Leucine-rich alpha-2-glycoprotein-1 (LRG1) has received much attention as a prognostic indicator in cancer therapy where high serum levels generally predict a poor outcome. Recently, it has been shown to play an active role in cancer progression and is being pursued as a novel target in cancer therapy. LRG1 acts in neovascularization of tumors resulting in weakened blood vessels and ineffective delivery of chemotherapeutic drugs. A monoclonal antibody (mAb) against LRG1 has shown efficacy in blocking this function of LRG1, normalizing the vasculature, and improving drug delivery in mice. Extracellular LRG1 is also anti-apoptotic and promotes cell proliferation and metastasis, all through epidermal growth factor receptor family signaling. In mice, anti-LRG1 antibody therapy has been shown to inhibit these effects of extracellular LRG1 and to enhance the anti-cancer effect of immune checkpoint blockade (ICB) therapy in mice. Pre-clinical testing of the humanized version of the LRG1 mAb is underway in the United Kingdom. Intracellular LRG1 has been reported to inhibit apoptosis by blocking the binding of Cyt c to apoptotic protease activating factor1 (Apaf-1) and to have other cytoplasmic functions. A nanoscale proteolysis targeting chimera (nano-PROTAC) with improved cytoplasmic delivery has been developed which enhanced apoptosis in tumors of mice. Targeting LRG1 in the aberrant angiogenesis of endothelial cells and the LRG1-Cyt c-Apaf-1 axis in cancer cells, along with other putative intracellular interactions of LRG1, show potential as supplementary, if not alternative, approaches to cancer therapy.
We report a deceptive presentation of Squamous Cell Carcinoma of the Cervix in a 54-year-old postmenopausal woman who presented with postmenopausal bleeding associated with lower abdominal pain for a 3-month duration, with a normal-looking ectocervix. She was diagnosed with squamous cell carcinoma on a pap smear and cervical biopsy. Magnetic resonance imaging revealed an irregular endometrial cavity contour, and a T2 hyperintense lesion was seen (2.3 × 0.8 cm) involving the posterior lip of the cervix at the junction of stroma and endocervix with a mural spread along the uterine myometrium. Histopathology after Wertheim's hysterectomy revealed a squamous cell carcinoma of the endocervix, Stage pT1b3, that had spread superficially to the endometrium, myometrium, and left salpinx. The detection of immunohistochemical expression of p16, p63, and negative for ER and PR in the lesions of the cervix and the endometrium suggests that these two lesions are etiologically related, favoring the possibility of endometrial SCC secondary to cervical SCC.
The uterine carcinosarcoma is a rare biphasic Malignant Mixed Mullerian Tumour (MMMT). It is a highly aggressive endometrial cancer phenotype, consisting of both epithelial and mesenchymal components. The presented case refers to a 65-year-old, P6L3 postmenopausal woman with postmenopausal bleeding and white discharge per vagina for one month with vulval leukoplakia. The ultrasound showed a thickened endometrium measuring 15 mm, and the Magnetic Resonance Imaging showed the uterus measuring 7.4 × 4.5 × 6 cm. The endometrium appeared heterogeneous, with a hyperintense lesion measuring 4.8 × 2.3 cm on T2W1. The myometrium appeared normal, and neither of the ovaries was visualized. The patient underwent surgery. The histopathological and immunohistochemical analysis suggested that high-grade Endometrial Carcinosarcoma with dual classifier positivity (MMRd-p53abn) more closely resembled single-classifier MMRd (Mismatch repair deficiency) than p53abn, with a good prognosis. Post-surgery, the patient was followed up on every three months. The patient received 6 cycles of adjuvant chemotherapy. Considering the highly invasive nature of uterine carcinosarcomas, the timely detection of this cancer by imaging, pathology findings and molecular classification is of extreme importance to improve the patient's survival and for management outcome.
Chimeric antigen receptor T-cell (CAR-T) therapy has produced remarkable therapeutic results in blood cancers, while its application to solid malignancies remains limited by a pooled objective response rate of approximately 9%. This gap stems from core biological obstacles: heterogeneous antigen expression, physical inaccessibility within dense stromal architectures, and immunosuppressive microenvironments that drive T-cell exhaustion through epigenetically fixed transcriptional programs. The period spanning 2024-2025 represents a pivotal turning point. GD2-targeting CAR-T cells delivered intracerebroventricularly achieved durable complete responses (including one sustained beyond 30 months) in H3K27M-mutated diffuse midline gliomas. CLDN18.2-targeting satricabtagene autoleucel demonstrated randomized superiority over physician's choice in advanced gastric cancer (progression-free survival HR 0.37). GPC3-targeting CAR-T cells armored with a dominant-negative TGF-β receptor achieved objective response rates of 50-57% in hepatocellular carcinoma, representing a three- to four-fold improvement over unarmored predecessors. These breakthroughs reflect a paradigm shift from potency-driven engineering toward resilience-based design: metabolic armoring via autocrine IL-10 and IL-15, epigenetic protection through DNMT3A disruption and c-Jun overexpression, logic-gated targeting via synNotch circuits, and microenvironmental shielding through dominant-negative receptors. Beyond the local microenvironment, emerging recognition of systemic neuroendocrine-immune dysregulation further informs CAR-T persistence and fitness considerations. This review synthesizes the mechanistic insights, engineering strategies, clinical evidence, and emerging platforms, including in vivo lentiviral CAR-T generation, that define the current landscape, and proposes a tiered framework for next-generation solid tumor CAR-T development, while explicitly acknowledging the limitations and unknowns that persist.
Breast cancer remains one of the leading causes of death among women worldwide, early detection is critical for improving survival. Conventional screening modalities such as mammography, MRI, biopsy, and ultrasound have been pivotal for patient care, but face limitations, including human variability, interpretive errors, operator dependence, and high rates of false positives and negatives which can lead to unnecessary treatment and financial distress. To overcome these challenges, a more accurate and predictive diagnostic tool is needed. This article compares traditional breast cancer screening methods with AI-integrated approaches demonstrating how artificial intelligence enhances diagnostic precision, efficiency, and predictive capability. AI-assisted mammography has been shown to detect 29% more cancers than traditional mammography without increasing false positives and reduces radiologist reading time by 40%. AI-assisted 3D digital breast tomosynthesis detects 1.6 additional cancers per 1,000 screenings and reduces recall rates by 2.2% compared to 2D mammography. In MRI, AI predicted breast cancer development up to one year in advance and correctly localize future cancer sites in 57% of cases. In ultrasound, AI significantly improves diagnostic accuracy, particularly for less experienced radiologists. In biopsy, AI-enabled digital assays for recurrence prediction achieve higher predictive accuracy, with pathologists using AI being 62% faster and 72% more accurate. Integrating AI into breast cancer redefines diagnostic excellence, shifting breast cancer management toward a more proactive, precise, and patient-centered approach. Future research should focus on external validation of AI models across larger and diverse populations, cost-effectiveness to ensure equitable access and ethical consideration to ensure responsible clinical adoption.
The MAPK and PI3K/AKT pathways are important components in cell growth and proliferation, which, when activated, result in cancer formation. Molecular alterations are the main cause of activation of the MAPK and PI3K/AKT pathways in the development of papillary thyroid carcinoma (PTC), the most common endocrine cancer. Activation of the MAPK pathway is usually caused by mutations in the BRAF, RAS, RET/PTC, and NTRK genes, while the activation of the PI3K/AKT pathway results from alterations in the PIK3CA, PTEN, and AKT genes. Moreover, hyperactivation of the MAPK pathway can be caused by overexpression of RTKs, GPCRs, and mutation in PTEN. Interactions between the two signaling pathways exacerbate tumor aggressiveness, dedifferentiation, radioiodine resistance, and response to targeted therapy in PTC. Recent developments in personalized medicine, including the introduction of new molecular diagnostic tools and targeted agents, have made considerable progress in the risk stratification and treatment strategies for papillary thyroid carcinoma. The current article reviews molecular mechanisms of activation of MAPK and PI3K/AKT pathways, their interaction, clinicopathological importance, and targeted treatments in papillary thyroid carcinoma.
INTRODUCTION:Angioleiomyoma is a rare, benign soft tissue tumor derived from smooth muscle cells with prominent vascular components. While more commonly found in the extremities, angioleiomyomas of the female genital tract, particularly the cervix, are extremely rare. Ultrasound helps in the diagnosis, but MRI is more definitive, as the vascular component of these tumors can often be highlighted with hyper intensity on T2-weighted images. Final confirmation of angioleiomyoma is by histopathological and immunohistochemistry studies. CASE REPORT:We present here the diagnosis and management by total excision of a case of a large sized cervical angioleiomyoma in a young female, which presented as persistent heavy menstrual bleeding and pelvic pain. CONCLUSIONS:Cervical angioleiomyoma, though rare, should be considered in the differential diagnosis of young females presenting with persistent heavy menstrual bleeding and pelvic pain.
BACKGROUND:Upper endoscopy with biopsy is the gold standard for diagnosing esophageal cancer. However, esophageal tumors can rarely escape endoscopic detection by growing in atypical patterns, such as entirely outside the esophageal lumen. CASE:We report a unique case of primary esophageal adenocarcinoma that presented with spinal cord compression due to local invasion of the T5 vertebral body, despite an initially normal upper endoscopy. A 68-year-old man developed progressive paraparesis and sensory loss due to a T5 pathological fracture. He had classic symptoms of esophageal cancer (dysphagia and weight loss), yet endoscopic evaluation one month prior showed no intraluminal tumor. Imaging revealed a posterior mediastinal mass contiguous with the esophagus and invading the T4-T6 vertebrae. Surgical resection of the epidural tumor confirmed poorly differentiated adenocarcinoma consistent with an esophageal primary. The patient declined chemoradiation and succumbed one month later. CONCLUSIONS:This unprecedented pattern of esophageal adenocarcinoma-growing extraluminally with isolated posterior extension to the spine-highlights the potential for esophageal cancer to present with no mucosal lesion on endoscopy. Clinicians should remain vigilant for malignancy in patients with high suspicion, even if initial endoscopic findings are benign.
Adaptor proteins serve as essential molecular scaffolds within the tumor microenvironment, linking activated receptors to downstream signaling pathways and coordinating the assembly of multiprotein complexes that modulate immune responses. Emerging evidence suggests that adaptor proteins play a critical role in shaping macrophage phenotypic plasticity. Tumor-associated macrophages exhibit functional heterogeneity and can adopt either anti-tumorigenic phenotypes that promote immune activation or pro-tumorigenic phenotypes that support tumor growth, metastasis, and immune evasion. The dynamic transition between these functional states is tightly controlled by intracellular signaling networks in which adaptor proteins function as key regulatory nodes. Based on available mechanistic studies, we systematically summarize adaptor molecules that govern signaling pathways driving macrophage polarization within the cancer condition. Additionally, this review underscores the significance of adaptor proteins as key modulators of macrophage phenotype and highlights their potential as therapeutic targets for reprogramming macrophages to enhance anti-tumor immunity. Collectively, we provide a conceptual framework for understanding adaptor-mediated immune regulation in cancer and support the development of targeted strategies to shape the tumor microenvironment.
BACKGROUND:Combined hepatocellular-cholangiocarcinoma (cHCC-CCA) is a rare and aggressive liver cancer, representing 2-5% of primary hepatic malignancies. Its mixed hepatocytic and cholangiocytic features pose major diagnostic challenges, and the absence of standardized treatment guidelines limits effective management. CASE PRESENTATION:A 61-yearold man with type 2 diabetes, hypertension, and chronic hepatitis B presented with right hypochondrial pain. Laboratory tests revealed elevated alpha-fetoprotein (247 ng/mL). Imaging showed a heterogeneous mass in liver segment V with capsular retraction, hilar lymphadenopathy, and atypical enhancement. Histological examination of the CT-guided liver biopsy suggested hepatocellular carcinoma. However, this proved to be a key diagnostic pitfall, as the complete resected specimen revealed a mixed tumor: final diagnosis of combined hepatocellularcholangiocarcinoma (cHCC-CCA) with approximately 20% hepatocellular and 80% cholangiocarcinoma components. Clinical Discussion: This case underscores the limitations of preoperative biopsy in diagnosing cHCC-CCA, highlighting the risk of misdiagnosis. Radiological features often reflect the predominant histological component but can be nonspecific due to tumor heterogeneity. Definitive diagnosis requires thorough histopathological examination with immunohistochemistry. CONCLUSIONS:cHCC-CCA poses a significant diagnostic and therapeutic challenge. Recognizing this mixed phenotype in complex liver masses is crucial. Histopathological confirmation and complete surgical resection remain key to optimal outcomes. Detailed case reports are essential to improve diagnostic criteria, elucidate molecular biology, and guide evidence-based management for this rare malignancy.
Oral squamous cell carcinoma (OSCC) is one of the most prevalent cancers worldwide, leading to significant illness and death, particularly in low- and middle-income countries. In addition to tobacco, alcohol, and human papillomavirus (HPV), several culturally ingrained practices, such as areca nut chewing, toombak, khat, reverse smoking, and hot mate drinking, remain underrecognized but important cultural factors contributing to OSCC globally. These exposures operate through the formation of nitrosamine-induced DNA adducts, oxidative stress, chronic inflammation, and thermal injury. Areca nut and toombak are associated with oral submucous fibrosis and carcinoma, while reverse smoking and mate are linked to thermal and polycyclic aromatic hydrocarbon-related effects. Khat is connected to oxidative and cytogenetic damage. This narrative review combines epidemiological, mechanistic, and public health evidence on cultural carcinogens in OSCC, emphasizing prevention strategies that honor cultural identity through education, harm reduction, and community involvement. Dermatologists specializing in mucocutaneous oncology can detect early lesions like leukoplakia, erythroplakia, and oral submucous fibrosis. Including oral mucosal screening in routine care provides an effective, affordable way to prevent diseases in high-risk populations. Culturally sensitive, dermatology-focused prevention can help reduce OSCC incidence and disparities while respecting community identity.
INTRODUCTION:Basal cell carcinoma (BCC) is one of the most common cutaneous malignancies and predominantly affects sun-exposed regions, particularly the head and neck. Although metastatic spread is rare, locally invasive growth may compromise functionally and aesthetically critical structures. Effective management therefore requires not only oncologic tumor control but also carefully planned reconstruction and long-term follow-up. MATERIALS AND METHODS:This study presents a structured narrative review of the literature combined with institutional clinical experience. Relevant publications on diagnosis, surgical management, reconstructive techniques, and postoperative strategies for head and neck BCC were identified through searches of PubMed, Embase, and the Cochrane Library. Clinical studies, systematic reviews, and guidelines published between 2000 and 2025 were analyzed and synthesized narratively due to heterogeneity in study designs and outcome measures. RESULTS:Surgical excision remains the cornerstone of curative treatment, with recommended margins depending on tumor risk stratification. Mohs micrographic surgery provides superior margin control in anatomically critical regions. Reconstruction must be individualized based on defect size, anatomical subunit involvement, and patient factors. Local flaps are commonly used for small- to medium-sized defects, whereas larger or deeply infiltrative tumors may require regional or free tissue transfer. DISCUSSION:Successful management of head and neck BCC requires interdisciplinary collaboration and individualized reconstructive planning. Advances in flap techniques, digital surgical planning, and systemic therapies have expanded treatment possibilities, enabling improved functional and aesthetic outcomes in complex cases.
Metastatic prostate cancer (PCa), especially when it involves the bone, remains a significant clinical challenge with limited therapeutic options. Our recent research identified Myeloid Differentiation Protein-2 (MD2/LY96) as a potential biomarker associated with poor prognosis and higher metastatic potential in PCa. In this Research Perspective, we build on those findings and present new preclinical data showing that pharmacological inhibition of MD2 markedly reduces tumor growth in a PCa mouse model of bone metastasis. Analysis of patient tumor tissues demonstrated that high MD2 expression is associated not only with metastasis but also with increased infiltration of T regulatory cells (Tregs) and myeloid-derived suppressor cells (MDSCs), indicating a role in promoting an immunosuppressive environment. Additionally, we show that soluble MD2 (sMD2) may serve as a non-invasive biomarker of metastatic burden and help predict resistance to poly ADP-ribose polymerase (PARP) inhibitor therapy. This Research Perspective aims to consolidate mechanistic and preclinical evidence supporting MD2 as a driver of prostate cancer metastasis and to evaluate the therapeutic potential of pharmacological MD2 inhibition in a bone metastasis model. These findings support MD2 as a novel therapeutic target and identify soluble MD2 as a promising predictive and prognostic biomarker in metastatic PCa, with mechanistic links to immune evasion and inflammatory signaling.
BACKGROUND:Mucinous ovarian carcinoma (MOC) is a rare subtype of epithelial ovarian cancer (3-5%), typically affecting women between 20 and 40 years old. It often presents diagnostic and management challenges. CASE REPORT:We present an exceptional case of a postmenopausal woman with abdominal pain disguised as a pelvic abscess. A 73-year-old postmenopausal woman presented with abdominal pain for 6 months and postmenopausal spotting for 1 month. Initial imaging (CT scan) suggested a pelvic abscess, which was managed conservatively. However, persistent symptoms and a complex adnexal mass prompted further evaluation. MRI revealed a multiloculated right adnexal mass, and tumour markers (CA-125, CEA, HE4) were elevated. Surgical staging included total abdominal hysterectomy, bilateral salpingo-oophorectomy, and omentectomy. Histopathology confirmed stage IC2 mucinous adenocarcinoma. Postoperative recovery was uneventful, and the patient received six cycles of carboplatin and paclitaxel as adjuvant chemotherapy. CONCLUSIONS:This case emphasizes the diagnostic challenge of MOC in postmenopausal women. Misinterpretation as benign pelvic pathology can delay appropriate treatment. Precise imaging, tumour markers, and a multidisciplinary approach are critical for early diagnosis and improved outcomes.
Lifestyle factors, such as physical activity and dietary modifications can beneficially modulate the gut microbiome of cancer patients, however their effects are often shaped by non-modifiable variables. This review and network analysis aims to synthesize current evidence on how both lifestyle and non-lifestyle factors affect the gut microbiome in cancer patients. A systematic search was conducted on Scopus, CINAHL, PubMed and Web of Science to produce 51 eligible studies for this review. A chi-square test of independence indicated that the distribution of gut bacteria function categories was significantly associated with the category of influencing factor (Χ2 = 390.87, p = 0.032). Across studies, high physical activity and healthy diets were associated with increased abundances of saccharolytic/short-chain fatty acids and lactic acid-producing bacteria, alongside decreased abundances of pathogenic or opportunistic bacteria. However, these associations may also be influenced by non-lifestyle characteristics such as chemotherapy, age, and cancer type or stage which could mask the benefits of lifestyle interventions. This study highlights the limited but growing evidence linking physical activity, diet and the gut microbiome in cancer populations. Progress in this field will require larger, more integrative designs that account for non-lifestyle confounders and apply advanced analytical approaches to capture complex interactions.
Dermatologic adverse events (AEs) are a well-recognized complication of EGFR-targeted therapies, often emerging early during treatment and contributing to dose interruptions, patient discomfort, and reduced adherence. The combination of amivantamab, a bispecific EGFR-MET antibody, with lazertinib, a third-generation EGFR tyrosine kinase inhibitor, has demonstrated significant survival benefits in EGFR-mutant advanced non-small cell lung cancer (NSCLC). However, this therapeutic advancement brings with it an increased incidence of cutaneous toxicity. At the 2025 European Lung Cancer Congress, interim findings from the phase II COCOON trial were presented, offering timely insight into a proactive approach to managing these toxicities. This commentary summarizes and contextualizes the COCOON study, which investigated whether a structured dermatologic prophylaxis regimen could mitigate moderate-to-severe skin AEs in patients receiving first-line amivantamab plus lazertinib. The prophylactic protocol included oral doxycycline or minocycline, ceramide-based moisturization, chlorhexidine nail care, and topical clindamycin, initiated at specified intervals. Compared to standard reactive care, this strategy halved the incidence of grade ≥2 dermatologic AEs (38.6% vs. 76.5%) and reduced grade ≥3 events and treatment discontinuations. The COCOON results emphasize the clinical value of anticipating EGFR inhibitor-related toxicities through multidisciplinary supportive care. By implementing straightforward, low-cost interventions, clinicians can significantly improve tolerability and maintain dose intensity, maximizing therapeutic benefit. As this data informs future updates to clinical practice guidelines, it reinforces the need to integrate dermatologic prevention into first-line treatment planning for EGFR-mutant NSCLC. This commentary highlights COCOON's relevance as a model for supportive care innovation in targeted oncology.
A sensitive nucleic acid detection approach based on tracing the inorganic phosphate (Pi) created during amplification by means of the colorimetric method has been presented. This method relies on nucleic acid amplification. Pyrophosphate (PPi), a result of the nucleic acid polymerization reaction, was hydrolyzed into inorganic phosphate (Pi) by the addition of inorganic pyrophosphatase. To create the phosphomolybdate precipitate, the obtained Pi could react with acid molybdate. The color of amplified sample was changed into green. Using high grade serous ovarian carcinoma (HGSOC) as an example, this tactic's usefulness was proven. Here, describe the Ercose (Eraser + Color Sensor) device proof-of-concept, which uses a straightforward strategy without sacrificing the accuracy of the outcomes. Ercose is a simple, quick, weightless and inexpensive. A low-cost, user-friendly color sensor is suggested for development in this study to identify the hue of the objects. The test objects were progressively illuminated by the sensor's RGB light emitting diodes, which served as the light sources. The analogue voltage data were converted to digital form and serially delivered to a graphical user interface (GUI). To determine the test objects colors, the digitized voltage values were employed (i.e., RGB values). The microcontroller arduino nano was managed by the GUI, which also showed the needed color values. The Ercose device can be used in a variety of real-world scenarios where standard spectrophotometer devices are not practical.
Amivantamab, a bispecific monoclonal antibody directed against the epidermal growth factor receptor (EGFR) and mesenchymal-epithelial transition factor (MET), has demonstrated significant clinical activity and is increasingly incorporated into frontline regimens for EGFR-mutant non-small cell lung cancer (NSCLC). Its increasing clinical use has, nevertheless, been paralleled by recognition of distinctive cutaneous adverse events, most commonly acneiform eruptions, paronychia, and xerosis among others. We present the first case of an erosive pustular dermatosis (EPD)-like reaction limited to a previously irradiated field in a patient receiving amivantamab for EGFR-mutant NSCLC. This case draws attention to the importance of recognizing EPD-like scalp ulcerations as a potential adverse event in patients receiving amivantamab, events that have not been recognized in clinical trials, particularly in the setting of recent or concurrent radiotherapy.
BACKGROUND:High grade serous ovarian cancer (HGSOC) recurs frequently and commercial tests have emerged for tumor-informed, cell-free DNA (cfDNA)-based detection of minimal residual disease. These tests are based on somatic single nucleotide variants prevalent in many cancers and thus are not well matched to HGSOC, which is dominated by structural genomic rearrangements. The purpose of this study was to evaluate the feasibility of a structural-variant (SV)-informed, cfDNA-based method for detecting clonal and subclonal HGSOC disease burden. METHODS:A method was developed for detecting patient-specific SV breakpoints using digital droplet PCR (ddPCR) with custom tumor-informed primer/probe pairs. Test parameters were first estimated using synthetic cfDNA generated by ultrasonication of genomic DNA from ovarian cancer cell lines. The optimized workflow was implemented in which whole genome sequencing of multisite pre-treatment HGSOC biopsies performed and high confidence SVs were called by multiple published SV callers. Real-time PCR and ddPCR were used for assay development. RESULTS:Following the optimized workflow, tumor-specific SV breakpoint-spanning primers/probe sets of four HGSOC patients' multisite biopsies were designed and validated by real-time PCR and ddPCR. Together with four HGSOCs, a total of 29 SVs breakpoints-spanning tumor-informed primers/probe sets were designed and validated in multisite biopsies. 15 validated tumor-specific SVs were selected for quantification in their corresponding liquid biopsies using the validated ddPCR, and 9 had measurements in liquid biopsies. CONCLUSIONS:Our result shows the detection of SVs from pre-treatment cfDNA using tumor-informed breakpoints-spanning ddPCR is feasible and may enable a novel and sensitive method for monitoring on-treatment disease burden.
OBJECTIVES:Through a genomics-based approach analyzing gene expression levels and adaptive immune receptor recombinations, we sought to determine whether MYC amplification was associated with a worse outcome and reduced immunogenicity. METHODS:MYC copy numbers and the presence of adaptive immune receptor (IR) recombination sequencing reads were quantified in genomics files representing prostate cancer samples. RESULTS:Our results showed that increased MYC amplification was found in metastatic stages of prostate cancer. Furthermore, increased MYC amplification was not only associated with worse progression-free survival but also with reduced immunogenicity in metastatic tumors, as determined by the recovery of a reduced numbers of adaptive IR recombination sequencing reads from tumor RNAseq and tumor whole genome sequence files. CONCLUSIONS:MYC amplification is associated with reduced tumor immunogenicity as assessed by the recovery of IR recombination reads from prostate cancer genomics files.
