11 research outputs found
Biomarkers as prognostic factors in endometrial cancer.
Endometrial cancer is the most common gynecologic malignancy in more developed countries. Approximately 75% of cases are diagnosed at an early stage with a tumor confined to the uterine corpus. Although most patients are cured by surgery alone, about 15-20% with no signs of locally advanced or metastatic disease at primary treatment recurs, with limited responsiveness to systemic therapy. The most common basis for determining the risk of recurrent disease has been classification of endometrial cancers into two subtypes. Type I, associated with a good prognosis and endometrioid histology and type II, associated with a poor prognosis and non-endometrioid histology. This review will focus primarily on the molecular biomarkers that have supported the dualistic model of endometrial carcinoma and help determine which patients would benefit from either adjuvant therapy or more aggressive primary treatment
Mutations in the KRAS gene in ovarian tumors.
RAS genes are the most frequently mutated oncogenes detected in human cancer. In this study we analyzed the presence of mutations at codon 12 of the KRAS gene in 78 women with ovarian tumor, including 64 invasive ovarian cancers and 14 borderline ovarian tumors, using an RFLP-PCR technique and we evaluated whether such alterations were associated with the selected clinicopathological parameters of the patients. KRAS codon 12 gene mutations were found in 6,2% of ovarian cancer tissue and in 14,3% of the borderline ovarian tumor. KRAS mutations were found with a significantly higher frequency in mucinous and borderline tumors compared to serous tumors (
The role of estrogens in angiogenesis in the female reproductive system
Podczas fizjologicznego cyklu menstruacyjnego w macicy dochodzi do powstawania nowych naczyń krwionośnych. Istnieją liczne dowody,
że to właśnie estrogeny wpływają na śródbłonki tych naczyń i modulują przebieg angiogenezy. Wykazano związek pomiędzy
estrogenami i ekspresją receptora estrogenowego na komórkach śródbłonka oraz ich aktywnością angiogenną. W niniejszej pracy przedstawiono
przegląd piśmiennictwa dotyczący roli estrogenów w angiogenezie zachodzącej w narządzie rodnym kobiet.Under physiological conditions, angiogenesis is routinely observed in the uterus. Multiple lines of evidence suggest that estrogen directly
modulates angiogenesis via effects on endothelial cells. A clear association between estrogen, estrogen receptor expression by endothelial
cells and angiogenic activity has been confirmed. This minireview will discuss the recent progress in research into the role of estrogens in
angiogenesis
Mutations of the KRAS oncogene in endometrial hyperplasia and carcinoma.
The aim of this study was to examine the prevalence and clinicopathological significance of KRAS point mutation in endometrial hyperplasia and carcinoma. We analysed KRAS in 11 cases of complex atypical hyperplasia and in 49 endometrial carcinomas using polymerase chain reaction associated with restriction fragment length polymorphism (PCR-RFPL). Point mutations at codon 12 of KRAS oncogene were identified in 7 of 49 (14,3%) tumor specimens and in 2 of 11 (18,2%) hyperplasias. No correlation was found between KRAS gene mutation and age at onset, histology, grade of differentiation and clinical stage. We conclude that KRAS mutation is a relatively common event in endometrial carcinogenesis, but with no prognostic value
Biomarkers as prognostic factors in endometrial cancer.
Endometrial cancer is the most common gynecologic malignancy in more developed countries. Approximately 75% of cases are diagnosed at an early stage with a tumor confined to the uterine corpus. Although most patients are cured by surgery alone, about 15-20% with no signs of locally advanced or metastatic disease at primary treatment recurs, with limited responsiveness to systemic therapy. The most common basis for determining the risk of recurrent disease has been classification of endometrial cancers into two subtypes. Type I, associated with a good prognosis and endometrioid histology and type II, associated with a poor prognosis and non-endometrioid histology. This review will focus primarily on the molecular biomarkers that have supported the dualistic model of endometrial carcinoma and help determine which patients would benefit from either adjuvant therapy or more aggressive primary treatment
Chimeric Antigen Receptor Design and Efficacy in Ovarian Cancer Treatment
Our increased understanding of tumour biology gained over the last few years has led to the development of targeted molecular therapies, e.g., vascular endothelial growth factor A (VEGF-A) antagonists, poly[ADP-ribose] polymerase 1 (PARP1) inhibitors in hereditary breast and ovarian cancer syndrome (BRCA1 and BRCA2 mutants), increasing survival and improving the quality of life. However, the majority of ovarian cancer (OC) patients still do not have access to targeted molecular therapies that would be capable of controlling their disease, especially resistant or relapsed. Chimeric antigen receptors (CARs) are recombinant receptor constructs located on T lymphocytes or other immune cells that change its specificity and functions. Therefore, in a search for a successful solid tumour therapy using CARs the specific cell surface antigens identification is crucial. Numerous in vitro and in vivo studies, as well as studies on humans, prove that targeting overexpressed molecules, such as mucin 16 (MUC16), annexin 2 (ANXA2), receptor tyrosine-protein kinase erbB-2 (HER2/neu) causes high tumour cells toxicity and decreased tumour burden. CARs are well tolerated, side effects are minimal and they inhibit disease progression. However, as OC is heterogenic in its nature with high mutation diversity and overexpression of different receptors, there is a need to consider an individual approach to treat this type of cancer. In this publication, we would like to present the history and status of therapies involving the CAR T cells in treatment of OC tumours, suggest potential T cell-intrinsic determinants of response and resistance as well as present extrinsic factors impacting the success of this approach
Mutations in the KRAS gene in ovarian tumors.
RAS genes are the most frequently mutated oncogenes detected in human cancer. In this study we analyzed the presence of mutations at codon 12 of the KRAS gene in 78 women with ovarian tumor, including 64 invasive ovarian cancers and 14 borderline ovarian tumors, using an RFLP-PCR technique and we evaluated whether such alterations were associated with the selected clinicopathological parameters of the patients. KRAS codon 12 gene mutations were found in 6,2% of ovarian cancer tissue and in 14,3% of the borderline ovarian tumor. KRAS mutations were found with a significantly higher frequency in mucinous and borderline tumors compared to serous tumors (p<0,01). Mutation frequency was correlated with the histological type of tumor, but not with stage, grade or patients age
Prognostic value of serum levels of SCC-Ag and CYFRA 21-1 in early-stage squamous cell carcinoma of the uterine cervix
Several markers present in tumor tissues and body fluids considerably aid in early diagnosis, enabling both correct decision- making qualifying patients to high-risk groups, monitoring of the patients’ response to treatment implemented and heralding the possibility of distant metastases or local recurrence. The paper presents correlations of elevated serum levels of CYFRA 21-1 and SCC-Ag with clinical stage, histological differentiation grade and survival rates of 89 patients with FIGO stage IB/IIA squamous cell carcinoma of the uterine cervix. Marker levels were assessed prior to surgery using immunoenzymatic assay kits. Two groups of patients were defined: I (n=31; 35%) surviving less than 5 years and II (n=58; 65%) surviving more than 5 years. CYFRA 21-1 levels exceeding 3.5 ng/ml were present in 42% of patients. Elevation of SCC-Ag level above 1.5 ng/ml was seen in 48% of patients. No correlations were noticed between elevation of serum levels of markers studied and clinical stage nor histological differentiation grade. Patients presenting marker levels below reference values benefited from longer survival. Patients surviving less than 5 years had a statistically significant elevation of baseline serum SCC-Ag levels (p5 lat. Stężenia CYFRA 21-1 wyższe niż 3,5 ng/ml stwierdzono u 42% chorych. Wzrost SCC-Ag powyżej 1,5 ng/ml wykazano u 48% pacjentek. Nie ujawniono zależności pomiędzy wzrostem stężeń badanych markerów a stopniem zaawansowania klinicznego, jak również zróżnicowaniem histologicznym raka. U chorych, u których stwierdzono niższe od wartości referencyjnych stężenia obu markerów, odnotowano dłuższy czas przeżycia. W grupie leczonych z czasem przeżycia krótszym niż 5 lat wykazano istotny statystycznie wzrost wartości wyjściowych stężeń SCC-Ag (p<0,001). Wyniki badań sugerują, że chore na raka płaskonabłonkowego szyjki macicy we wczesnych stadiach zaawansowania klinicznego, u których przed leczeniem odnotowano podwyższone stężenia CYFRA 21-1 i SCC-Ag, wymagają neoadiuwantowej chemioterapii poprzedzającej leczenie operacyjne. Słowa kluczowe: płaskonabłonkowy rak szyjki macicy, CYFRA 21-1, SCC-Ag, surowica