Zinc transporter LIV1: A promising cell surface target for triple negative breast cancer.

Breast cancer is one of the leading causes contributing to the global cancer burden. The triple negative breast cancer (TNBC) molecular subtype accounts for the most aggressive type. Despite progression in therapeutic options and prognosis in breast cancer treatment options, there remains a high rate of distant relapse. With advancements in understanding the role of zinc and zinc carriers in the prognosis and treatment of the disease, the scope of precision treatment/targeted therapy has been expanded. Zinc levels and zinc transporters play a vital role in maintaining cellular homeostasis, tumor surveillance, apoptosis, and immune function. This review focuses on the zinc transporter, LIV1, as an essential target for breast cancer prognosis and emerging treatment options. Previous studies give an insight into the role of LIV1 in fulfilling the most important hallmarks of cancer such as apoptosis, metastasis, invasion, and evading the immune system. Normal tissue expression of LIV1 is limited. Higher expression of LIV1 has been linked to Epithelial-Mesenchymal Transition, histological grade of cancer, and early node metastasis. LIV1 was found to be one of the attractive targets in the therapeutic hunt for TNBCs. TNBCs are an immunogenic breast cancer subtype. As zinc transporters are known to serve as the metabolic gatekeepers of immune cells, this review bridges tumor infiltrating lymphocytes, TNBC and LIV1. In addition, the suitability of LIV1 as an antibody-drug conjugate (Seattle genetics [SGN]-LIV1A) target in TNBC, represents a promising strategy for patients. Early clinical trial results reveal that this novel agent reduces tumor burden by inducing mitotic arrest, immunomodulation, and immunogenic cell death, warranting further investigation of SGN-LIV1A in combination with immuno-oncology agents. Priming the patient's immune response in combination with SGN-LIV1A could eventually change the landscape for the TNBC patient population.

Analysis of Morbidity, Mortality and Survival Pattern Following Surgery for Borderline Ovarian and Malignant Ovarian Tumour in Tertiary Care Centre.

BACKGROUNDS: To analyse the morbidity, mortality and survival pattern following surgery for borderline ovarian and malignant ovarian tumours. METHODS: The medical records of 57 consecutive patients with invasive and borderline epithelial ovarian cancer patients registered and operated in our tertiary centre between 2015 to 2017 were reviewed. Patients were followed up for a minimum of 18 months to maximum of 42 months at an interval of 3 months with CA125 values. Various prognostic factors were analysed. The data descriptive statistics of frequency and percentage analysis were used for categorical variables and mean and standard deviation were used for continuous variables. RESULTS: The most common age group was 51 years and above with the majority (56.2%) of women belonging to postmenopausal age group (32/57). In our study, 30 out of 57 women (52.6%) had stage III disease, 17 women had stage I disease (29.8%) and 7 women had stage 2 disease (12.3%). Majority of the women had serous epithelial ovarian tumour (47 out of 57 patients), which contributed to 82.4%. Grade 1 and 2 morbidity was encountered in 8 patients. Six patients had wound infection (grade 1), and 2 patients required blood transfusions (grade 2). One patient had grade 3 morbidity requiring re-laparotomy. Borderline tumours and early-stage epithelial ovarian tumours had good prognosis, less morbidity and good survival. The overall median survival was 25 months. CONCLUSIONS: With meticulous perioperative care, surgery for ovarian cancer in the primary and interval setting can be done with minimal morbidity and no postoperative mortality, especially in patients with co-morbidities. Grade is an important prognostic factor affecting the survival of patients with epithelial ovarian cancers undergoing surgery. Lymph node dissection helps achieve local control but may not improve the survival.

Molecular dysregulations underlying the pathogenesis of endometriosis.

Endometriosis is a crippling disease characterized by the presence of endometrium-like tissue or scar outside the uterine cavity, commonly confined to the peritoneal and serosal surfaces of the pelvic organs. 10-15% of women in reproductive age are estimated to be affected by endometriosis. Most of these patients present with infertility and suffer from pelvic pain. The benign disease rarely progresses to malignancy. Regardless of its high prevalence, the pathogenesis of the disease is not fully understood. Treatment options for endometriosis are limited and are often based on a symptomatic approach. The unavailability of proper diagnostic approaches, fewer therapeutic options, and sparse understanding of molecular alterations are responsible for the continued disease burden. Exploring the molecular elements causing the pathogenesis of endometriosis may lead to a number of breakthroughs in the treatment of the illness, such as the discovery of new biomarkers for diagnosis and therapeutic targets that can be a guide to better prognosis and reduced recurrence. The goal of this review is to provide the reader a critical understanding of the disease by summarizing the genetic, immunological, hormonal, and epigenetic deregulations that support the molecular basis for development of endometriotic cyst, with a special focus on the study models needed to analyze these changes in the endometriotic microenvironment.