TCHP antibody Polyclonal Antibodies Primary antibodies
- Known as:
- TCHP (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100712
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- TCHP antibody Polyclonal Antibodies Primary antibodies
Ask about this productRelated genes to: TCHP antibody Polyclonal Antibodies Primary antibodies
- 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 Polyclonal Antibodies Primary antibodies
Related articles to: TCHP antibody Polyclonal Antibodies Primary antibodies
- : 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 - The bulky xanthene-bridged diamido-barium complex, [(EtNONTCHP)Ba(η6-toluene)] 1-Ba (EtNONTCHP = 4,5-bis{(TCHP)N}-2,7-diethyl-9,9-dimethyl-xanthene, TCHP = 2,4,6-tricyclohexylphenyl), has been prepared and exists as a weakly associated polymer in the solid-state. While this is unreactive toward tetramethylsilane (TMS), its lighter analogues [(EtNONTCHP)M(η6-toluene)] 1-M (M = Ca and Sr) coordinate to TMS giving the 1:1 complexes [(EtNONTCHP)M(η6-toluene)(κ2-H,H-TMS)] 2-M (M = Ca or Sr). In the solid-state, the TMS ligands in these species appear to ligate the metal centers in a κ2-H,H-mode. NMR spectroscopic studies imply that the TMS ligands of 2-M dissociate from the metal center, even in noncoordinating solvents. A theoretical analysis of the strength and nature of the metal-TMS bonding in 2-M has been carried out. First, precursor complexes 1-M were computed to be strong Lewis acids, which coordinate the poorly nucleophilic TMS ligand, to give 2-M. DFT analyses revealed the strength of bonding between TMS and the 1-M fragments to be weak (ΔG298 K° = -6.6 and -6.9 kcal mol-1 for 2-Ca and 2-Sr, respectively). ETS-NOCV and NBO analyses of the bonding in 2-Ca indicated that, while electrostatic interactions between the TMS and 1-Ca units dominate (ca. 68%), both dispersion (ca. 20%) and orbital (ca. 12%) interactions make significant contributions to the total attractive energy. - Source: PubMed
Parr Joseph MEvans Matthew JMcKay Alasdair IUnsworth Sophie GJones Cameron - Haematuria is a rare complication in patients receiving docetaxel, carboplatin, trastuzumab, and pertuzumab (TCHP) chemotherapy for breast cancer, with only a few cases reported. Here, we describe a 65-year-old woman with HER2-positive T2N1 breast cancer who developed visible haematuria and acute kidney injury (AKI) after her first cycle of neoadjuvant TCHP therapy. Ultrasound and computed tomography (CT) imaging of the renal tract demonstrated mild bilateral hydronephrosis and moderate bilateral hydroureter associated with inflammatory fat stranding, with findings most consistent with chemotherapy-associated inflammatory ureteritis and cystitis. Initial management included continuous bladder irrigation, intravenous fluids, and empirical antibiotic therapy. However, persistent haematuria and worsening renal function despite supportive treatment prompted initiation of oral prednisolone 60 mg once daily for presumed inflammatory urothelial toxicity. The patient showed a marked clinical response within 72 hours of corticosteroid initiation, with resolution of haematuria and recovery of renal function to baseline. Following multidisciplinary team (MDT) discussion, and given poor tolerance of systemic therapy alongside significant treatment-related anxiety, a decision was made to proceed directly to surgery rather than continue neoadjuvant chemotherapy. This case highlights chemotherapy-associated urothelial toxicity as a rare but clinically significant adverse effect of TCHP therapy and the need for early recognition and multidisciplinary management. A focused review of previously reported cases is also presented. - Source: PubMed
Publication date: 2026/06/08
Mathiyalagan NavinRahul EricSarwar Muhammad AdeelAli Eiman AbdelmoneimKhan Sarah - Five base-stabilized beryllium Grignards of the type LBeBrY (L = IDipp (1,3-bis(dipropylphenyl)imidazol-2-ylidene), IPr (1,3-dipropyl-4,5-dimethylimidazol-2-ylidene), CDP (hexaphenylcarbodiphosphorane), Y = Dur (2,3,5,6-tetramethylphenyl = duryl); L = IPr, Y = Tchp (2,4,6,-tricyclohexylphenyl); L = CAAC (1-(2,6-dipropylphenyl)-2,2,4,4-tetramethylpyrrolydin-5-ylidene, Y = Tmp (2,6-tetramethylpyrrolidine)) were synthesized by salt metathesis from LBeBr or ligand exchange at (EtO)BeBrY. Single-crystal X-ray diffraction analyses show that the angle between the beryllium and carbon ligand planes depends mainly on L, varying from coplanar (L = CDP) to orthogonal (L = IDipp), via 50-70° for L = IPr. In contrast, (CAAC)BeBrDur and (CAAC)BeBrTmp display coplanar and near-orthogonal arrangements, respectively. Energy decomposition analysis in combination with natural orbitals for chemical valence (EDA-NOCV) calculations rationalize these trends as arising from a balance of steric repulsion, stabilizing London dispersion interactions between L and Y, and small but non-negligible BeBrY→L (L = carbene) or L→BeBrY (L = CDP) π-donation components. Reduction of LBeBrAr led to complex product mixtures, presumably owing to Schlenk-type equilibria as well as the formation of highly reactive [LBeY] and LBeHY intermediates involved in ligand decomposition reactions. Only the one-electron reduction of (CAAC)BeBrTmp afforded a stable linear [(CAAC)BeTmp] radical, which EPR spectroscopy and DFT calculations indicate is a CAAC- rather than a Be-centered radical. - Source: PubMed
Publication date: 2026/06/09
Czernetzki CorinnaArrowsmith MerleKroll ThomasGärtner AnnalenaKrummenacher IvoBraunschweig Holger