9 research outputs found
Regression Analysis Associated with Survival among XDR-TB patients with HIV-coinfection (n = 129).
<p>Regression Analysis Associated with Survival among XDR-TB patients with HIV-coinfection (n = 129).</p
Demographic, Clinical, Sputum, and TB& HIV Treatment Characteristics Among Survivors & Non-survivors of XDR-TB (n = 142).
*<p>not individually included in regression analysis.</p>**<p>p<0.05.</p>$<p>ttest.</p>§<p>Chi-square.</p>€<p>Kruskal-Wallis.</p
Modifiable & Non-Modifiable Clinical Characteristics of XDR-TB Patients.
<p>Modifiable & Non-Modifiable Clinical Characteristics of XDR-TB Patients.</p
The <i>KRAS-</i>variant is significantly associated with developing ovarian cancer post-menopausally compared to pre-menopausally.
<p>The <i>KRAS-</i>variant is significantly associated with developing ovarian cancer post-menopausally compared to pre-menopausally.</p
The <i>KRAS-</i>variant is significantly associated with uninformative breast and ovarian cancer patients.
<p>The <i>KRAS-</i>variant is significantly associated with uninformative breast and ovarian cancer patients.</p
The <i>KRAS</i>-variant is significantly associated with the risk of developing additional cancers beyond breast and ovarian cancer.
<p>The <i>KRAS</i>-variant is significantly associated with the risk of developing additional cancers beyond breast and ovarian cancer.</p
Prevalence of the <i>KRAS-</i>variant in uninformative patients.
<p>Prevalence of the <i>KRAS-</i>variant in uninformative patients.</p
Estrogen withdrawal, increased breast cancer risk and the KRAS-variant
<p>The <i>KRAS</i>-variant is a biologically functional, microRNA binding site variant, which predicts increased cancer risk especially for women. Because external exposures, such as chemotherapy, differentially impact the effect of this mutation, we evaluated the association of estrogen exposures, breast cancer (BC) risk and tumor biology in women with the <i>KRAS</i>-variant. Women with BC (<i>n</i> = 1712), the subset with the <i>KRAS</i>-variant (<i>n</i> = 286) and <i>KRAS</i>-variant unaffected controls (<i>n</i> = 80) were evaluated, and hormonal exposures, <i>KRAS</i>-variant status, and pathology were compared. The impact of estrogen withdrawal on transformation of isogenic normal breast cell lines with or without the <i>KRAS</i>-variant was studied. Finally, the association and presentation characteristics of the <i>KRAS</i>-variant and multiple primary breast cancer (MPBC) were evaluated. <i>KRAS</i>-variant BC patients were more likely to have ovarian removal pre-BC diagnosis than non-variant BC patients (p = 0.033). In addition, <i>KRAS</i>-variant BC patients also appeared to have a lower estrogen state than <i>KRAS</i>-variant unaffected controls, with a lower BMI (<i>P</i> < 0.001). Finally, hormone replacement therapy (HRT) discontinuation in <i>KRAS</i>-variant patients was associated with a diagnosis of triple negative BC (<i>P</i> < 0.001). Biologically confirming our clinical findings, acute estrogen withdrawal led to oncogenic transformation in <i>KRAS</i>-variant positive isogenic cell lines. Finally, <i>KRAS</i>-variant BC patients had greater than an 11-fold increased risk of presenting with MPBC compared to non-variant patients (45.39% vs 6.78%, OR 11.44 [3.42–37.87], <i>P</i> < 0.001). Thus, estrogen withdrawal and a low estrogen state appear to increase BC risk and to predict aggressive tumor biology in women with the <i>KRAS</i>-variant, who are also significantly more likely to present with multiple primary breast cancer.</p