in serum may be suggested as an new biochemical marker of cancer process useful in oncological diagnosis.

Adult↗

PubMedDate not supplied

Hypersensitivity reaction to carboplatin during treatment for ovarian cancer: successful resolution by replacement with cisplatin.

Development of hypersensitivity reactions to carboplatin (CP) during cancer treatment makes optimal chemotherapy difficult to achieve. Many approaches have previously been used following the development of reactions to CP. We report on a patient with ovarian cancer who developed a hypersensitivity reaction to CP. The patient was successfully treated following replacement of carboplatin with cisplatin.

Aged↗

PubMed2003

Inflammatory pancreatic diseases in older patients: recognition and management.

The aging process influences and modifies the clinical picture and treatment modalities of inflammatory pancreatic diseases in elderly patients. The two major categories of inflammatory exocrine pancreatic diseases seen in the elderly are acute pancreatitis (AP) and chronic pancreatitis (CP). In elderly patients with AP, the presence of concomitant diseases affecting renal, hepatic and cardiopulmonary function make the early clinical assessment of the severity of AP inaccurate at the time of admission to hospital. In addition, the classical multifactorial scoring system routinely utilised in clinical practice to determine the severity of AP may overscore elderly patients because increasing age is associated with more points. Contrast-enhanced computed tomography is particularly useful in assessing the severity of AP and is required in all patients suspected with severe AP. It should be repeated after a certain time period to monitor the disease. The most important aspect of the management of elderly patients with severe AP is the prevention and treatment of systemic and local complications. Treatment of AP should address the removal of aetiological factor(s) and support of organ systems and hydroelectrolytic/caloric balance; specific treatments (antiproteases, antibacterials) should also be administered to patients with severe AP. Surgery is indicated mainly when infection occurs following pancreatic necrosis and/or fluid collection. However, in selected patients with a high anaesthetic risk, alternative, less invasive drainage options (percutaneous, endoscopic) should be considered. CP rarely occurs in older age, and it should be suspected based on clinical findings. The greatest challenge is the differentiation between CP and pancreatic cancer. Treatment of CP in the elderly should be directed at controlling the symptoms, by management of diabetes and exocrine insufficiency because pain and complications are rare in elderly patients with CP. Compliance with treatment should be periodically assessed if insulin and/or oral enzyme supplementation is required. Careful evaluation of nutritional status and its prompt correction is also important.

Acute Disease↗

PubMed2026

Genome-wide CRISPR screens map synthetic lethal interactions across recurrent cancer driver alterations.

Synthetic lethality (SL) provides a treatment paradigm for targeting cancer with alterations in driver genes that are not conventionally druggable, including tumor suppressor genes. We execute a series of genome-wide CRISPR screens using functionally validated isogenic cell lines and conduct a large-scale SL analysis using data from the cancer dependency map (DepMap). We chart SL interactions across 15 driver alterations: FBXW7, CCNE1, CDK12, ARID1A, KMT2D, DNMT3A, TET2, KEAP1, STK11, IDH1, SF3B1, SRSF2, U2AF1, chromosome 18q loss, and chromosome 13q loss. We show validation of several SL interactions, including ARID1A and the hexosamine biosynthetic pathway aminotransferase GFPT1, STK11 with CAMK protein kinase MARK2, FBXW7 and the CDK1 regulatory kinase PKMYT1, and CCNE1 amplification and the anaphase-promoting complex or cyclosome (APC/C). In summary, this study offers a rich resource of genetic interactions across cancer drivers enabling the discovery of biological insights and drug targets for future therapeutic development.

CP: cancer↗

PubMed2025

Genetic mapping and predictive modeling of paralog synthetic lethality.

Paralogs are abundant in the human genome and thought to be a primary source of synthetic lethality, yet the vast paralogome remains largely uncharacterized. A digenic screen of 36,648 paralogous pairs in the human genome revealed that synthetic lethalities were infrequent and varied in penetrance in different tumor backgrounds. We hypothesized that the variable penetrance of synthetic lethalities resulted from complex polygenic interactions with different cellular contexts. A machine learning classifier of a subset of paralog pairs tested across 49 cancer models revealed that endogenous perturbations in related pathways predicted paralog synthetic lethality. Further, predictive modeling of paralog synthetic lethality showed that the strength of synthetic lethal interactions was largely due to the overlap and essentiality of the protein-protein interaction networks shared by the paralog pairs. Collectively, this study tested 36,648 digenic paralog interactions and delineated the key feature classes that underlie the heterogeneity of paralog synthetic lethalities.

Humans↗

PubMed2003

Evolving strategies for prostate cancer chemoprevention trials.

Prostate cancer chemoprevention (CP) can be defined as the use of natural and synthetic agents that inhibit, reverse or regress precancer and delay progression to invasive cancer. During the past two decades several CP strategies have evolved. The first generation of CP trials tested the efficacy of antioxidants and vitamins including B-carotene, vitamin A, retinol, 13 cis retinoic acid, vitamins E, C and selenium. Although these trials were disappointing, provocative hypotheses were generated for selenium and vitamin E that set the stage for future prostate trials. In the 1990s, the NCI launched a second generation of large CP trials aimed at breast and prostate cancer. One of these trials is the PCPT, testing the efficacy of a 5 alpha-reductase inhibitor-finasteride to prevent prostate cancer in 18,000 men. Although PCPT is still in progress, the NCI recently launched a second large primary prostate CP trial called SELECT, testing the efficacy of selenium and vitamin E in 32,400 men. The Prostate Cancer Progress Report to the Director of NCI in 1998 challenged the research community to design more efficient CP trials for prostate cancer. In response, the NCI has evolved a third generation of CP trials. This involves pharmacologically driven translational science research including agents and their targets, biomarker endpoints, suitable clinical models for testing agents and efficient trial designs employing high risk cohorts and surrogate endpoints. In summary, a dual strategy for CP is being developed which includes public health measures and a medical intervention approach.

Antioxidants↗

PubMed2004

[Cancer procoagulant activity in serum and neoplastic tissue in cases of cervical and uterine carcinoma].

OBJECTIVES: Cancer procoagulant (CP) is a sulfhydryl proteinase thought to be synthesized mainly by neoplastic cells. Consequently, increased CP activity in blood serum was interpreted as being associated with the presence of a proliferative process in the host's body. To date, CP activity has not been systematically studied in cases of genital carcinoma. The present study is aimed at evaluation of CP activity in women with genital carcinoma. DESIGN: A case-controlled study backed up by histopathological examination. MATERIALS AND METHODS: Peripheral blood was sampled preoperatively in a sterile manner from an antecubital vein, from 16 women with cervical carcinoma and 15 women with uterine carcinoma. Blood for the reference group of 12 healthy women was obtained in an identical manner after an overnight fast. The CP activity in serum was determined using the coagulative method according to Gordon and Benson, and was expressed as coagulation time in seconds (s). The CP activity in 10% tissue homogenates (in saline) of genital cancer was determined by the chromogenic method according to Colucci et al. RESULTS: The mean CP activity in serum of women with cervical carcinoma (78.28 +/- 15.25 s) and of women with uterine carcinoma (79.63 +/- 12.02 s) was significantly different (P < 0.0001) from the respective values found in healthy women (281.33 +/- 43.19 s). The CP activity in neoplastic tissue was 28.50 +/- 6.40 nmol pNa/mL for cervical carcinoma, and 28.31 +/- 3.92 nmol pNa/mL for uterine carcinoma, both values being significantly higher (P < 0.0009) than the activity found in the normal tissues. There was no established relationship between neoplastic CP activity and FIGO staging of the disease. CONCLUSIONS: This is the first study to demonstrate the concomitant presence of CP activity in serum and neoplastic tissue of women with genital carcinoma. These patients have decreased coagulation time and thus are likely to develop coagulation disturbances in the course of their cancer. There may be a role for CP as a tumor marker of genital carcinoma.

Adult↗