Endometrial Adenocarcinoma Research Articles

Classification of endometrial adenocarcinoma using histopathology images with extreme learning machine method

Classification of endometrial adenocarcinoma using histopathology images with extreme learning machine method

LCI139: In silico design of a novel multitarget small molecular inhibitor for the treatment of PTEN-mutant endometrial adenocarcinoma

LCI139: In silico design of a novel multitarget small molecular inhibitor for the treatment of PTEN-mutant endometrial adenocarcinoma

Molecular markers of response to enzalutamide-based therapy in advanced or recurrent endometrioid endometrial adenocarcinoma (ENPAC study)

Molecular markers of response to enzalutamide-based therapy in advanced or recurrent endometrioid endometrial adenocarcinoma (ENPAC study)

An unusual case of aggressive endometrial adenocarcinoma metastasis to the clivus: illustrative case.

Though endometrial carcinomas are a relatively common cancer of the female genitourinary tract, they rarely metastasize. Similarly, clival metastases make up a tiny fraction of all brain metastases. To the authors' knowledge, an endometrial carcinoma clival metastasis has never been described in the literature; therefore, the authors present the following unusual case of a 69-year-old female with a history of an initially grade 2 endometrial adenocarcinoma that metastasized to her clivus. Endometrial carcinoma has the potential to metastasize to the clivus. Endometrial carcinoma, even when initially low grade, can metastasize intracranially. Prompt diagnosis with tissue biopsy and radiation is the mainstay of treatment, although the prognosis remains poor. https://thejns.org/doi/10.3171/CASE24392.

A Comprehensive Review of TRPS1 as a Diagnostic Immunohistochemical Marker for Primary Breast Carcinoma: Latest Insights and Diagnostic Pitfalls

Background/Objectives: Immunohistochemical expression of TRPS1 (trichorhinophalangeal syndrome type 1) protein is usually used by pathologists to confirm breast origin for triple-negative breast cancers (TNBC) or metastatic carcinomas of unknown primary. However, recent studies have reported TRPS1 expression in a variety of non-breast lesions. This review aims to provide a comprehensive evaluation of TRPS1 expression across various tumor types, highlighting both its diagnostic utility and potential pitfalls that may arise in clinical practice. Methods: A thorough search of the PubMed database on TRPS1 immunoexpression in tumor pathology was conducted. While the gene itself has been known for several decades, most studies regarding its use in immunohistochemistry emerged in the late 2010s. Particular emphasis was placed on case reports and cohort studies that examined the implications of TRPS1 expression in non-breast tissues, as well as variations in the results between commercially available TRPS1 clones, which may influence the staining intensity and specificity. Results: TRPS1 demonstrated a strong diagnostic utility in identifying primary breast lesions, particularly in TNBC cases. However, its expression in a growing number of non-breast cancers, such as lung adenocarcinoma, prostate adenocarcinoma, urothelial carcinoma, ovarian high-grade serous carcinoma, and endometrial adenocarcinoma, as well as up to 96% of synovial sarcomas with SS18-SSX fusion, emphasizes the need for caution when interpreting TRPS1 positivity and suggests a multi-marker approach in order to increase the diagnostic accuracy. Conclusions: While TRPS1 remains a highly sensible immunohistochemical marker for confirming breast primary lesions, pathologists should be aware of its low specificity and incorporate complementary diagnostic methods in order to ensure accurate clinical management. Further research should focus on elucidating the molecular pathways regulating TRPS1 expression in various tumor types, which may better define its clinical utility.

PERITONEAL KERATIN GRANULOMAS MIMICKING PERITONEAL CARCINOMATOSIS: A POTENTIAL DIAGNOSTIC PITFALL

Abstract Introduction/Objective Keratin granulomas from a primary uterine cancer can present as peritoneal tumor nodules, mimicking peritoneal carcinomatosis. Endometrial adenocarcinomas with viable peritoneal tumor implants and/or involvement of bladder or bowel mucosa are categorized as stage IV disease. We present a rare case of endometrial adenocarcinoma of the uterus with squamous differentiation and multiple peritoneal nodules of keratin granulomas, masquerading as peritoneal carcinomatosis. Methods/Case Report A 68-year-old female with insignificant past medical history presented with complaints of postmenopausal bleeding for the past four months. Physical examination was unremarkable. Transvaginal ultrasound showed a 4.9 cm echogenic mass in the uterus. The endometrial biopsy showed squamous debris with atypical cells suspicious of malignancy. Endometrial curettings revealed endometrial adenocarcinoma, endometrioid type with squamous differentiation, FIGO Grade 1. Subsequently, she underwent hysterectomy with bilateral salpingo- oophorectomy. Intraoperatively, multiple suspicious nodules on the sigmoid colon and in the pelvis were identified, of which excisional biopsies and pelvic peritoneal washing were taken. Microscopic examination of the resection confirmed endometrial adenocarcinoma, FIGO Grade 1, nuclear grade 1, with extensive foreign body giant cell reaction to dead squamous cells (ghost cells). Cytologic examination of the peritoneal washing was unremarkable and excisions of the sigmoid serosal and peritoneal nodules showed pink eosinophilic laminated nodules surrounded by inflammatory cells including plasma cells, lymphocytes and multinucleated giant cells without any viable tumor cells. Results (if a Case Study enter NA) NA Conclusion Keratin granulomas are a foreign body reaction to keratin deposition from the squamous component of endometrioid adenocarcinoma. The pathogenesis of this foreign body response to keratin is considered to be a trans- tubal spread of keratin through retrograde shedding from the fallopian tubes. In the absence of viable tumor cells, it appears to have no negative prognostic significance. Careful microscopic examination of peritoneal keratin granulomas is imperative to avoid erroneous upstaging of the tumor and the subsequent advanced treatment.

Gastric and Gastrointestinal-like Immunophenotypes In Conventional Endometrial Endometrioid Adenocarcinomas Including Endometrioid Adenocarcinomas with Mucinous Differentiation: Frequency and Diagnostic Implications

Abstract Introduction/Objective Mucinous carcinomas of the gastric/gastrointestinal type (MCG) are now recognized as a rare, clinically aggressive subtype of endometrial cancer [EMCa]. However, neither their full morphologic spectrum, nor their defining immunophenotype, has been clearly defined. Previous proposals for their recognition include at least focal immunohistochemical expression of gastrointestinal markers, minimality or absence of ER and possibly PAX8 expression, and the absence of an endometrioid carcinoma component. Herein, we assess the frequency of gastric and gastrointestinal immunophenotypes in conventional endometrioid carcinomas without any discernible gastric/gastrointestinal-type morphology. Methods/Case Report Immunohistochemical analyses for CK7, CK20, CDX2, ER, SATB2, MUC6, PAX8 were performed on 81 EMCa, comprised of consecutively archived cases of low grade endometrioid carcinoma (n=47), FIGO grade III endometrioid carcinoma (n=12), and endometrioid carcinomas with mucinous differentiation (n=22). None showed goblet cells or gastric-type morphology. Expression levels were quantified as H-scores on a standardized 0-300 scale. Results (if a Case Study enter NA) Significant subsets of all 3 groups showed expression of MUC6, CDX2, SATB2 and CK20, without any significant differences between the groups. 56%, 62%, 23% and 25% of cases expressed MUC6, CDX2, CK20 and SATB2 respectively. 37% co-expressed MUC6 and CDX2, 12% co-expressed CDX2 and CK20, 6% co-expressed MUC6, CDX2 and CK20 and 2.5% co-expressed CDX2, CK20 and SATB2. The expression levels were generally low across all groups, with average H scores for positive cases being 49.5 [range 1-250] for MUC6, 33.7 [range 1-285] for CDX2, 24.0 [range 1-270] for CK20, and 30.5 [range; 2-220] for SATB2. There was no statistically significant correlation between the expression of any of the 4 markers (CK20, CDX2, SATB2 or MUC6) and low ER or PAX8 expression. However, the only 2 cases with high CDX2 expression (H: >/=200) were also associated with low ER (H<50) expression, and one of these concurrently showed high CK20 (H: 270) and low PAX8 (H: 2) expression, suggestive of true intestinal differentiation. Conclusion MUC6, SATB2, CDX2, and CK20 are not uncommonly expressed at low levels in endometrioid carcinoma. As such, the expression of these markers cannot be the sole basis for defining the clinically aggressive EMCa with true gastric/gastrointestinal differentiation, and for distinguishing them from conventional endometrioid carcinomas.

Synchronous endometrial and minor salivary gland carcinomas – role of molecular diagnostics amid lack of clinical suspicion

Abstract Introduction/Objective Synchronous malignancies account for 3-5% of all tumor diagnoses but can be challenging to detect if one or both tumors are rare histologic subtypes and clinical suspicion is lacking. Molecular diagnostics are critical for accurate diagnosis in these difficult cases to guide appropriate patient care. Methods/Case Report We report the case of a 49-year-old female who was diagnosed with a high-grade, mixed- histology endometrial adenocarcinoma a few years back. She was found to have hilar and mediastinal nodal carcinoma of uncertain differentiation a couple of months after her initial diagnosis, clinically labelled as metastatic endometrial carcinoma. Following neoadjuvant chemotherapy, her hysterectomy showed complete pathologic response, and was found to be POLE ultramutated on NGS. Follow-up PET scan in 2023 showed progression of hilar/endobronchial thickening, as well as interval increase in size of mediastinal nodes, again presumed to be endometrial metastases, despite the POLE mutant status. Repeat sampling was performed from both the sites, along with comprehensive molecular profiling. Cytology from the nodes and surgical pathology from the endobronchial lesion showed similar morphology consisting of hyperchromatic basaloid cells in cribriform arrangement with tubular structures containing myxoid stromal material, negative for PAX-8, ER, p40, and TTF1 immunostains, inconsistent with endometrial metastasis. Molecular studies including FISH and NGS showed MYB1::NFIB fusion characteristic of adenoid cystic carcinoma and absence of POLE mutation, definitively refuting the clinically suspected progression of endometrial metastasis. Molecular testing confirmed that the endobronchial tumor and mediastinal nodal involvement were caused by a second primary, distinct from her POLE-ultramutated endometrial carcinoma which disappeared with chemotherapy. Her extended molecular workup also revealed a pathogenic mutation in BRIP1, suggesting a genetic cancer predisposition syndrome requiring referral for genetic counseling. Results (if a Case Study enter NA) NA Conclusion Molecular pathology is an invaluable tool for unravelling diagnostic complexity. Pathologists must integrate cytomorphology, molecular genetics and knowledge of cancer biology to steer the clinical teams towards the best patient care.

The vasculogenic mimicry, CD146+ and CD105+ microvessel density in the prognosis of endometrioid endometrial adenocarcinoma: a single-centre immunohistochemical study

The microvessel compartment is crucial in the tumour microenvironment of endometrioid adenocarcinoma (EA). This study investigated the role of vasculogenic mimicry (VM), CD146, and CD105 microvessel density in the clinical prognosis of EA. A total of 188 EA cases were analyzed, with VM channels and microvessels detected using PAS/CD31, CD146, and CD105 staining. Mann-Whitney and Fisher exact tests were used to compare the study groups according to the evaluated criteria. ROC analysis included determination of the confidence interval (CI) and area under the ROC curve. The Mantel-Cox test was used to analyze progression-free survival. Multivariate Cox proportional hazard analysis was performed using stepwise regression. Results showed that VM channels and CD146 and CD105 microvessels were significantly higher (p < 0.0001) in cases with unfavourable prognosis. Univariate survival analysis highlighted the significant role of these factors in progression-free survival, while multivariate Cox analysis identified VM and CD146+ vessels as predictive factors. This study demonstrates, for the first time, that VM, CD146, and CD105-positive vessels are involved in EA prognosis, suggesting their potential as independent prognostic indicators and targets for antiangiogenic therapy. However, these findings require further validation through large-scale studies.

Toxicokinetic Profiles and Potential Endocrine Disruption Effects at the Reproductive Level Promoted by Siloxanes Used in Consumer Products.

Siloxanes, commonly known as silicones, are polymeric compounds made up of silicon and oxygen atoms bonded together alternately. Within this group of substances are linear methyl-siloxanes and cyclic methyl-siloxanes, with octamethylcyclotetrasiloxane (D4) and decamethylcyclopentasiloxane (D5) being the most produced and used industrially. Due to their versatility, high production volume, stability, and local presence in environmental matrices and biological fluids such as breast milk, fat, and plasma, siloxanes have been considered persistent organic pollutants, representing a public health problem. This represents a public health concern, especially when different investigations have reported potential endocrine effects at the reproductive level in experimental animals exposed to D4 and D5. The objective of this study was to review the potential reproductive and endocrine effects derived from siloxanes present in personal care products (PCPs). The results of the literature review confirmed that D4 and D5 were the most used siloxanes as additives in PCP because they improve the emollient properties of the cosmetic and the physical appearance of hair and skin. Similarly the toxicological effects of siloxanes, particularly D4, D5, and D6 included significant endocrine disruption, reproductive toxicity, and liver toxicity. Studies in SD and F-344 rats, commonly used to assess these effects, have shown that D4 has low estrogenic activity, binding to ER-α receptors, whereas D5 does not bind to estrogen receptors. D4 exposure has been associated with increased uterine weight and estrous cycle alterations, leading to prolonged exposure to estrogens, which raises the risk of endometrial hyperproliferation and carcinogenesis. Recent research highlights that D5 exposure disrupts follicle growth, endometrial receptivity, and steroidogenesis, resulting in infertility and hormonal imbalances, potentially causing disorders like endometriosis and increased cancer risk. Chronic exposure to D5 has been linked to the development of uterine endometrial adenocarcinoma, with higher doses further elevating this risk.

Race- associated molecular differences in uterine serous carcinoma.

Endometrial cancer (EMCA) is the most common gynecologic malignancy, and new diagnoses are increasing in the United States. Black patients are more likely to present with advanced stage, be diagnosed with high-risk uterine serous carcinoma (USC) and die of their cancer. Patients with endometrial adenocarcinoma who received tumor FoundationOne CDx testing at our institution between January 2017 and August 2022 were identified. Genomic alterations, demographic and clinical characteristics were collected. Descriptive statistics and Fisher's exact test were used to analyze data. A total of 289 patients (29.4% Black and 52.6% White) with advanced or recurrent endometrial adenocarcinoma underwent FoundationOne CDx testing. USC comprised 26.3% (76 of 289) of tested tumors. Of USC tumors, 33 of 76 (44%) were of Black race. USC occurred more frequently in Black patients (33 of 85 [38.8%] Black patients compared to 30 of 152 [19.7%] White patients, p<0.05). Among USC, CCNE1 amplification occurred more frequently in Black patients than in White patients (12 of 33 [36.36%] vs 2 of 30 [6.67%], p<0.05) while PI3K/AKT/mTOR pathway mutations occurred less frequently (16 of 33 [48.5%] vs 26 of 33 [86.7%], p=0.17). Among patients with CCNE1 amplification 73.3% (11 of 15) progressed on or within 12 months of first-line platinum-based therapy. CCNE1 amplification had significantly shorter median overall survival (97.3 months vs 44.3; HR (95%CI): 7.1 (10.03, 59.4) p< 0.05). Black patients constituted 44% of patients with USC in our study and had an increased frequency of CCNE1 amplification. Patients whose tumors harbored CCNE1 amplification had shorter overall survival. Identifying actionable mutations in this high unmet need population is crucial to improving outcomes among Black patients with uterine malignancy. Development of new targeted-therapies will need to keep these alterations at the forefront as trials are being designed.

Oncologic outcomes based on lymphovascular space invasion in node-negative FIGO 2009 stage I endometrioid endometrial adenocarcinoma: a multicenter retrospective cohort study

BackgroundThe 2023 International Federation of Gynecology and Obstetrics (FIGO) staging system includes lymphovascular invasion quantification as a staging criterion for endometrioid endometrial carcinomas; no lymphovascular invasion and focal invasion (≤4...

"Diagnosis and Management of Endometrial Adenocarcinoma Complex with Pyometra in a Bitch -A Rare Case Report Diagnosis and Management of Endometrial Adenocarcinoma Complex with Pyometra in a Bitch -A Rare Case Report "

"Diagnosis and Management of Endometrial Adenocarcinoma Complex with Pyometra in a Bitch -A Rare Case Report Diagnosis and Management of Endometrial Adenocarcinoma Complex with Pyometra in a Bitch -A Rare Case Report "

Abstract C165: Interrogating the Tumor and Immune Microenvironment of Endometrial Cancers Among a Diverse Cohort of Cases

Abstract Endometrial cancer (EC) is the sixth most common gynecological malignancy, with an increasing incidence worldwide over the last two decades. African American women are more likely to be diagnosed with endometrial cancer than Caucasian women. Unfortunately, African American women are more frequently diagnosed with high-grade EC, which occurs 2-3 times more often compared to their white and Hispanic counterparts. Additionally, African American women have higher mortality rates from EC than Caucasian women, highlighting a significant cancer disparity among these patients. Uterine EC disparities are induced by complex ecosystems composed of cellular niches with distinct genotypes, phenotypes, and spatial transcriptomic landscapes. In estrogen-dependent EC tumorigenesis, the endometrium undergoes uncontrollable proliferation, progressing from normal to atypical hyperplasia and ultimately to carcinoma. The heterogeneity of EC tumors complicates therapeutic targeting, rendering EC a challenging disease to cure. This study aims to investigate the genetic and transcriptomic features found in the tumor microenvironment of African American patients with EC. Previous research has shown that the molecular classification of EC tumors can be categorized as estrogen-driven, hypermutant, microsatellite instable, or lacking a specific molecular profile. Current models do not adequately reflect the oncogenic origin and pathological progression in patients. The cohort of EC cases includes primary, metastatic, and normal tumor tissues classified as Uterine Endometrial Adenocarcinoma, along with two Serous Papillary cases with varying tumor grades (low to high grade). Spatial transcriptomics and whole exome sequencing were performed on these samples. Spatial transcriptomics will identify the alterations in gene expression and the spatial landscape of the cell neighborhoods driving tumor heterogeneity. Whole exome sequencing will provide insight into the germline and somatic variants present in EC, offering a deeper understanding of the potential genetic drivers in African American patients. The genes expressed across the EC tumor landscape are implicated in cell proliferation, epithelial- mesenchymal transition, DNA damage response, and immune response. The analysis will also show the transition of normal to malignant endometrium harboring high tumor mutational burden and microsatellite instability when comparing paired samples. This comprehensive approach aims to elucidate the genetic and transcriptomic underpinnings contributing to the disparities observed in African American patients with EC, ultimately informing better-targeted therapies and improving outcomes. Citation Format: Danyelle Paine, John Carpten. Interrogating the Tumor and Immune Microenvironment of Endometrial Cancers Among a Diverse Cohort of Cases [abstract]. In: Proceedings of the 17th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2024 Sep 21-24; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2024;33(9 Suppl):Abstract nr C165.

Unraveling the Complexity: Endometrial Adenocarcinoma in a Young Woman—A Case Report

Unraveling the Complexity: Endometrial Adenocarcinoma in a Young Woman—A Case Report

Functional Analysis of RE1 Silencing Transcription Factor as a Putative Tumor Suppressor in Human Endometrial Cancer.

Uterine cancer is the most common gynecologic malignancy in the United States, with endometrioid endometrial adenocarcinoma (EC) being the most common histologic sub-type. Considering the molecular classifications of EC, efforts have been made to identify additional biomarkers that can assist in diagnosis, prognosis, and individualized therapy. We sought to explore the relationship of Repressor Element 1 (RE1) silencing transcription factor (REST), which downregulates neuronal genes in non-neuronal tissue, along with matrix metalloproteinase-24 (MMP24) and EC. We analyzed the expression of REST and MMP24 in 31 cases of endometrial cancer and 16 controls. We then explored the baseline expression of REST and MMP24 in two EC cell lines (Ishikawa and HEC-1-A) compared to a benign cell line (t-HESC) and subsequently evaluated proliferation, migration, and invasion in the setting of loss of REST gene expression. REST and MMP24 expression were significantly lower in human EC samples compared to control samples. REST was highly expressed in EC cell lines, but decreasing REST gene expression increased proliferation (FC: 1.13X, p < 0.0001), migration (1.72X, p < 0.0001), and invasion (FC: 7.77X, p < 0.05) in Ishikawa cells, which are hallmarks of cancer progression and metastasis. These findings elicit a potential role for REST as a putative tumor suppressor in EC.

Molecular characteristics and oncogenic role of CHD family genes: a pan-cancer analysis based on bioinformatic and biological analysis

Chromodomain helicase DNA-binding protein (CHD) gene family, an ATP (adenosine triphosphate) -dependent chromatin remodeler family, is involved in multiple developmental process and tumor development. However, there have been none pan-cancer analyses of this family. The expression levels, survival profiles, mutation profiles and immune infiltration of the CHD family genes from TCGA and TARGET database were analyzed using online tools or R packages. Interestingly, all types of CHD gene expressions were associated with the prognosis of Neuroblastoma, Acute lymphoblastic leukemia-Phase 3 and Acute Myeloid Leukemia (All P < 0.05). Knock down of CHD7 and CHD9 in K562 (human erythromyeloblastoid leukemia) and HEC-1-B (human endometrial adenocarcinoma) cells significantly inhibit cell proliferation and migration (P < 0.05). Proliferation, colony formation and migration assays were performed in CHD7 and CHD9 knockdown K562 and HBC-1-B cell lines. Mechanisms were also analyzed by PPI and GO ontology for our experiments. Histone modification, especially the methylation of H3K4, might be involved in CHD7 and CHD9 related oncogenesis. Through bioinformatic analysis, we showed CHD genes significantly affected the prognosis of different tumor types, including childhood tumor. Our findings provide new insights into the function and mechanism of CHD gene family, especially in CHD7 and CHD9.

Granulosa cell tumor of the ovary associated with Endometrial Cancer

Sex cord–stromal tumors (SCST) of the ovary comprise 5% to 8% of all ovarian malignancies. Granulosa cell tumors (GCT) are the most common type of malignant ovarian SCST accounting for 2% to 5% of all ovarian malignancies. Most tumors secrete estrogen. This can lead to an estrogen dependent endometrial hyperplasia and in some cases endometrial cancer. We report the case of a 62 year old woman with endometrial adenocarcinoma and adult granulosa cell tumor of the ovary who presented with postmenopausal bleeding and adnexal mass. She underwent total abdominal hysterectomy with bilateral salpingo-oophorectomy, infracolic omentectomy, and pelvic lymphadenectomy, and the specimen was submitted for histopathological examination. Concomitant adult GCT and endometrial Cancer is rare. This diagnosis requires a high index of suspicion along with imaging and histopathology.

Retained PAX2 expression associated with DNA mismatch repair deficiency in endometrial endometrioid adenocarcinoma.

Loss of expression of tumour suppressor PAX2 and MMR deficiency (dMMR) has been frequently seen in endometrial endometrioid adenocarcinoma (EEC). However, the relationship between PAX2 expression and MMR status is unknown. We studied the PAX2 expression and examined its association with MMR status at the protein and genetic levels in 180 cases of EEC. Overall, total loss of PAX2 expression was found in about 70%, while retained PAX2 expression was seen in 30% of EEC. Among 125 cases with loss of PAX2, 68.8% were found in EECs with pMMR, while 31.2% were seen in those with dMMR. Among 55 cases of EECs with retained PAX2 expression, 92.7% were EECs with dMMR and 7.3% were those with pMMR (P < 0.001). While dMMR cases with MLH1 hypermethylation show almost equal retained or loss of PAX2 expression (52% versus 48%), dMMR with genetic alterations had significantly more retained PAX2 expression than loss of PAX2 (92.3% versus 7.7%), regardless of somatic or germline mutations. Loss of PAX2 was observed in 97.3% of dMMR with MLH1 hypermethylation compared to 2.7% of dMMR with genetic alterations (P < 0.001). Aggressive features such as higher tumour grades (FIGO 2-3) and advanced clinical stage (T2-T4) were significantly more frequently seen in dMMR with retained PAX2 expression, compared those to pMMR with loss of PAX2 expression. Our study demonstrates a close correlation between retained PAX2 expression and dMMR in EEC. The molecular mechanism and clinical significance linking these two pathways in EEC remains to be unravelled.

IN VITRO CYTOTOXIC ACTIVITIES OF PLATINUM(II) COMPLEXES CONTAINING 1H-BENZO[d]IMIDAZOLE AND 1H-1,3-DIAZOLE DERIVATIVES

Objective: This study aimed to synthesize and evaluate the cytotoxic activities of four platinum(II) complexes with 2-substituted or nonsubstituted 1H-benzo[d]imidazole and 1H-1,3-diazole derivatives as carrier ligands (L1-L4), which may have potent cytotoxic activity and low side effects. Material and Method: K1-K4 complexes were synthesized by heating and mixing K2PtCl4 and the appropriate L1-L4. The chemical structures of K1-K4 were elucidated by Infrared and 1H Nuclear Magnetic Resonance spectroscopic methods. In vitro, cytotoxic effects of K1-K4 complexes against prostate (DU-145), endometrial adenocarcinoma (Ishikawa), and breast cancer (MCF-7) cell lines were tested by the MTT method. Result and Discussion: According to the IC50 values of the tested cell lines, K1 and K2 derivatives bearing unsubstituted 1H-benzo[d]imidazole (L1) and 1H-1,3-diazole (L2) were found to be the most effective compounds among these synthesized complexes.