jabbrv-ltwa-all.ldf jabbrv-ltwa-en.ldf Background Plasmablastic myeloma (PBM) is a rare, aggressive subtype of multiple myeloma (MM) with poor prognosis. On the other hand, plasmablastic lymphoma (PBL) is also an aggressive large B-cell lymphoma with plasmacytic phenotype, which is generally treated with anti-lymphoma drugs. Importantly, PBM is difficult to distinguish from PBL, because clinical features of both diseases closely overlap. We report two cases of PBM accompanied by apparent extramedullary lesions. Case Case1: A 38-year-old female complained of fatigue. She presented pancytopenia, splenomegaly, the soft tissue lesion over the chest wall and multiple osteolytic lesions. Initially, pathology of the soft tissue established a diagnosis of PBL. She received two cycles of EPOCH, leading to considerable improvement. She then received daratumumab (Dara) and Lenalidomide (Len), achieving remission for two years. Case2: A 60-year-old-male was evaluated for multiple tumors of pancreas and retroperitoneum. Biopsy of pancreatic tumor identified plasmacytoid cells, whereas biopsy of bone marrow showed no evidence of plasma cells. Therefore, he was initially diagnosed as multiple plasmacytoma, and received 3 cycles of chemotherapy with Bortezomib (Bor), lenalidomide, and dexamethasone, but in vain. Once Bor was replaced to Dara, he rapidly developed panperitonitis and ascites filled with plasmablasts, and eventually died of multiple organ failure. Conclusion As there has been no standard care for PBM, our cases raise a possibility that combination therapy of anti-myeloma and anti-lymphoma drugs from the first may provide good outcome. In addition, Ki-67 proliferation index is an useful finding to diagnose as PBM. Keywords plasmablastic myeloma (PBM), plasmablastic lymphoma (PBL), Ki-67

Introduction: Despite constant improvements, incontinence is one of the most relevant and quality-of-life-reducing side effects of radical prostatectomy (RP) and, in addition to patient-specific factors such as age, the experience of the surgeon/center and the surgical technique used play an important role. Aim of the study was to present current real-world data on incontinence after RP from one of the largest German rehabilitation centers in 2022 and to compare it to the results from the same institution in 2016. Material and Methods: Retrospective, unicentric, univariate analysis of data from 1394 men after RP in 2022 at admission and discharge. Incontinence defined as ≥1 pad/day was evaluated by quantitative measuring all day incontinence under a defined graduation and compared to the results of 2016. Results: Median age for both cohorts was 66 years with minor differences in preoperative PSA levels. Despite different surgical approaches, no significant change in postoperative incontinence rates in 2016 and 2022 were noted at discharge (76.9 vs. 77.9%, p=0.56). A notable increase in patients with Gleason score 3+4 and a shift towards robotic surgery were observed in 2022. While nerve sparing led to a significant improvement in continence (p < 0.01), lymphadenectomy and T-stage were not related to any significant increase in incontinence rates. Comparing age groups within the cohort, patients >69 years exhibited the highest risk of postoperative incontinence and least likelihood of regaining continence during rehabilitation (p < 0.01). Men treated at a certified prostate cancer center had significantly (p<0.01) lower incontinence rates. Conclusion: Our study shows little improvement in short term post-operative incontinence rates after radical prostatectomy in Germany in the last six years and known risk factors for post-operative incontinence like age, nerve-sparing surgery and level of experience were reproduced in our analyses. We conclude to carefully select patients for RP and to strongly advice treatment at certified centers.

Background: Undifferentiated embryonal sarcoma of the liver (UESL) is an aggressive mesenchymal tumor that usually occurs in children. When it occurs in adults, it poses a diagnostic challenge for the medical team. The clinical manifestations are not specific, imaging studies show a hepatic mass with a mixed component (solid and cystic). To date, surgical resection with neoadjuvant therapy has yielded satisfactory results in terms of survival. Case: We present the case of a 19-year-old patient, which, to our knowledge is the only case reported in Central America, which was surgically resected and received adjuvant chemotherapy. The patient has been followed for 34 months, and she remains free of disease. Conclusion: The presented case highlights the need to raise awareness about UESL in the Central American region and promote a comprehensive diagnostic and therapeutic approach to improve disease-free survival in these patients.

Background: Supposed ‘spontaneous’ remissions in chronic lymphocytic leukemia/CLL are extremely rare. By the most stringent immunophenotypic criteria, there are only seven cases to date of unexplained, immune system effected cures. A historic review of this phenomenon is presented as context for this eighth case of CLL immunophenotypic reversal. Case history: A 59-year-old, molecular biologist, stage I CLL, whose diagnosis and recovery were both thoroughly documented, not content to watch and wait, chose to treat himself, after individual tumour susceptibility testing, with evidence based, biological response modifiers, which initially seemed to keep his CLL stable. This included 1mg of hydroxocobalamin injected i.m. daily. However, after some years his lymphocytosis began slowly to drift upwards. At that point, he was persuaded to change his injection protocol to methylcobalamin, at 50 mg i.m. a day, a dose whose clinical safety is sufficiently well established, and a form of cobalamin that the research literature shows has anticancer actions. Outcome: This change in cobalamin form and dose proved a critical turning point. Complete disappearance of the lymphocytosis also coincided with a severe infection and an even further temporary increase of the parenteral methylcobalamin dose, both catalytic factors. In the 4th & 5th years following this, the patient’s repeated immunophenotyping showed no clonal disease present. A brief review of the field of cobalamin in cancer research and treatment is given, with discussion of the various mechanisms by which cobalamins may impact on cancer/CLL. Historic analysis reveals that cyanocobalamin is generally cancer promotional, whereas hydroxocobalamin, methylcobalamin and adenosylcobalamin are cancer protective and cytotoxic. It is hypothesised that the actions of cobalamin in cancer aetiology and oncogenesis/progression are intertwined with those of nitric oxide, which tumours regulate to dupe the immune system to their presence, by causing a functional cobalamin deficiency in the host.

Thymic neuroendocrine tumors are rare malignant tumors with neuroendocrine functions located in the anterior mediastinum thymic region. They exhibit a high degree of malignancy and can early invade surrounding fat,pericardium, pleura, major blood vessels, and lungs,posing a significant risk of recurrence.Here, we report a case of recurrent thymic cancer treated with complete surgical resection, replacement of the innominate vein, superior vena cava formation, and iodine ion insertion.A 51-year-old male diagnosed with stage lllA malignant thymoma in November 2021, accompanied by lymph node metastasis,involving the peripheral left lung.The patient underwent six cycles of adjuvant immunotherapy with pembrolizumab and cisplatin plus etoposide, along with one course of radiotherapy postoperatively.Subsequently, the patient received regular immunotherapy and follow-up at our hospital. In October 2023,chest CT revealed tumor recurrence, with infiltration into the pericardium, bilateral innominate veins, superior vena cava, and brachiocephalic artery.Subsequently, the patient underwent a midline thoracotomy for extensive resection of recurrent thymic tumor,enlargement of pericardial resection, left innominate vein-to-right atrial artificial grafting,superior vena cava formation,and iodine-125radioisotope brachytherapy.Aggressive surgical intervention combined with adjuvant therapy is an essential treatment modality for locally advanced thymic cancer involving the superior vena cava and surrounding blood vessels.

Background: Laryngeal Squamous Cell Carcinoma (LSCC) is a commonly occurring malignancy in the head and neck region. However, due to the heterogeneity of primary tumor sites, tumor behavior, and molecular mechanisms, there is currently no consensus on the accuracy of clinicopathological prognostic factors for individual cases. Tumor histopathologic behavior remains a crucial factor in predicting aggressiveness. Recent studies have shown that peritumoral tumor budding (TB) combined with cell nest size (CNS) is a reliable marker for predicting lymph node metastasis, advanced cancer prognosis, and therapeutic response in SCCs of different origins. Materials and methods: In this retrospective cross-sectional study, we analyzed 128 LSCC cases that underwent total laryngectomy at Amir Alam Hospital. We evaluated TB and CNS based on the Boxberg et al. study. Results: Our study demonstrated a significant correlation between TB, and nodal involvement (P value=0.015), vascular invasion (P value=0.035), and mortality rate (P value=0.001), as well as a significant statistical correlation between high TB and extra-laryngeal extension (P value=0.006), clinical stage (P value=0.011), and mortality rate (P value=0.001). Moreover, small nest size was also associated with the clinical stage (P value=0.047), extra-laryngeal extension (P value=0.015), and mortality rate (P value=0.001). Based on our results, TB, CNS, and clinical stage are independent prognostic factors for mortality rate and are correlated with disease-free survival. Conclusion: Given the effect of TB and CNS on the overall prognosis and survival of patients with LSCC, evaluating these two factors on routine H&E microscopic examination of LSCC specimens is recommended to facilitate individualized risk assessment and treatment planning.

Background: Small cell lung cancer (SCLC) harbours the most aggressive phenotype of all lung cancers to correlate with its bleak prognosis. The aggression of SCLC is partially attributable to its strong metastatic tendencies. The biological processes facilitating the metastasis in SCLC are still poorly understood and garnering a deeper understanding of these processes may enable the exploration of additional targets against this cancer hallmark in the treatment of SCLC. Recent findings: This narrative review will discuss the proposed molecular mechanisms by which the cancer hallmark of activating invasion and metastasis is featured in SCLC through important steps of the metastatic pathway. The review will discuss SCLC VEGF family expression and vascular mimicry as a means of vasculogenesis, and the role of tumour heterogeneity, DLL3, NFIB, selectin, and B1 integrin in enabling epithelial to mesenchymal transition and subsequent invasion, and the molecular markers expressed by SCLC to assist organ-specific homing during metastasis. The review will also discuss a recent article observing mir-1 mrna upregulation as a potential therapeutic option in targeting the metastatic activity of SCLC. Conclusion: Treatment of SCLC remains a clinical challenge due to its recalcitrant and aggressive nature. Amongst the many hallmarks used by SCLC to enable its aggressive behaviour, that of its ability to invade surrounding tissue and metastasise is particularly notable and understanding the molecular mechanisms in SCLC metastasis can identify therapeutic targets to attenuate SCLC aggression and improve mortality.

The prognosis of high-risk neuroblastomas (NB) that are resistant to first-line induction chemotherapy is relatively poor. This study explored the mechanism of resistance to first-line chemotherapeutics mediated by TXNDC17 and its potential solutions in NB. The genetic and clinical data of patients with NB were obtained from the Therapeutically Applicable Research to Generate Effective Treatments dataset. TXNDC17 and BECN1 expressions in NB cells were up- and downregulated by transfection with plasmids and shRNA, respectively. Autophagy-related proteins were detected by western blot. Cell viability was determined using cell proliferation and toxicity experiments. Apoptotic cells were detected using flow cytometry. Overall, 1076 pediatric and adolescent patients with NB were enrolled in this study. The 10-year overall survival (OS) rates and event-free survival (EFS) rates for the patients with mutation of BECN1 were 37.4% ± 9.1% and 34.5% ± 8.8%, respectively. For patients with mutation of TXNDC17, the 10-year OS and EFS were 41.4% ± 5.9% and 24.3% ± 5.1%, respectively, which were significantly lower than those in the unaltered group. The overexpression of BECN1 and TXNDC17 reduced NB sensitivity to cisplatin (DDP), etoposide (VP16), and cyclophosphamide (CTX). Autophagy mediated by BECN1 was regulated by TXNDC17, and this process was involved in the resistance to DDP, VP16, and CTX in NB. Suberoylanilide hydroxamic acid (SAHA) can enhance the sensitivity of NB cells to chemotherapeutics by inhibiting TXNDC17, ultimately decreasing autophagy-mediated chemoresistance. Acquired resistance to first-line chemotherapeutics was associated with autophagy mediated by BECN1 and regulated by TXNDC17, which can be reversed by SAHA.

Dexamethasone (Dex), a synthetic glucocorticoid that acts by binding to the glucocorticoid receptor (GR), has been widely applied to treat leukemia and lymphoma, however the precise mechanism underlying Dex action is still not well elucidated. DOT1L, a histone H3-lysine79 (H3K79) methyltransferase, has been linked to multiple cancer types, particularly mixed lineage leukemia (MLL) gene rearranged leukemia, but its contribution to lymphoma is yet to be delineated. Analysis from TCGA database displayed that DOT1L was highly expressed in lymphoma and leukemia. In the present study, we initially demonstrated that DOT1L served as a newly target gene controlled by GR, and downregulation of DOT1L was critical for the killing of B lymphoma cells by Dex. Further study revealed that Dex had no impact on the transcriptional activity of DOT1L promoter, rather it reduced the mRNA level of DOT1L through decreasing mRNA stability. In addition, knockdown of DOT1L remarkably inhibited the B lymphoma cells growth. Overall, our findings indicated that DOT1L may serve as a potential drug target and a promising biomarker of Dex sensitivity when it comes to treating B lymphoma.

Myeloid neoplasms, including acute myeloid leukemia, have been traditionally among the less investigated cancer types concerning germline predisposition. Indeed, myeloid neoplasms with germline predisposition are challenging to identify because often display similar clinical and morphological characteristics of sporadic cases and have similar age at diagnosis. However, a misidentification of familiarity in myeloid neoplasms have a critical impact on clinical management both for the carriers and their relatives. We performed a thorough genomic analysis using a large custom gene panel, the Myelo-Panel, targeted on cancer predisposing genes. In particular, we assessed both germline and somatic variants in 4 families, each with two siblings, who developed hematological neoplasms: 7 acute myeloid leukemia and 1 Philadelphia-positive chronic myeloid leukemia. In each family, we identified at least one novel potentially predisposing variant, affecting also genes not included in the current European LeukemiaNet guidelines for AML management. Moreover, we suggest reclassification of 2 germline variants as pathogenic: likely pathogenic p.S21Tfs*139 in CEPBA and VUS p.K392Afs*66 in DDX41. Our data underline how familiar predisposition to hematological neoplasms is currently underestimated and call for revision of clinical practices that should include thorough reconstruction of family history and genetic testing with gene panels targeted for cancer predisposing genes.

Objective: It is already established that thoracic radiation therapy (TRT) enhances the outcomes of patients with extensive-stage small cell lung cancer (ES-SCLC) after chemotherapy response. This investigation aimed to elucidate TRT’s impact on ES-SCLC patients during immunotherapy. Methods: This retrospective research was authorized by our institute IRB and included histopathology-confirmed ES-SCLC cases that underwent chemoimmunotherapy with or without TRT as primary treatment at our hospital between October 2018 to March 2022. With the help of propensity score matching, the selection bias was minimized. The research endpoints were progression-free survival (PFS) and overall survival (OS), which were determined via Kaplan-Meier, from first-line treatment initiation time. Survivals in different cohorts were compared with the help of a Log-rank test. Furthermore, Cox proportional hazards regression was applied to examine factors linked with survival. With the help of subgroup analyses, the influencing factors on TRT were assessed. Results: This investigation analyzed 172 patients who were followed up for a median of 20.1 months. The median PFS and OS for patients receiving TRT were 11.3 and 24.4 months, respectively, while for those without TRT, the values were 15.9 and 6.6 months (p < 0.001 and p = 0.006, respectively). According to the multivariate Cox regression assessment, thoracic radiotherapy was an independent favourable factor for both OS and PFS. Per the subgroup analysis, patients in all subgroups may have OS beneficial after TRT. Conclusions: Thoracic radiation therapy may improve PFS and OS in ES-SCLC cases undergoing chemoimmunotherapy as the primary treatment. Further investigation by randomized controlled studies is needed for confirmation.

Abstract Introduction: Upper abdominal metastases of bladder cancer are very rare. This case report describes the first ever patient with bladder cancer progression initially presenting with gastric outlet obstruction due to peritoneal carcinomatosis of upper gastrointestinal system. Case report: We present the case of a 78-years-old male patient with diagnosed high risk NMIBC (high grade pT1 + CIS) who was admitted to hospital with vomiting. At the time, patient was between 2. and 3. BCG instillation cycle, following two transurethral resections. Routine urological follow-up one month before admission showed no signs of tumour. Gastroscopy revealed duodenal stenosis without intraluminal lesions. First CT- scans showed inflammation of the fat tissue surrounding duodenum without clear signs of metastases. Laparoscopic exploration described lesions typical for peritoneal carcinomatosis. Pathohistological analysis of taken samples proved urothelial cancer cells, confirming the diagnosis of metastatic bladder cancer. Conclusion: This case report presented an unusual presentation of bladder cancer that could help clinicians in everyday practice, as it might bring focus to a progression potential of the bladder cancer, eventually encouraging improvement in diagnostics and therapy. Keywords: non-muscle invasive bladder cancer, NMIBC, metastatic bladder cancer, peritoneal carcinomatosis, gastric outlet obstruction

Background: Glioblastoma multiforme (GBM) poses a significant health challenge as the most common primary malignancy of the adult central nervous system. Gender and age-related differences in GBM influence prognosis and treatment complexities. This multicenter retrospective study explores gender and age disparities in GBM patients, investigating their impact on occurrence and survival outcomes. Methods: This STROBE-compliant retrospective study involved GBM patients who received medical care in Guilan Province, Iran. Patients’ data, including age, gender, tumor location, and histopathological diagnosis date, was collected from medical records. Results: In a cohort of 164 GBM patients, the average age was 54 years, with higher prevalence in men (59.8%) as well as patients ≤60 years (64.6%). The tumor sites exhibited overlapping features in 68% of cases, with the frontal and temporal lobes being the most prevalent specific locations. The mean survival was 12.88 ± 14.14 months, one-year survival of 45%, with women showing higher one-year survival (60% vs. 40%) and longer mean survival (16.14 ± 17.35 vs. 10.75 ± 11.15 months). Patients ≤60 years had higher one-year survival (75% vs. 35%). In subgroup analysis, women had significantly higher survival rates in patients ≤60 years. However, among patients over 60, women exhibited a more significant reduction in survival rates, and no statistically significant difference was observed between males and females in this age group. Discussion: While the biological mechanisms behind gender disparities in GBM remain unclear, studies suggest the potential involvement of sex hormones. Age-related differences, in line with the prior research, highlight the complexity of managing older GBM patients. Conclusion: This study underscores age and gender disparities in GBM occurrence and prognosis, emphasizing the necessity for further investigations and innovative approaches to address the potential pathogenesis.

Glioblastoma (GBM) is a malignant brain tumor that frequently occurs alongside other central nervous systems (CNS) conditions. Glutamate release and aberrant cellular behavior are shared features of both CNS diseases and GBM cells. Neither their origin nor the ways in which CNS disorders affect the development or behavior of GBM are well understood. Using data from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) datasets–where both healthy and cancerous samples were analyzed–we used a quantitative analytical framework to identify differentially expressed genes (DEGs) and cell signaling pathways that might be related to GBM. Then, we performed gene ontology studies and hub protein identifications to estimate the roles of these DEGs after finding disease-gene connection networks and signaling pathways. Using the GEPIA Proportional Hazard Model and the Kaplan-Meier estimator, we widened our analysis to identify the important genes that may play a role in both progression and the survival of patients with GBM. Totally, 890 DEGs, including 475 and 415 up- and down-regulated were identified, respectively. Our results revealed SQLE, DHCR7, delta-1 phospholipase C ( PLCD1), and MINPP1 genes are high expression, and the Enolase 2 ( ENO2) and hexokinase-1 ( HK1) genes are low expressions. Hence, our findings suggest novel mechanisms that affect the occurrence of GBM development, growth, and/or establishment and may also serve as secretory biomarkers for GBM prognosis and possible targets for therapy.

Background: Recent advances in cancer genome analysis and the practice of precision medicine have made it possible to identify fractions with rare genetic alterations. EGFR-amplified cancers are known to be rare fractions across organs and have a poor prognosis. The use of anti-EGFR antibody for EGFR-amplified cancers has been promising, but the evidence is not yet clear. Case: In this report, we describe the case of a 48-year-old man diagnosed with advanced gallbladder cancer. The patient was administered Gemcitabine plus Cisplatin, followed by S-1 monotherapy; however, disease progression was observed after two cycles of each regimen. Comprehensive genomic profiling test revealed EGFR-amplification, and the patient was treated with combination therapy with the anti-EGFR antibody Necitumumab, Gemcitabine, and Cisplatin. After two cycles of treatment, showed a reduction in tumor size, and the treatment response was evaluated as partial response. On day 90, after five cycles of treatment, tumor progression was confirmed. In addition, after disease progression, liquid biopsy revealed acquired pathogenic gene alterations suggesting anti-EGFR antibody resistance. Conclusions: This report supports the clinical benefit of anti-EGFR antibody for EGFR-amplified biliary tract cancers and the importance of genomic analysis in personalized therapy and drug resistance research.

Paclitaxel (PTX) has been used as a chemotherapeutic agent for several malignancies including breast cancer and efforts to increase the efficiency of PTX are continuing. In this study, FDA-approved 4-aminopyridine (4-AP), a voltage-gated potassium channel blocker, was used in combination with PTX in MCF-7 and MDA MB 231 cell lines it has been confirmed that K+ (potassium) channels are involved in the cell cycle. Viability was determined with trypan blue, a clonogenic assay was performed, and the cell cycle was determined with a flow cytometer and immunochemistry. To gain an insight into the mechanism, intracellular K+ concentration, intracellular Ca2+ (calcium) concentration, and transmembrane potential measurements were made with corresponding fluorescent dyes. Apoptotic cell number was determined using Annexin /PI method by flow cytometer. Viability decreased with combination therapy and the clonogenic assay proved decreased colony formation. Apoptotic cell number was increased after treatment with the combination in both cell lines. Cell cycle measurements showed G1 arrest for both MCF-7 and MDA MB 231 cell lines upon 4-AP treatment. PTX caused G1 arrest in MCF-7 cells and S phase arrest in MDA MB 231 cells. Combination treatment caused S phase arrest in MCF-7 cells and S phase and G2/M phase arrest in MDA MB 231 cells. Intracellular K+ concentration was increased after all treatments in both cell lines. Ca2+ concentration was increased significantly after combination treatment. Depolarization in the transmembrane potential was observed after all treatments in both cell lines. Biophysical parameters like the transmembrane potential and ion fluxes have been defined in cancer progression which can provide new aspects for cancer treatments. This study shows that the combination of 4-AP with PTX is a promising alternative the mechanism of which needs further investigation considering the results obtained for Ca2+, K+, and membrane potential.

Background: Squamous cell carcinoma of the prostate (SCCP) is a neoplasm that comprises fewer than 1% of all primary prostate cancer diagnoses. Given its rarity, there is a paucity of data regarding the treatment of this disease. The limited literature points to the potential of local therapy in conjunction with chemotherapy to improve patient mortality. Methods: Using the National Cancer Initiative’s Surveillance, Epidemiology, and End Results (SEER) database, we conducted a retrospective analysis for patients diagnosed with primary SCCP between 2000 and 2018. We analyzed patient demographics, tumor characteristics, such as histology, and patient outcomes based on treatment modality. We generated Kaplan-Meier five-year overall survival (5y OS) curves for these variables. Results: A total of 66 patients were identified. Five-year overall survival was 18%; median overall survival was 13 months. Patients with Grade II and below disease had an increased 5y OS of 48%, compared to 10% for patients with Grade III and Grade IV disease (p < 0.05). Analysis of the 5y OS based on disease histology revealed patients with papillary SCC had a 5y OS of 50%, compared to 26% for patients with papillary carcinoma, not otherwise specified. Analysis of 5y OS stratified by treatment modality revealed no statistically significant change with any treatment (surgery, radiotherapy, and chemotherapy). Conclusions: The literature on SCCP remains sparse; the rarity of this disease limits analysis. While the investigation undertaken in this paper does not find any change in 5y OS regardless of treatment modality, the variation in 5y OS based on histologic classification of SCCP points to a potential route for the future treatment of this disease.

Abstract The risk factors and clinical prediction of cardiovascular disease comorbidities in patients with breast cancer have not been fully clarified. We conducted this retrospective case-control study. The univariable and multivariable cox regression was used to screen the risk factors of cardiovascular comorbidities in breast cancer patients, and construct a clinical prediction model, followed by prediction efficacy test and internal validation. A total of 144 cases were included and divided into two groups based on the low and high expression levels of apoB (n=46 in apoBlow and n=98 in apoBhigh group). Univariable and multivariable cox regression found that apoB, age and HER2 were the key factors responsible for the myocardial ischemia occurrence in breast cancer patients. These factors were used to constructed the clinical prediction model with combination area under curve (AUC) of 0.583, and the decision curve analysis (DCA) suggested that there would be therapeutically clinical net benefit in the model-predicted population in the predicted threshold interval between 0.35 to 0.70. Finally, Kaplan-meier plot indicated HER2(+) category and apoBhigh lead to the most occurrence of myocardial ischemia in breast cancer patients. Moreover, the 3-year disease-free survival (DFS) was not found difference between the apoBlow and apoBhigh subgroups. The clinical prediction model was constructed using three key factors, and it was indicated HER2(+) and apoBhigh lead to the most occurrence of myocardial ischemia in breast cancer patients. This study may be helpful in providing clinical evidence for the early prediction of cardiovascular comorbidities in breast cancer patients.