Gynecology and Reproductive Endocrinology

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (629)348-3199

Rapid Communication - Gynecology and Reproductive Endocrinology (2024) Volume 8, Issue 3

Advances in Understanding and Managing Endometrial Adenocarcinoma

Qi Wan Yang *

School of Biosciences, The University of Porto is a Portuguese public research university located in Porto, Portugal

*Corresponding Author:
Qi Wan Yang
School of Biosciences
The University of Porto is a Portuguese public research university located in Porto
Portugal
E-mail: yang_wan@gmail.com

Received: 22-Apr-2024, Manuscript No. AAGGS-24-138556; Editor assigned: 26-Apr-2024, PreQC No. AAGGS-24-138556(PQ); Reviewed:11-May-2024, QC No. AAGGS-24-138556; Revised:18-May-2023, Manuscript No. AAGGS-24-138556(R); Published: 25-May-2023, DOI: 10.35841/2591-7994-8.3.203

Citation: Yang QW. Advances in understanding and managing endometrial adenocarcinoma. 2024;8(3):203

Visit for more related articles at Gynecology and Reproductive Endocrinology

Introduction

Endometrial adenocarcinoma (EA) is the most common form of endometrial cancer, accounting for more than 80% of cases. This type of cancer originates in the glandular cells of the endometrium, the lining of the uterus. The incidence of EA has been increasing globally, with risk factors including obesity, diabetes, hypertension, and unopposed estrogen exposure. The rising prevalence underscores the importance of advancements in understanding, diagnosing, and managing this malignancy[1].

EA typically arises due to the prolonged exposure of the endometrium to estrogen without the counterbalancing effect of progesterone. This hormonal imbalance can be endogenous, as seen in conditions like polycystic ovary syndrome (PCOS), or exogenous, due to hormone replacement therapy. Genetic predispositions, such as Lynch syndrome, also significantly increase the risk of developing EA. Molecular alterations, including mutations in PTEN, PIK3CA, KRAS, and ARID1A genes, play a crucial role in the pathogenesis of EA. Understanding these genetic changes has opened new avenues for targeted therapies[2].

The diagnosis of EA involves a combination of clinical evaluation, imaging, and histopathological examination. Symptoms often include abnormal uterine bleeding, particularly in postmenopausal women, pelvic pain, and sometimes an enlarged uterus palpable on physical examination. Transvaginal ultrasound is typically the first imaging modality used, offering insights into endometrial thickness. An endometrial biopsy remains the gold standard for diagnosis, allowing for histological assessment and grading of the tumor.

Recent advancements have improved diagnostic accuracy and early detection. Liquid biopsy, analyzing circulating tumor DNA (ctDNA) from blood samples, is emerging as a non-invasive diagnostic tool. Moreover, advancements in molecular imaging techniques, such as PET/CT with novel radiotracers, are enhancing the sensitivity and specificity of EA detection[3].

The primary treatment for EA is surgical, involving hysterectomy with bilateral salpingo-oophorectomy. The extent of surgery depends on the stage and grade of the tumor. Minimally invasive surgical techniques, such as laparoscopic and robotic-assisted surgeries, have gained popularity due to their reduced morbidity and faster recovery times compared to open surgery.

Adjuvant therapies, including radiation and chemotherapy, are tailored based on the tumor stage and risk factors. Radiation therapy, either as external beam radiation or brachytherapy, is often employed to reduce local recurrence. Chemotherapy, typically involving platinum-based agents, is used in advanced stages or recurrent disease[4,5].

Hormonal therapy is a cornerstone for treating hormone receptor-positive EA, with progestins, tamoxifen, and aromatase inhibitors being commonly used. The advent of targeted therapies and immunotherapy has revolutionized the management of advanced EA. Agents targeting the PI3K/AKT/mTOR pathway, immune checkpoint inhibitors such as pembrolizumab, and drugs targeting microsatellite instability (MSI) or mismatch repair (MMR) deficiency are showing promising results in clinical trials.

The prognosis of EA largely depends on the stage at diagnosis, histological grade, and molecular characteristics. Early-stage EA generally has a favorable prognosis with a five-year survival rate exceeding 90%. However, advanced stages or high-grade tumors have a poorer prognosis[7].

Regular follow-up is crucial for detecting recurrences early. Follow-up protocols typically involve physical examinations, imaging, and serum markers, though no consensus exists on the optimal surveillance strategy. Recent studies suggest that incorporating ctDNA analysis could enhance the detection of minimal residual disease and guide personalized follow-up schedules.

Ongoing research is focused on understanding the molecular underpinnings of EA to develop more effective targeted therapies. The Cancer Genome Atlas (TCGA) project has provided a comprehensive genomic landscape of EA, identifying distinct molecular subtypes with potential therapeutic implications [8].

Immunotherapy is a rapidly evolving field in EA treatment. Studies have shown that tumors with high MSI or MMR deficiency respond well to immune checkpoint inhibitors. Combining immunotherapy with other modalities, such as radiation or targeted therapies, is being explored to enhance treatment efficacy.

Additionally, efforts are being made to develop predictive biomarkers to tailor treatment plans better. Molecular profiling and next-generation sequencing are increasingly used to identify actionable mutations and guide precision medicine approaches [9].

Endometrial adenocarcinoma remains a significant health concern due to its rising incidence and the complex interplay of risk factors and molecular alterations driving its pathogenesis. Advances in diagnostic techniques, surgical methods, and the advent of targeted and immunotherapies have significantly improved patient outcomes. However, challenges remain, particularly in managing advanced stages and recurrent disease. Continued research into the molecular mechanisms and the development of novel therapeutic strategies are essential to further enhance the prognosis and quality of life for patients with EA.

In conclusion, the evolving landscape of EA management highlights the importance of a multidisciplinary approach, incorporating the latest advancements in diagnostics, surgery, and systemic therapies. Personalized medicine, guided by molecular profiling, holds the promise of transforming the future of EA treatment, offering hope for improved survival and quality of life for affected women [10].

References

  1. Fox H, Buckley CH. The endometrial hyperplasias and their relationship to endometrial neoplasia.Histopathology. 1982;Sep 6:493-510.

Indexed at, Google Scholar, Crossref

  1. Grimelius L . A silver nitrate stain for alpha-2 cells in human pancreatic islets. Acta Soc Med Ups. 1968;73:243-270.

Indexed at, Google Scholar

  1. Burger RA, Brady MF, Bookman MA, et al.  Incorporation of bevacizumab in the primary treatment of ovarian cancer. N Engl J Med. 2011;365:2473-2483.
  2. Albores-Saavedra J, Rodríguez-Martínez HA, Larraza-Hernández O. Carcinoid tumors of the cervix.Pathol Annu. 1979;14 :273-291.

Indexed at, Google Scholar

  1. Ueda G, Yamasaki M, Inoue M, et al. Immunohistological demonstration of calcitonin in endometrial carcinomas with and without argyrophil cells.Nihon Sanka Fujinka Gakkai Zasshi. 1980;32:960-964.

Indexed at, Google Scholar, Crossref

  1. Tateishi R, Wada A, Hayakawa K, et al. Argyrophil cell carcinomas (apudomas) of the uterine cervix. Light and electron microscopic observations of 5 cases.Virchows Arch A Pathol Anat Histol. 1975;366:257-274.

Indexed at, Google Scholar, Crossref

  1. Proks C, Feit V. Gastric carcinomas with argyrophil and argentaffin cells.Virchows Arch A Pathol Anat Histol. 1982;395:201-206.

Indexed at, Google Scholar

  1. Partanen S, Syrjänen K. Argyrophilic cells in carcinoma of the female breast.Virchows Arch A Pathol Anat Histol. 1981;391:45-51.

Indexed at, Google Scholar

  1. Perren TJ, Swart AM, Pfisterer J, et al. A phase 3 trial of bevacizumab in ovarian cancer. N Engl J Med. 2011;365:2484-2496.

Indexed at, Google Scholar, Crossref

  1. Katsumata N, Yasuda M, Takahashi F, et al. Dose-dense paclitaxel once a week in combination with carboplatin every 3 weeks for advanced ovarian cancer: a phase 3, open-label, randomised controlled trial. Lancet. 2009;374:1331-1338.

Indexed at, Google Scholar, Crossref

Get the App