TCHP antibody
- Known as:
- TCHP (anti-)
- Catalog number:
- orb100712
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- TCHP antibody
Related genes to: TCHP antibody
- Gene:
- TCHP NIH gene
- Name:
- trichoplein keratin filament binding
- Previous symbol:
- -
- Synonyms:
- MGC10854, TpMs
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-27
- Date modifiied:
- 2016-03-14
Related products to: TCHP antibody
Related articles to: TCHP antibody
- Neoadjuvant chemotherapy (NAC) is the standard of care for locally advanced breast cancer, yet the molecular predictors of pathological response remain incompletely defined, particularly regarding microRNA (miRNA) dynamics. We investigated paired pre- and post-NAC miRNA expression profiles in relation to molecular subtype, residual cancer burden (RCB), and clinical timing parameters. Seven patients with invasive breast cancer (Luminal A = 3, Luminal B = 1, TNBC = 2, HER2+ = 1) who received NAC (AC-T or TCHP) were included in this pilot study. Small-RNA sequencing (NovaSeq X Plus, CeGaT GmbH, project S17293) was performed on 14 FFPE specimens (7 pre-NAC core needle biopsies, 7 post-NAC surgical specimens). Differential expression analysis used the paired Wilcoxon signed-rank test with Benjamini-Hochberg correction. Spearman correlations assessed associations between miRNA expression, RCB score, and clinical timing intervals. Candidate miRNAs were subsequently annotated using experimentally validated miRNA-target interactions. After filtering (≥ three counts in ≥ three samples), 759 miRNAs were analysed. No miRNA reached strict significance (adj < 0.05, |logFC| > 1.0) after multiple testing correction, consistent with the limited statistical power ( = 7). Under exploratory criteria ( < 0.10, |logFC| > 0.5), 156 candidate miRNAs were identified: 70 upregulated and 86 downregulated post-NAC. Leading candidates included hsa-miR-139-3p (+2.60), hsa-miR-139-5p (+2.36), and hsa-miR-1323 (+1.55) as upregulated, and hsa-miR-429 (-2.53), hsa-miR-141-3p (-1.79), and hsa-miR-1277-5p (-1.25) as downregulated post-NAC. The single patient achieving the lowest residual disease burden (P3, Luminal B, RCB-I, score 1.32) displayed a distinct pre-treatment miRNA profile, separating from all other pre-NAC specimens on principal component analysis and characterised by higher baseline hsa-miR-139-3p/-5p and lower baseline hsa-miR-429 and hsa-miR-141-3p expression, suggesting that baseline miRNA expression patterns may contribute to differential chemotherapy response. RCB score showed a non-significant positive trend with post-NAC Ki-67 (ρ = +0.71, = 0.07). This pilot study identifies NAC-modulated candidate miRNAs in breast cancer and establishes a paired FFPE-based small-RNA-sequencing workflow applicable in routine clinical settings. The distinct pre-treatment profile of the single best responder generates the testable hypothesis that baseline expression of tumour suppressor miRNAs of the miR-139 family, together with low miR-200-family expression, may track chemosensitivity. As no candidate reached statistical significance after multiple testing correction and none has been validated in an independent cohort or by an orthogonal method, all findings are exploratory and hypothesis-generating. The results support larger prospective validation studies examining miRNA signatures as predictive biomarkers of NAC response across breast cancer molecular subtypes. - Source: PubMed
Publication date: 2026/08/31
Komporaly Isabela AndaGheorghe Adelina SilvanaIovănescu Elena AdrianaGeorgescu BogdanStănculeanu Dana Lucia - Serpentine supravenous hyperpigmentation (SSH) is a rare dermatological complication of intravenous chemotherapy characterized by linear hyperpigmented streaks along superficial veins. Bullous SSH represents an exceptionally rare variant with only a few previously reported cases in the literature. We report the case of a 50-year-old woman with HER2-positive breast cancer who developed bullous SSH 5 days after her first cycle of TCHP (docetaxel, carboplatin, trastuzumab, pertuzumab) chemotherapy. The patient presented with linear erythematous streaks and small tense bullae along the infusion vein on her right forearm. Treatment with topical mometasone furoate 0.1% ointment resulted in complete resolution within 2 weeks. Preventive strategies described for SSH include use of contralateral arm venous access, thorough saline flushing after chemotherapy infusion, consideration of central venous access when feasible, and, in selected cases, modification of the chemotherapy regimen. In our patient, subsequent chemotherapy cycles were administered using contralateral arm venous access with thorough saline flushing (same flushing protocol as Cycle 1), without recurrence of SSH. The patient completed all six planned cycles and subsequently achieved pathologic complete response. This case is the first to demonstrate that conservative management of bullous SSH with topical mometasone furoate, combined with contralateral venous access and thorough saline flushing, enables successful rechallenge and uninterrupted continuation of planned oncological treatment with pathologic complete response as the outcome. - Source: PubMed
Publication date: 2026/08/21
Nair Gayathri RKoutsis JamesPoels DeepaliAgar NitaWarrier SanjayKumar Sanjeev - Super-bulky bis(anilido)acridanide pro-ligands (NNN)H (NNN = 4,5-bis(anilido)-2,7,9,9-tetramethylacridanide, anilido = NAr, Ar = DCHP, 2,6-dicyclohexylphenyl; TCHP, 2,4,6-tricyclohexylphenyl) have been prepared in high yields. The reaction of (NNN)H with trimethylaluminium affords bimetallic complex [AlMe(NNN)] which reacts with iodine to form the corresponding monometallic complex [Al(NNN)(I)]. The reduction of [Al(NNN)(I)] with sodium and potassium containing reducing agents was explored. From potassium reductions, only complexes K[Al(NNN)(I)] (from K/KI) and [Al(NNN)(TMEDA)] (from KC/TMEDA, TMEDA = N,N,N',N'-tetramethyl ethylenediamine) could be isolated. In contrast, aluminium(III) hydride [Na(CH)][Al(NNN)(H)] was formed from reduction of [Al(NNN)(I)] in benzene with excess sodium metal (mirror). This complex is unstable and readily decomposes in the presence of ethers, such as 2.2.2-cryptand, to give the aluminium(III) complex [Al(NNN)(2.2.2-cryptand)]. - Source: PubMed
Publication date: 2026/08/21
Evans Matthew JParr Joseph MJones Cameron - : Neoadjuvant dual HER2 blockade combined with chemotherapy is the standard treatment approach for patients with high-risk early-stage or locally advanced HER2-positive breast cancer. However, the optimal chemotherapy backbone and the predictive value of systemic inflammatory biomarkers remain subjects of ongoing investigation. This study aimed to compare pathologic complete response (pCR) rates between neoadjuvant dose-dense doxorubicin/cyclophosphamide followed by paclitaxel plus trastuzumab and pertuzumab (ddAC+THP) and docetaxel, carboplatin, trastuzumab, and pertuzumab (TCHP), and to evaluate the predictive performance of pretreatment inflammatory biomarkers. In this multicenter retrospective study, patients with HER2-positive breast cancer treated with neoadjuvant ddAC+THP or TCHP between 2019 and 2025 at three tertiary centers were evaluated. Pretreatment inflammatory biomarkers, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and hemoglobin, albumin, lymphocyte, and platelet (HALP) score, were calculated from baseline laboratory parameters. Receiver operating characteristic analyses were performed to determine optimal cutoff values, and logistic regression analyses were used to identify predictors of pCR. A total of 197 patients were included, of whom 138 received ddAC+THP and 59 received TCHP. Overall, 125 patients (63.5%) achieved pCR. The pCR rate was numerically higher in the ddAC+THP group than in the TCHP group (65.2% vs. 59.3%), although the difference was not statistically significant ( = 0.431). Among the evaluated biomarkers, SIRI demonstrated the highest discriminatory performance for predicting pCR (AUC: 0.725, 95% CI: 0.652-0.797), followed by NLR (AUC: 0.673, 95% CI: 0.595-0.750). In multivariable analysis, hormone receptor positivity (OR: 0.291, 95% CI: 0.131-0.645; = 0.002) and elevated SIRI (>0.845) (OR: 0.088, 95% CI: 0.036-0.216; < 0.001) were independently associated with lower odds of achieving pCR. No significant difference in pCR was observed between treatment regimens across predefined subgroup analyses. Neoadjuvant ddAC+THP and TCHP achieved comparable pCR outcomes in patients with HER2-positive breast cancer. SIRI was independently associated with a lower likelihood of achieving pCR and showed acceptable discriminatory performance. These findings suggest that SIRI may represent an exploratory, readily available inflammatory biomarker for pCR risk stratification; however, prospective validation is required before clinical application. - Source: PubMed
Publication date: 2026/07/16
Şahin GökhanDişli Ahmet KürşadSirvan FiratMıdık Mustafa MuratBoyraz Nur EvsanBelen ObenŞahin Taha KorayNuransoy Cengiz AyşeKuş FatihGökdere SılaGöker ErdemÇakar BurcuAksoy Sercanİnanç MevlüdeGüven Deniz CanYıldırım Hasan Çağrı - Primary breast squamous cell carcinoma (PBSCC) with HER2-positive status is exceptionally rare, with fewer than 100 cases reported globally, and HER2 positivity occurring in only 5.8-7.1% of these cases. No established treatment standards exist for this entity. We present the case of a 43-year-old woman with HER2-positive PBSCC who exhibited a poor response to neoadjuvant TCHP therapy (Miller-Payne grade 2). Local recurrence occurred just 3 months after mastectomy. Second-line therapy with pyrotinib plus capecitabine provided 9 months of disease control before lung metastasis emerged. Subsequent molecular profiling revealed a E545K mutation (VAF 40.3%), co-amplified with and . Although third-line treatment with trastuzumab deruxtecan (T-DXd) achieved a partial response, the progression-free survival (PFS) was limited to only 5 months. A repeat biopsy confirmed HER2 downregulation (from 3+ to 2+), identifying antigen loss as a key mechanism of acquired resistance. A review of the literature indicates that the pathological complete response rate of HER2-positive PBSCC to standard HER2-targeted therapy is remarkably low, far inferior to the 50-60% pCR rates achieved with dual HER2 blockade in HER2-positive invasive ductal carcinoma. This case underscores that upon failure of HER2-targeted therapy accompanied by HER2 antigen loss, the treatment strategy should pivot towards molecularly-guided precision therapy. Based on evidence such as that from the TRIUMPH trial, priority should be given to agents targeting the detected alterations, such as or inhibitors, rather than persisting with HER2-targeted approaches. - Source: PubMed
Publication date: 2026/07/09
Yang FangGuo SiyuLi PingYang MengqiWu Xuan