CD2 overexpression

CD276 is significant upregulation in ESCC tissues and facilitates the EMT process in ESCC cells via the TGF-β/SMAD signaling, thus promoting the progression of ESCC.

Our results showed that CD24 expression may induce a cellular quiescence-like state and resistance to platinum-based chemotherapeutic agents in ovarian cancer via miR-130a and 301a upregulation. CD24-miR-130a/301a-CDK19 signaling axis could be a prognostic marker for or a potential therapeutic target against ovarian cancer recurrence.

Here we show the experimental development of a third-generation CAR-NK therapy strategy against the CD25 based on the scFV of the clinically approved monoclonal humanized antibody, Basiliximab... We show here for the first time the potential use of an NK cell-mediated CAR therapy strategy targeting CD25 which has been shown to be upregulated in CML blast crisis. The experimental data show a significantly increased and selective in vitro and in vivo cytotoxicity of CD25 CAR-NK92 cells against CD25-expressing leukemia cells as compared to WT-NK92 cells. These results suggest that targeting CD25 by a CD25 CAR based on Basilixiamb's scFV might be an interesting tool in BC-CML and in all acute leukemias overexpressing CD25.

Our findings have important implications in future practice, overexpression of CD24 in OSCC was associated with poor prognosis correlating to the clinical findings, large-scale comprehensive studies are needed further to confirm our findings. In addition to histological features, CD24 can be used as marker for OSCC.

HeLa cells were injected to induce xenograft tumors in mice, and a CTSK inhibitor, MK-0822, was used to confirm the regulation of CTSK and paclitaxel sensitivity by CD200-CD200R in vivo. In vivo, CTSK inhibition significantly suppressed the effects of CD200-CD200R overexpression on the response to paclitaxel by suppressing the CTSK-mediated NF-κB pathway. CD200-CD200R regulates CTSK-mediated NF-κB pathway to affect cisplatin or paclitaxel sensitivity in cervical cancer, which provides a possible immunotherapeutic target and combination strategy for advanced cervical cancer.

One of the potential targets is CD26, to which we have developed and evaluated the efficacy and safety of the humanized monoclonal antibody YS110...Furthermore, in a systemic dissemination model in which HSB2 was administered intravenously, CD26-3G inhibited tumor growth more potently than 2G, resulting in greater survival benefit. The third-generation CD26-targeted CAR-T-cell therapy may be a promising treatment modality for T-cell malignancies.

CD27 overexpression will suppress the viability of the KYSE150 and TE3 cells. Our findings suggested that the degree of CD27 expression could serve as an esophageal cancer prognosis biomarker.

Chemoresistant CD24/CD44GFP-ZEB1 cells depicted 1000-fold higher IC-50 values of doxorubicin and decreased activation of JNK-p38 stress kinase molecular signaling-dependent mammosphere forming efficiency to evade apoptosis. Thus, ZEB1 and its downstream effectors are plausible therapeutic targets for the mitigation of breast cancer chemoresistance in patients.

For one category-unit increase in three ordinal F. nucleatum categories (negative vs. low vs. high), multivariable-adjusted odds ratios (with 95% confidence interval) of the low, intermediate and high CD274 categories (vs. negative) were 0.78 (0.41-1.51), 0.64 (0.32-1.28) and 0.50 (0.25-0.99), respectively (P  = 0.032). Tumor CD274 expression level was inversely associated with the amount of F. nucleatum in colorectal cancer tissue, suggesting that different immunosuppressive mechanisms (i.e. PDCD1 immune checkpoint activation and tumor F. nucleatum enrichment) tend to be used by different tumor subgroups.

Our study provides evidence that CD271 could prevent the switch between low to high-risk cSCC tumors. Because CD271 contributes to maintaining active differentiative paths and favors the response to therapies, it might be a promising target for future pharmaceutical development.

Upon triggering immunogenicity with X-ray radiation, our hydrogel encapsulating efferocytosis inhibitor MRX-2843 enabled a cascade regulation to orchestrate polarization, efferocytosis, and phagocytosis of peritoneal macrophages for realizing robust phagocytosis of tumor cells and powerful antigen presentation, offering a potent approach for ovarian cancer therapy via bridging the innate effector function of macrophages with their adaptive immune response. Moreover, our hydrogel is also applicable for potent treatment of inherent CD24-overexpressed triple-negative breast cancer, providing an emerging therapeutic regimen for the most lethal malignancies in women.

HER2 antibody-drug conjugate (ADC) is the newest additions to HER2-targeted therapy with Trastuzumab emtansine and Trastuzumab deruxtecan being recently approved by the FDA. We further demonstrated that these MR.HER2-CAR T cells are more effective in killing HER2-low breast tumor cells than unmodified HER2-CAR T cells. Thus, MR.HER2-CAR T cell therapy is a promising candidate for a novel HER2-targeted therapy that is effective while having low toxicity.

Remarkably, we observed that the MRCAR T cells inhibit tumor growth more effectively than unmodified CAR T cells in both Huh7 human hepatocellular carcinoma (GPC3-MRCAR) and A549 human non-small cell lung cancer (HER2-MRCAR) mouse models. Thus, MR-CAR T cell therapy represents a promising approach to improve CAR T cell therapy against solid tumors.

In summary, we have discovered a novel therapeutic anti-CD25 mAb that can deplete Treg cells without blocking IL-2 signaling. As demonstrated in our preclinical tumor models, it has a good potential to induce effective antitumor immune responses in TME and tumor growth inhibition especially in combination with PD-1/PD-L1 treatment.

Next, BMSC-exos carrying miR-187 contributed to repressed cell malignant features as well as limited tumorigenicity and tumor metastasis. Collectively, this study demonstrated that BMSC-derived exosomal miR-187 restrained prostate cancer by reducing CD276/JAK3-STAT3-Slug axis.

In vivo studies to further understand the translational significance of this metabolic axis is underway. Taken together, our study demonstrates, for the first time, that CD24 presents a novel metabolic vulnerability that can target BCSCs to gain a therapeutic advantage in the treatment of drug-resistant TNBC patients.

The grafting of CD271-overexpressing cells resulted in a significantly lower metastatic capacity and promoted the recruitment of macrophages within the site of injection. Therefore, our results indicate an inverse correlation between CD271 expression and malignancy level and CD271 could potentially have a role in the switch between the less aggressive to the high-risk cSCC

In this research, CD24 cells accounted for the vast majority of TNBC cells, and they were insensitive to Taxol but sensitive to ferroptosis agonists and effectively escaped phagocytosis by tumor-associated macrophages...This system achieved dual antitumor effects, ultimately promoting cell death and thus inhibiting TNBC tumor growth, with some tumors even disappearing. The composite nanoprecision treatment system reported in this paper is a potential strategic tool for future use in the treatment of TNBC.

Finally, we reported the use of a novel strategy for the generation of anti-CD20 mAbs, with human and canine cross-reactivity, by exploring our rabbit derived single-domain antibody platform. Overall, these results support the rationale of using CD20 as a target for veterinary settings and the development of novel therapeutics and immunodiagnostics.

This study demonstrated the functional roles of CD26 in inducing CRC migration, invasion, angiogenesis and metastasis and identified the potential involvement of MMP1 and CAV1 in such process. CD26 is an attractive therapeutic target for combating tumor progression to improve the prognosis of CRC patients.

The same was true for a subgroup who were treated with multidrug regimens with or without mogamulizumab...These results suggest ATLL patients with CD28 overexpression have more aggressive clinical course and are more refractory to treatment with multidrug chemotherapy. CD28 overexpression appear to be a novel unfavorable prognostic marker in ATLL patients, and further prospective studies are warranted to establish its prognostic significance.

Finally, CD271 upregulation inhibited mROS production, revealing the presence of a negative feedback loop in mROS regulation. These results indicate that targeting CD271 can activate cell death pathways to inhibit melanoma progression and potentially overcome resistance to targeted therapy.

CAR-T cells were detected by flow cytometry using the RQR8-specific CD34 antibody. The BCMA-CD24 CAR was found to be expressed on roughly 13% of T-cells. To determine the selective lysis by the CAR-T cells, we performed co-culture killing assays in which MM cell lines over-expressing CD24 (ARP-1 CD24OE or OCI CD24OE cells) were incubated with CAR-T cells.

Conclusion Our study shows that anti-MM cytotoxicity from primary healthy donor CD3+ T cells is attenuated by CD200 expression on MM cells. We also demonstrate that this inhibitory mechanism in CD3+ T cells is mediated via DOK2, providing a potential target for immunotherapeutic approaches in MM.

The immune checkpoint CD200 upregulated immune-related genes through β-catenin signaling, reprogrammed the TIME, and exerted protumor effects. Ad5sCD200R1 injection could be an effective targeted strategy to enhance antitumor immunoediting.

Mantle cell lymphoma (MCL) is a neoplasm of mature lymphocytes committed to the B-cell lineage. This neoplasm has an aggressive clinical course, with poor response to standard treatment and short overall survival. MCL typical immunophenotype has been described as a mature monoclonal B-cell population with expression of CD19, CD20, CD43, CD45, CD79 and CD5; and negative expression of CD10, CD23 and CD200. Overexpression of cyclin D1 as detected by immunohistochemistry is characteristic of this disease. CD117 or c-kit is a surface protein encoded by the proto-oncogene c-kit which is expressed in normal hematopoietic and neoplastic cells, usually of myeloid lineage. There are few published studies with assessment of CD117 expression on mature B-cell neoplasms (MBCN). In this report, we described a MCL case with aberrant CD117 coexpression as demonstrated by flow cytometry immunophenotyping (FCI). Patient was a 64 year-old male with leukocytosis (39.20 x 109/l) and lymphopenia with normal red blood cell and platelet counts. Peripheral blood FCI with a screening panel evidenced an abnormal population representing 64% of nucleated cells, with expression of CD19, CD45(bright) and CD117. Additional staining of myeloid and lymphoid markers was performed. The neoplastic cells had positive expression of cytCD79a, CD5, CD19, CD20(bright), CD27, CD38, CD45(bright), CD43, CD79b, CD81, HLA-DR and kappa light chain; and were negative for cytCD3, cytMPO, CD10, CD11c, CD23, CD25, CD33, CD34, CD103, CD200 and lambda light chain. CD117 PE (clone 104D2, EXBIO, Praha, CZE) staining was repeated and positive expression was confirmed. FCI findings were compatible with the diagnosis of MCL with aberrant CD117 coexpression. After initial chemotherapy, patient had persistent leukocytosis (19.10 x 109/l) with anemia (hemoglobin of 11.1 g/l). Bone marrow aspirate FCI showed persistence of 37% of neoplastic cells. Unfortunately, patient died from causes unrelated to the disease before the next chemotherapy cycle. CD117 expression is a common finding in acute myeloid leukemia, being less frequently expressed in precursor lymphoid neoplasms and rarely identified in mature neoplasms. There are few studies evaluating CD117 expression in MBCN since its assessment is not part of the diagnostic panels. Assessment of c-kit mRNA expression in different types of lymphomas only identified its expression in CD30-positive cases. A CD117-positive B-cell non-Hodgkin lymphoma (NHL) carrying the t(14;18) translocation has been described in a case report. In another study, CD117 overexpression was identified in 2 out of 17 MCL cases using immunohistochemistry. Also, CD117 expression was identified in four out of 30 diffuse large B-cell lymphoma (DLBCL) cases. There is one large study assessing the distribution and expression of KIT in 824 cases of malignant lymphoma where CD117 expression was assessed with tissue microarray, and only one B-cell follicular lymphoma had positive CD117 expression. The role of CD117 expression on MBCN is still unclear, however, the abnormal expression of this marker has the potential to be used for FCI minimal residual disease (MRD) assessment. In Conclusion , CD117 expression can be found in MCBN such as MCL and expansion of FCI panel in order to better characterize such abnormal populations is necessary for the correct diagnosis.

The expression of CD276 showed a weak but statistically significant positive correlation with tumor diameter, but we did not find a significant association between CD276 expression and other histopathological clinical factors, or the response to initial therapy. A search of published data identified the monoclonal antibody (inhibitor) enoblituzumab as a potential drug for patients diagnosed with MTC overexpressing CD276.

PIK3CA-mutated PTEN-lost tumors (n = 33) showed higher prevalence of CD274-positivity (82%) than PIK3CA-wild-type PTEN-lost tumors (n = 204; 70% CD274-positivity) and PTEN-expressed tumors (n = 147; 50% CD274-positivity) (P = .003). Our findings support the role of PI3K signaling in the CD274/PDCD1 pathway.

Hsp70 may regulate CD24 expression. Co-expression of CD24 and Hsp70 may be a prognostic biomarker for lung cancer.

Higher infiltration of CD204-positive macrophages into the tumour-microenvironment might be prognostically important in CRC.

We introduce our recent studies focusing on AT-rich interactive domain 1A gene mutations and programmed death ligand-1 overexpression/CD274 copy-number amplification, which are recurrently identified in EBV (+) GC. Finally, based on those findings, we propose potential therapeutic options using candidate-targeted therapies against EBV (+) GC.

Treatments to reduce immune evasion, as well as the use of other natural and pharmacological immune activators, should include prior pharmacological inhibition of steroidogenesis. Attempts to combine these with tumor cell proliferation inhibitors, if they do not affect cells of the immune system, may produce interesting results.

While these data support the rational to target CD25, ALL cells did not appear to be in-vitro sensitive to basiliximab, an antibody able to target the Il2RA, but in-vivo investigations are needed to better assess the effects of this therapeutic approach in ALL context...Targeting CD25 receptor with anti-CD25 antibodies or peptide mimetics could be an effective strategy for targeting leukemic cells. Additionally, high CD25 expression could be exploited for the development of CAR-T therapy

While these data support the rational to target CD25, ALL cells did not appear to be in-vitro sensitive to basiliximab, an antibody able to target the Il2RA, but in-vivo investigations are needed to better assess the effects of this therapeutic approach in ALL context...Targeting CD25 receptor with anti-CD25 antibodies or peptide mimetics could be an effective strategy for targeting leukemic cells. Additionally, high CD25 expression could be exploited for the development of CAR-T therapy

While these data support the rational to target CD25, ALL cells did not appear to be in-vitro sensitive to basiliximab, an antibody able to target the Il2RA, but in-vivo investigations are needed to better assess the effects of this therapeutic approach in ALL context...Targeting CD25 receptor with anti-CD25 antibodies or peptide mimetics could be an effective strategy for targeting leukemic cells. Additionally, high CD25 expression could be exploited for the development of CAR-T therapy

While these data support the rational to target CD25, ALL cells did not appear to be in-vitro sensitive to basiliximab, an antibody able to target the Il2RA, but in-vivo investigations are needed to better assess the effects of this therapeutic approach in ALL context...Targeting CD25 receptor with anti-CD25 antibodies or peptide mimetics could be an effective strategy for targeting leukemic cells. Additionally, high CD25 expression could be exploited for the development of CAR-T therapy

NPM/B23 silencing enhanced phagocytosis by macrophages through decrease of CD24 on cancer cells. Restoration of CD24 expression in NPM/B23-silenced cancer cells inhibited macrophage-mediated phagocytosis.

In conclusion, CD4IL-10 have a cytotoxic profile and can kill the majority of pAML blasts. Thus, CD4IL-10 is a novel cell therapy which could control GvHD and support GvL in pAML patients transplanted with allo-HSCT.

Overall, our results demonstrated a significant CD24 overexpression in human and canine prostate cancer, although its prognostic value may be questionable. However, tumors overexpressing CD24 may be a reliable model for new target therapies and dogs could be used of a unique preclinical model for these studies.