" A new study shows women who undergo surgical treatment for endometriosis have a lower risk of developing ovarian cancer. The Swedish research also found that hormonal treatments for endometriosis did not lower the risk." http://www.m.webmd.boots.com/a-to-z-guides/news/20130411/endometriosis-surgery-ovarian-cancer
" There is sufficient evidence to conclude that there is an increased risk of developing clear-cell and endometrioid epithelial ovarian cancer for women with histologically verified endometriosis. Nonetheless, prospective cohort studies assessing the relation between endometriosis and ovarian cancer will increase knowledge in this field." http://www.ncbi.nlm.nih.gov/m/pubmed/24011403/
From 2014:
" Genetic studies have demonstrated that endometriotic lesions have mutations in genes directly related to neoplasms, in particular the p53, KRAS, PTEN, and ARID1Agenes, which suggests a direct transition from a subset of endometriotic lesions to invasive carcinomas. The identification of both genetic and epigenetic biomarkers including microRNAs are essential for identifying patients at risk for the transition to neoplasia." http://www.sciencedirect.com/science/article/pii/S1553465013004305
From 2012:
"According to the article published today, women with endometriosis have an odds ratio of about 1.5 of developing an invasive ovarian cancer compared to the general female population.
“From this point of view, these data are “reassuring” in comparison with some previous reports indicating a much higher risk. An odds ratio of 1.5 means that a woman with endometriosis has a life-time risk of developing an ovarian cancer of about 1.5% instead of 1%”
WES President, Paolo Vercellini
said World Endometriosis President, Professor Paolo Vercellini.
Whereas the study showed no link between endometriosis and high-grade serous, mucinous, serous borderline, or mucinous borderline ovarian cancers, the authors stress that their paper describes for the first time an association between endometriosis and low-grade serous ovarian cancers translating to a doubling of the risk in women with a history of endometriosis.
Professor Vercellini agrees this is an important finding, but does offer another word of caution:
This finding only has pathogenic and not clinical implications, as the incidence of this cancer subtype is limited to 336 out of 7911 cases in this pooled analysis and thus the practical consequences are modest.
Indeed he stresses that it is important to be cautious with the definition of endometriosis in general as a precursor lesion for clear-cell and endometrioid ovarian cancers, as reasonably only atypical endometriosis should be considered a definite precursor lesion [2].
Furthermore, without the specification of which sub-types of endometriosis, the lack of information on subsequent treatment with or without danazol, and the possible differential recalling rate between cases and controls, there are still some uncertainties that need to be resolved in future studies.
In particular, future studies need to determine whether the association is causal with a clear temporal relationship or merely association due to exposure to shared risk factors." http://endometriosis.ca/news/article/ovarian-cancer-risk-in-women-with-endometriosis/
Thursday, July 24, 2014
Wednesday, July 23, 2014
Endo selective destroying medicine? may be possible!
Wow! Amazing piece of research find by Matthew Rosser in the UK:
"Researchers have identified a protein (called z13) that selectively binds to and is absorbed by, endometriotic cells. In a way, finding this protein has been like the child’s toy where you have a box with different shaped holes in it and you have to find the right shaped peg to fit in the hole, except imagine you have a box with tens of thousands of different holes and tens of thousands of accompanying pegs, not an easy task. Now that this protein has been discovered it means we have a way to target endometriosis specifically and ignore all other tissue and organs in the body.
What the researchers then did was attach other proteins to z13 which would induce cells to die. Effectively, what they now had was an endo seeking missile. So far the researchers have tested this on peritoneal endometriosis in baboons and found that the targeted proteins caused the endometriotic cells to die whilst leaving the surrounding tissue unharmed.
One of the best things about this approach, from a patient perspective, is that this is completely non-hormonal; no messing around with the ovaries, no pumping the whole body with hormones, just targeting the disease itself.
Cautious optimism aside, it may be a while before we see this approach translated into humans and there are still many more tests to be done to make sure it is safe. Nevertheless this shows that research is not continuously bogged down in the old ‘hormone therapy’ mindset and people are exploring new and exciting possibilities and, whilst this may not be a cure, it is a step in the right direction.
Matthew Rosser at 10:40"
http://endo-update.blogspot.co.uk/2014/07/endo-seeking-missile.html?m=1
"Researchers have identified a protein (called z13) that selectively binds to and is absorbed by, endometriotic cells. In a way, finding this protein has been like the child’s toy where you have a box with different shaped holes in it and you have to find the right shaped peg to fit in the hole, except imagine you have a box with tens of thousands of different holes and tens of thousands of accompanying pegs, not an easy task. Now that this protein has been discovered it means we have a way to target endometriosis specifically and ignore all other tissue and organs in the body.
What the researchers then did was attach other proteins to z13 which would induce cells to die. Effectively, what they now had was an endo seeking missile. So far the researchers have tested this on peritoneal endometriosis in baboons and found that the targeted proteins caused the endometriotic cells to die whilst leaving the surrounding tissue unharmed.
One of the best things about this approach, from a patient perspective, is that this is completely non-hormonal; no messing around with the ovaries, no pumping the whole body with hormones, just targeting the disease itself.
Cautious optimism aside, it may be a while before we see this approach translated into humans and there are still many more tests to be done to make sure it is safe. Nevertheless this shows that research is not continuously bogged down in the old ‘hormone therapy’ mindset and people are exploring new and exciting possibilities and, whilst this may not be a cure, it is a step in the right direction.
Matthew Rosser at 10:40"
http://endo-update.blogspot.co.uk/2014/07/endo-seeking-missile.html?m=1
Tuesday, July 22, 2014
My current yoga poses that help
I have a current rotation of yoga poses that really seems to help. On my spunky days I do the more active ones; other days, just the stretchy ones.
Start out in child's pose.
Come up onto your hands and knees and do a few cat/cow poses.
Then this little baby for some reason helps my low back feel better:
While you're there, thread the needle for your arms- again, makes my hips and low back feel better.
Then maybe do a few sun salutations to warm up.
For my more spunky days, I add in a warrior series, half moon pose, three legged dog, and other such poses.
Intersperse some of these babies in:
Standing forward fold
Add in a twist to each side (make sure to keep your hips even).
A forward lunge, a low lunge, or one of my favorites- lizard lunge.
Twists seem to be helpful to me as do quad stretches so this one pulls double duty:
Another good quad stretch
Side stretch
After a warrior 2, this is nice:
Tree pose also seems to help me a lot too. I do it while I'm brushing my teeth, stirring the pots while making supper, wherever I can fit it in.
This twist also feels good on my outer hips and releases a lot of the tightness I tend to hold there:
Cobbler's pose helps quite a bit as well. I will sit like this in the recliner with my laptop, using the arm rests to hold my legs.
*********One of the best ones to help my hips- thread the needle pose*************
***************Head to knee pose is another essential for me:*****************
Reclining is good for the hamstring- it releases it's pull on my pelvic floor.
Going out to the side and then to the other side is another good release
Comforting- do this in bed a lot:
Another good twist- and reclining too!
This side stretch is good:
Or doing a spinal rotation:
Another one that I do in bed a lot to help release tension:
And another happy child's pose:
Or garland pose throughout the day is good for some release (can do it sans pillows):
And remember:
How I feel at the end of a good yoga session:
Study: excision of endo only has 36% chance reop rate, not always associated with recurrence
"CONCLUSIONS: Laparoscopic excision of endometriosis significantly reduces pain and improves quality of life for up to 5 years. The probability of requiring further surgery is 36%. Return of pain following laparoscopic excision is not always associated with clinical evidence of recurrence." http://humrep.oxfordjournals.org/content/18/9/1922.long
Friday, July 18, 2014
estrogen may increase nerve pain signals in endo
Elevated peritoneal expression and estrogen regulation of nociceptive ion channels in endometriosis.
Greaves E1, Grieve K, Horne AW, Saunders PT.
Author information
Abstract
Context: Ovarian suppression is a common treatment for endometriosis-associated pelvic pain. Its exact mechanism of action is poorly understood although it is assumed to reflect reduced production/ action of estrogens. Objective: To measure expression of mRNAs encoded by nociceptive genes in the peritoneum of women with chronic pelvic pain (CPP) with or without endometriosis; to investigate whether estrogens alter nociceptive gene expression in human sensory neurons. Design: Human tissue analysis and cell culture. Setting: University Research Institute Patients: Peritoneal biopsies were obtained from women with CPP and endometriosis (n=12), CPP and no endometriosis (n=10), and with no pain or endometriosis (n=5). Endometriosis lesions were obtained from women with endometriosis (n=18). Main outcome measures: mRNAs encoding ion channels (P2RX3, SCN9A, SCN11A, TRPA1, TRPV1) and the neurotransmitter TAC1 were measured in tissue samples and in human embryonic stem cell-derived sensory neurons treated with estrogens. Results: TRPV1, TRPA1 and SCN11A mRNAs were significantly higher in the peritoneum from women with endometriosis (p<0.001, p<0.01). TPRV1, SCN9A and TAC1 were elevated in endometriosis lesions (p<0.05). P2RX3 mRNA was increased in the peritoneum of women with CPP, with and without endometriosis (p<0.05). Incubation of sensory neurons with E2 increased TRPV1 mRNA (p<0.01); the ERβ-selective agonist DPN increased concentrations of TRPV1, P2RX3, SCN9A and TAC1 mRNAs. Conclusions: Estrogen-dependent expression of TRPV1 in sensory neurons may explain why ovarian suppression can reduce endometriosis-associated pain. Strategies directly targeting ion channels may offer an alternative option for management of CPP.
PMID: 25029427 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25029427
Greaves E1, Grieve K, Horne AW, Saunders PT.
Author information
Abstract
Context: Ovarian suppression is a common treatment for endometriosis-associated pelvic pain. Its exact mechanism of action is poorly understood although it is assumed to reflect reduced production/ action of estrogens. Objective: To measure expression of mRNAs encoded by nociceptive genes in the peritoneum of women with chronic pelvic pain (CPP) with or without endometriosis; to investigate whether estrogens alter nociceptive gene expression in human sensory neurons. Design: Human tissue analysis and cell culture. Setting: University Research Institute Patients: Peritoneal biopsies were obtained from women with CPP and endometriosis (n=12), CPP and no endometriosis (n=10), and with no pain or endometriosis (n=5). Endometriosis lesions were obtained from women with endometriosis (n=18). Main outcome measures: mRNAs encoding ion channels (P2RX3, SCN9A, SCN11A, TRPA1, TRPV1) and the neurotransmitter TAC1 were measured in tissue samples and in human embryonic stem cell-derived sensory neurons treated with estrogens. Results: TRPV1, TRPA1 and SCN11A mRNAs were significantly higher in the peritoneum from women with endometriosis (p<0.001, p<0.01). TPRV1, SCN9A and TAC1 were elevated in endometriosis lesions (p<0.05). P2RX3 mRNA was increased in the peritoneum of women with CPP, with and without endometriosis (p<0.05). Incubation of sensory neurons with E2 increased TRPV1 mRNA (p<0.01); the ERβ-selective agonist DPN increased concentrations of TRPV1, P2RX3, SCN9A and TAC1 mRNAs. Conclusions: Estrogen-dependent expression of TRPV1 in sensory neurons may explain why ovarian suppression can reduce endometriosis-associated pain. Strategies directly targeting ion channels may offer an alternative option for management of CPP.
PMID: 25029427 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25029427
Wednesday, July 16, 2014
cardiovascular risk decreased after surgical treatment of endo
"Regression of endothelial dysfunction in patients with endometriosis after surgical treatment: a 2-year follow-up study
Authors
Abstract
STUDY QUESTION How does endothelial function change in women with endometriosis after surgical treatment?
SUMMARY ANSWER Surgical treatment of endometriosis leads to endothelial function improvement, resulting in reduction of cardiovascular risk.
WHAT IS KNOWN ALREADY Some recent studies have demonstrated that in young women with endometriosis, even if structural alterations are absent, endothelial dysfunction, expressed as flow-mediated dilation (FMD) impairment, can nevertheless occur. However, there are no data about changes of endothelial function in women with endometriosis after surgical treatment of endometriosis.
STUDY DESIGN, SIZE, DURATION This is a follow-up study carried out in 68 women enrolled in a previous study. Endothelial function was evaluated 2 years after surgical procedure and compared with baseline values.
PARTICIPANTS/MATERIALS, SETTING, METHODS Twenty-two patients who had undergone surgical treatment of endometriosis (named as patients with STE) and 10 control subjects without endometriosis, from the original study sample participated in this follow-up study. Assessment of endothelial function by FMD evaluation and measurements of serum markers of endothelial activation and inflammation were done in all these subjects.
MAIN RESULTS AND THE ROLE OF CHANCEAfter a 2-year follow-up period, FMD increased significantly with respect to baseline values among patients with STE [average pre- to post-difference: 5.07%, 95% confidence intervals (CI) 3.50, 6.63%; P < 0.001] but not among controls (average pre- to post-difference: 1.56%, 95% CI −0.55, 3.67%; P = 0.13). Follow-up FMD values were not significantly different between patients with STE and controls (average difference 1.50%, 95% CI −1.24, 4.23%; P = 0.27). Follow-up markers of inflammation and endothelial cells activation were similar among patients with STE and controls.
LIMITATIONS, REASONS FOR CAUTIONAlthough this study represents the first in the literature assessing endothelial function after surgical treatment of endometriosis, further longitudinal studies are desirable to define better the real risk that women with a history of endometriosis will develop cardiovascular events.
WIDER IMPLICATIONS OF THE FINDINGSEndothelial dysfunction may be a better predictor of future cardiovascular events than traditional risk factors and the improvement in endothelial function we observed in patients after STE may have significant implications for their future cardiovascular risk.
STUDY FUNDING/COMPETING INTEREST(S)No external funding has been either sought or obtained for this study. There are no conflicts of interest to declare." http://m.humrep.oxfordjournals.org/content/29/6/1205
Authors
Abstract
STUDY QUESTION How does endothelial function change in women with endometriosis after surgical treatment?
SUMMARY ANSWER Surgical treatment of endometriosis leads to endothelial function improvement, resulting in reduction of cardiovascular risk.
WHAT IS KNOWN ALREADY Some recent studies have demonstrated that in young women with endometriosis, even if structural alterations are absent, endothelial dysfunction, expressed as flow-mediated dilation (FMD) impairment, can nevertheless occur. However, there are no data about changes of endothelial function in women with endometriosis after surgical treatment of endometriosis.
STUDY DESIGN, SIZE, DURATION This is a follow-up study carried out in 68 women enrolled in a previous study. Endothelial function was evaluated 2 years after surgical procedure and compared with baseline values.
PARTICIPANTS/MATERIALS, SETTING, METHODS Twenty-two patients who had undergone surgical treatment of endometriosis (named as patients with STE) and 10 control subjects without endometriosis, from the original study sample participated in this follow-up study. Assessment of endothelial function by FMD evaluation and measurements of serum markers of endothelial activation and inflammation were done in all these subjects.
MAIN RESULTS AND THE ROLE OF CHANCEAfter a 2-year follow-up period, FMD increased significantly with respect to baseline values among patients with STE [average pre- to post-difference: 5.07%, 95% confidence intervals (CI) 3.50, 6.63%; P < 0.001] but not among controls (average pre- to post-difference: 1.56%, 95% CI −0.55, 3.67%; P = 0.13). Follow-up FMD values were not significantly different between patients with STE and controls (average difference 1.50%, 95% CI −1.24, 4.23%; P = 0.27). Follow-up markers of inflammation and endothelial cells activation were similar among patients with STE and controls.
LIMITATIONS, REASONS FOR CAUTIONAlthough this study represents the first in the literature assessing endothelial function after surgical treatment of endometriosis, further longitudinal studies are desirable to define better the real risk that women with a history of endometriosis will develop cardiovascular events.
WIDER IMPLICATIONS OF THE FINDINGSEndothelial dysfunction may be a better predictor of future cardiovascular events than traditional risk factors and the improvement in endothelial function we observed in patients after STE may have significant implications for their future cardiovascular risk.
STUDY FUNDING/COMPETING INTEREST(S)No external funding has been either sought or obtained for this study. There are no conflicts of interest to declare." http://m.humrep.oxfordjournals.org/content/29/6/1205
Saturday, July 12, 2014
Genetics and Endometriosis
Is there a genetic component to endometriosis? Current research says yes, although there are other factors that come into play.
"Multifactorial or polygenic disorders, such as endometriosis, are determined by multiple genes with allelic variations. Early studies by the groups of Simpson and Lamb [2,3] suggested that endometriosis has a heritable component. Endometriosis is a common, chronic, inflammatory and estrogen-dependent gynecological disease that develops as a consequence of a combination of genetic predisposition and environmental factors." http://genomemedicine.com/content/2/10/75
"Endometriosis is a benign disease with high prevalence in women of reproductive age estimated between 10 and 15% and is associated with considerable morbidity. Its etiology and pathogenesis are controversial but it is believed to involve multiple genetic, environmental, immunological, angiogenic, and endocrine processes. Altered expressions of growth factors, cytokines, adhesion molecules, matrix metalloproteinases, and enzymes for estrogen synthesis and metabolism have been frequently observed in this condition. The possibility of genetic basis of endometriosis is demonstrated in studies of familial disease, in which the incidence of endometriosis is higher for first-degree relatives of probands as compared to controls....
"This condition is considered as benign disorder, but exhibits cellular proliferation, cellular invasion, and neo angiogenesis. The glandular epithelium occasionally exhibits cytological atypia and/or hyperplasia (3) as well as DNA aneuploidy (4). The malignant potential of the endometriotic epithelial cells has been suggested in some cases considering the monoclonal methylation pattern of the HUMARA alleles and their invasive and metastatic ability in vitro (5, 6). In this context, previous studies supported the hypothesis that progression of endometriotic lesions to frank malignancy can occur although with a very rare incidence (7–11). However, the significance of the so-called malignant potential of endometriotic cells is controversial since monoclonal cells growth pattern was described in various benign lesions (5).
"There is strong evidence that the endometrium of women with endometriosis has an increased capacity to proliferate, implant, and grow in the peritoneal cavity (2). Morphological studies of tissue sections have demonstrated that the endometriotic glands have a wide range of morphologic development presenting a pattern ranging from poorly to highly differentiated glandular structures. Such morphological variations occur from gland to gland even within cellular areas in the same gland (19). Adequate morphological changes of the endometriotic glands were found in implants only during the proliferative phase of the menstrual cycle, whereas secretory changes were completely missing during the luteal phase (19). These changes include histological differentiation and induction of secretory proteins such as prolactin (PRL) (20), insulin-like growth factor binding protein-1 (IGF-BP1) (21), and extracellular matrix proteins such as fibronectin (22). In addition, several markers are aberrantly expressed in endometriotic cells in comparison to the normal cell elements, including the gap junction connexins (Cx) (23), β-cadherins (24), metalloproteinases (25), and P450 aromatase (26). Altogether, these features indicate a high degree of dedifferentiation in comparison to the normal situation....
"From the collected molecular data, it is evident that one or several genes may be disrupted by mutations or loss of DNA sequences in this condition. Loss of some protein functions may effect the regulation of several emerging down stream pathways, including the EGFR-axis, E-cadherin dynamics, transcriptional regulation, cell cycle regulation (proliferation/apoptosis), and cell adhesion. Divergences from mature endometrial epithelium to endometriotic epithelium must involve abnormal gene expression, which may directly cause or reinforce the alterations caused by changes of one or several genes undergoing germinal alterations. Within this context, the treatment strategies of endometriosis centered mainly toward ovarian function suppression and indirect limitation of cell growth and activity of endometriosis remain insufficient (73, 74).
"Multifactorial or polygenic disorders, such as endometriosis, are determined by multiple genes with allelic variations. Early studies by the groups of Simpson and Lamb [2,3] suggested that endometriosis has a heritable component. Endometriosis is a common, chronic, inflammatory and estrogen-dependent gynecological disease that develops as a consequence of a combination of genetic predisposition and environmental factors." http://genomemedicine.com/content/2/10/75
"Endometriosis is a benign disease with high prevalence in women of reproductive age estimated between 10 and 15% and is associated with considerable morbidity. Its etiology and pathogenesis are controversial but it is believed to involve multiple genetic, environmental, immunological, angiogenic, and endocrine processes. Altered expressions of growth factors, cytokines, adhesion molecules, matrix metalloproteinases, and enzymes for estrogen synthesis and metabolism have been frequently observed in this condition. The possibility of genetic basis of endometriosis is demonstrated in studies of familial disease, in which the incidence of endometriosis is higher for first-degree relatives of probands as compared to controls....
"This condition is considered as benign disorder, but exhibits cellular proliferation, cellular invasion, and neo angiogenesis. The glandular epithelium occasionally exhibits cytological atypia and/or hyperplasia (3) as well as DNA aneuploidy (4). The malignant potential of the endometriotic epithelial cells has been suggested in some cases considering the monoclonal methylation pattern of the HUMARA alleles and their invasive and metastatic ability in vitro (5, 6). In this context, previous studies supported the hypothesis that progression of endometriotic lesions to frank malignancy can occur although with a very rare incidence (7–11). However, the significance of the so-called malignant potential of endometriotic cells is controversial since monoclonal cells growth pattern was described in various benign lesions (5).
"There is strong evidence that the endometrium of women with endometriosis has an increased capacity to proliferate, implant, and grow in the peritoneal cavity (2). Morphological studies of tissue sections have demonstrated that the endometriotic glands have a wide range of morphologic development presenting a pattern ranging from poorly to highly differentiated glandular structures. Such morphological variations occur from gland to gland even within cellular areas in the same gland (19). Adequate morphological changes of the endometriotic glands were found in implants only during the proliferative phase of the menstrual cycle, whereas secretory changes were completely missing during the luteal phase (19). These changes include histological differentiation and induction of secretory proteins such as prolactin (PRL) (20), insulin-like growth factor binding protein-1 (IGF-BP1) (21), and extracellular matrix proteins such as fibronectin (22). In addition, several markers are aberrantly expressed in endometriotic cells in comparison to the normal cell elements, including the gap junction connexins (Cx) (23), β-cadherins (24), metalloproteinases (25), and P450 aromatase (26). Altogether, these features indicate a high degree of dedifferentiation in comparison to the normal situation....
"From the collected molecular data, it is evident that one or several genes may be disrupted by mutations or loss of DNA sequences in this condition. Loss of some protein functions may effect the regulation of several emerging down stream pathways, including the EGFR-axis, E-cadherin dynamics, transcriptional regulation, cell cycle regulation (proliferation/apoptosis), and cell adhesion. Divergences from mature endometrial epithelium to endometriotic epithelium must involve abnormal gene expression, which may directly cause or reinforce the alterations caused by changes of one or several genes undergoing germinal alterations. Within this context, the treatment strategies of endometriosis centered mainly toward ovarian function suppression and indirect limitation of cell growth and activity of endometriosis remain insufficient (73, 74).
"Future studies should concentrate on modifying and extending the use of the molecular biology techniques. Cytogenetic analysis with improved culture techniques of endometriotic tissue, capable of simulating the normal endometriotic environment, may help to prevent selective in vitro growth pressures. CGH and cDNA microarray studies has only been used to date on a limited number of primary endometriotic samples, yet has given us important informations (41, 75). Gene expression profiling, allelotyping, and FISH studies need to investigate the various types of endometriotic samples and more regions of the genome. As techniques are improving and examination of archival material is now possible it should be easier to correlate clinical data with the phenotypical features and genotype of primary lesions. This will certainly yield informations important for the early diagnosis and prognosis of patients.
"Finally, the anatomical and the immuno-histochemical features of the ectopic organic structures identified in fetal female reproductive tract suggest that endometriotic as well as neoplastic disease in adult women may develop on the basis of misplaced endometrial glands and/or embryonic cell remnants."
Above from Frontiers in Surgery: http://journal.frontiersin.org/Journal/10.3389/fsurg.2014.00016/full
"Endometriosis is a benign gynecological disease characterized by the presence and growth of endometrial cells outside the uterus. Genetic, endocrine, immunological, and environmental factors have been suggested in its pathogenesis. A great number of studies have related genetic polymorphisms as a factor that contributes to the development of endometriosis. This review presents a detailed description of the contribution of genetic polymorphisms in genes that regulate vascular function and tissue remodeling in endometriosis (alpha 2-HS glycoprotein [AHSG], epidermal growth factor receptor [EGFR], vascular endothelial growth factor [VEGF], endostatin, plasminogen activator inhibitor 1 [PAI-1], angiotensin I-converting enzyme [ACE], and matrix metalloproteinases [MMPs]). Some polymorphisms of the VEGF (-460 C/T, +405 G/C, +936 C/T), PAI, MMP-1, 2, and 3 genes were widely studied, while polymorphisms of the AHSG, EGF, endostatin, and VEGF (-1154 G/A, -2578 A/C) genes were not. In this latter case, additional studies are required to confirm the findings of the few studies that have analyzed these single nucleotide polymorphisms (SNPs). Additionally, studies that found a positive or negative association of SNP with endometriosis emphasize the relevance of studies with a large number of control cases to confirm their findings. The haplotype analysis was performed only for the VEGF (-460, +405, -1154 and -2578), ACE (-240/2350) and MMP-1, 2, 3, and 9 genes, and in most of them, there was no association with endometriosis. Of the eight works that analyzed haplotypes of the VEGF gene, five did not associate them with endometriosis. Haplotypes of ACE and MMP-2 genes were not associated with endometriosis, while those of MMP-1, 3, and 9 genes were related to a high risk for the disease." lots more details at http://www.scielo.br/scielo.php?pid=S0104-42302012000500022&script=sci_arttext&tlng=en
"They have identified two new genetic variants that increase the risk of developing the disease, particularly moderate-severe stages.... The first is a variant on chromosome 7 believed to be involved in regulating nearby genes, probably those involved in the development of the womb and its lining. The second variant was found on chromosome 1, close to the gene WNT4. This is important for hormone metabolism and the development of the female reproductive tract, especially the ovaries, making it an important biological candidate for involvement in endometriosis.
"Our study is a breakthrough because it provides the first strong evidence that variations in DNA make some women more likely to develop endometriosis," says Dr Zondervan. "We now need to understand the effect of these variations on cells and molecules in the body."" http://www.well.ox.ac.uk/dec-10-genetic-variants-in...
"Our study is a breakthrough because it provides the first strong evidence that variations in DNA make some women more likely to develop endometriosis," says Dr Zondervan. "We now need to understand the effect of these variations on cells and molecules in the body."" http://www.well.ox.ac.uk/dec-10-genetic-variants-in...
"We conducted a genome-wide association meta-analysis of 4,604 endometriosis cases and 9,393 controls of Japanese1 and European2 ancestry. We show that rs12700667 on chromosome 7p15.2, previously found to associate with disease in Europeans, replicates in Japanese (P = 3.6 × 10−3), and we confirm association of rs7521902 at 1p36.12 near WNT4. In addition, we establish an association of rs13394619 in GREB1 at 2p25.1 with endometriosis and identify a newly associated locus at 12q22 near VEZT (rs10859871). Excluding cases of European ancestry of minimal or unknown severity, we identified additional previously unknown loci at 2p14 (rs4141819), 6p22.3 (rs7739264) and 9p21.3 (rs1537377). All seven SNP effects were replicated in an independent cohort and associated at P <5 × 10−8 in a combined analysis. Finally, we found a significant overlap in polygenic risk for endometriosis between the genome-wide association cohorts of European and Japanese descent (P = 8.8 × 10−11), indicating that many weakly associated SNPs represent true endometriosis risk loci and that risk prediction and future targeted disease therapy may be transferred across these populations." http://www.nature.com/ng/journal/v44/n12/full/ng.2445.html
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