Endometrial carcinoma recurrence according to race and ethnicity: An NRG Oncology/Gynecologic Oncology Group 210 Study

Abstract

Non-Hispanic black (NHB) women are more likely to experience an endometrial carcinoma (EC) recurrence compared with Non-Hispanic white (NHW) women. The extent to which tumor characteristics, socioeconomic status (SES), and treatment contribute to this observation is not well defined. In the NRG Oncology/Gynecology Oncology Group (GOG) 210 Study we evaluated associations between race and ethnicity with EC recurrence according to tumor characteristics with adjustment for potential confounders. Our analysis included 3,199 non-Hispanic white, 532 non-Hispanic black and 232 Hispanic women with EC. Recurrence was documented during follow-up. We used Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between race and ethnicity with EC recurrence in models stratified by histologic subtype (low-grade endometrioid, high-grade endometrioid, serous, mixed cell, carcinosarcoma, clear cell) or stage (I, II, III) and adjusted for age, SES, body mass index, smoking status, and treatment. In histologic subtype-stratified models, higher EC recurrence was noted in NHB women with low-grade endometrioid (HR=1.94, 95% CI=1.21-3.10) or carcinosarcomas (HR=1.66, 95% CI=0.99-2.79) compared with NHWs. In stage-stratified models, higher EC recurrence was noted among NHB women with stage I (HR=1.48, 95% CI=1.06-2.05) and Hispanic women with stage III disease (HR=1.81, 95% CI=1.11-2.95). Our observations of higher EC recurrence risk among NHB and Hispanic women, as compared with NHW women, were not explained by tumor characteristics, SES, treatment or other confounders. Other factors, such as racial differences in tumor biology or other patient factors, should be explored as contributors to racial disparities in EC recurrence. This article is protected by copyright. All rights reserved.

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Integrated genome analysis of uterine leiomyosarcoma to identify novel driver genes and targetable pathways

Abstract

Uterine leiomyosarcomas (uLMS) are rare, aggressive malignancies for which limited treatment options are available. To gain novel molecular insights into uLMS and identify potential novel therapeutic targets, we characterized 84 uLMS samples for genome-wide somatic copy number alterations, mutations, gene fusions and gene expression, and performed a data integration analysis. We found that alterations affecting TP53, RB1, PTEN, MED12, YWHAE and VIPR2 were present in the majority of uLMS. Pathway analyses additionally revealed that the PI3K/AKT/mTOR, estrogen-mediated S-phase entry and DNA damage response signaling pathways, for which inhibitors have already been developed and approved, frequently harbored genetic changes. Furthermore, a significant proportion of uLMS was characterized by amplifications and overexpression of known oncogenes (CCNE1, TDO2), as well as deletions and reduced expression of tumor suppressor genes (PTEN, PRDM16). Overall, it emerged that the most frequently affected gene in our uLMS samples was VIPR2 (96%). Interestingly, VIPR2 deletion also correlated with unfavorable survival in uLMS patients (multivariate analysis; HR=4.5, CI=1.4-14.3, p=1.2E-02), while VIPR2 protein expression was reduced in uLMS versus normal myometrium. Moreover, stimulation of VIPR2 with its natural agonist VIP decreased SK-UT-1 uLMS cell proliferation in a dose-dependent manner. These data suggest that VIPR2, which is a negative regulator of smooth muscle cell proliferation, might be a novel tumor suppressor gene in uLMS. Our work further highlights the importance of integrative molecular analyses, through which we were able to uncover the genes and pathways most frequently affected by somatic alterations in uLMS. This article is protected by copyright. All rights reserved.

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The Prevalence and Concordance of Human Papillomavirus Infection in Different Anogenital Sites among Men and Women in Liuzhou, China: A Population-Based Study

Abstract

Human papillomavirus (HPV) infection is the pathogenesis of anogenital cancers and genital warts in both men and women, whereas there is a scarcity of large studies focused on HPV prevalence in different anogenital sites of both sexes in the same population. From May to July 2014, 2309 men and 2378 women aged 18-55 were enrolled from a community in Liuzhou, China. Penis/glans penis/coronary sulcus (PGC) and perianal/anal canal (PA) specimens of men, and vaginal (VA), vulvar (VU) and PA specimens of women, were collected and genotyped for HPV. The prevalence of any HPV tested in PGC and PA samples from men and VA, VU, and PA samples from women was 10.9%, 3.8%, 14.2%, 13.3% and 8.4%, respectively. The concordance of VA and VU was highest (kappa = 0.74), followed by VU and PA (0.44), VA and PA (0.39), and PGC and PA (0.16). Besides sex behavior, ever having used a towel supplied by a hotel was a risk factor for both external genital and PA HPV infection. Our data indicated that women were more of a major reservoir for oncogenic HPV infection of both genital sites and PA sites than was men. In both sexes, the genital sites were more likely than PA sites to harbor HPV infection. The concordance rates of HPV infection between genital sites and PA infection were poor. This article is protected by copyright. All rights reserved.

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Cancers, Vol. 9, Pages 141: An Exploration into the Origins and Pathogenesis of Anaplastic Large Cell Lymphoma, Anaplastic Lymphoma Kinase (ALK)-Positive

Cancers, Vol. 9, Pages 141: An Exploration into the Origins and Pathogenesis of Anaplastic Large Cell Lymphoma, Anaplastic Lymphoma Kinase (ALK)-Positive

Cancers doi: 10.3390/cancers9100141

Authors: Suzanne Turner

T-cell non-Hodgkin lymphoma is a heterogeneous disease ranging from malignancies arising from thymic T cells halted in development, through to mature, circulating peripheral T cells. The latter cases are diagnostically problematic with many entering the category of peripheral T-cell lymphoma, not otherwise specified (PTCL, NOS). Anaplastic large cell lymphoma (ALCL) is one of the exceptions to this whereby aberrant expression of anaplastic lymphoma kinase (ALK) and the distinctive presence of cell surface CD30 places this entity in its own class. Besides the expression of a well-studied oncogenic translocation, ALCL, ALK+ may also have a unique pathogenesis with a thymic origin like T lymphoblastic lymphoma but a peripheral presentation akin to PTCL. This perspective discusses evidence towards the potential origin of ALCL, ALK+, and mechanisms that may give rise to its unique phenotype.

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Cancers, Vol. 9, Pages 141: An Exploration into the Origins and Pathogenesis of Anaplastic Large Cell Lymphoma, Anaplastic Lymphoma Kinase (ALK)-Positive

Cancers, Vol. 9, Pages 141: An Exploration into the Origins and Pathogenesis of Anaplastic Large Cell Lymphoma, Anaplastic Lymphoma Kinase (ALK)-Positive

Cancers doi: 10.3390/cancers9100141

Authors: Suzanne Turner

T-cell non-Hodgkin lymphoma is a heterogeneous disease ranging from malignancies arising from thymic T cells halted in development, through to mature, circulating peripheral T cells. The latter cases are diagnostically problematic with many entering the category of peripheral T-cell lymphoma, not otherwise specified (PTCL, NOS). Anaplastic large cell lymphoma (ALCL) is one of the exceptions to this whereby aberrant expression of anaplastic lymphoma kinase (ALK) and the distinctive presence of cell surface CD30 places this entity in its own class. Besides the expression of a well-studied oncogenic translocation, ALCL, ALK+ may also have a unique pathogenesis with a thymic origin like T lymphoblastic lymphoma but a peripheral presentation akin to PTCL. This perspective discusses evidence towards the potential origin of ALCL, ALK+, and mechanisms that may give rise to its unique phenotype.

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Recall of Fertility Discussion by Adolescent Female Cancer Patients: A Survey-Based Pilot Study

Journal of Adolescent and Young Adult Oncology , Vol. 0, No. 0.


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