Search

Tumor calcification is considered to have the superiority of integrating tumor diagnosis and treatment, and it also has been found to be a predictor of favorable prognosis. However, selecting suitable nanocarriers and therapeutic drugs to maximize the tumor calcification efficiency are key factors for improving calcification‐medicated theranostics. This study performs a multi‐channel calcification nanoinitiator (CalNI, i.e., BP‐Cur‐Ca@PKLAK) by loading curcumin (Cur) and depositing Ca2+ on black phosphorus (BP) and combined carrying mitochondria‐targeting cytotoxic peptide KLAK to boost a triple‐induced tumor calcification. CalNI preferentially accumulates inside tumor mitochondria and induces multilevel calcification promotion by the three combined effects of (i) the degradation of BP into PO43− provides the phosphorus source required for calcification; (ii) burst of calcium ions can directly induce cellular calcium overload; (iii) Cur can inhibit calcium efflux thus further aggravate intracellular calcium stress. Moreover, KLAK exhibited enhanced mitochondrial synergistic toxic effects. Notably, the potential function of CalNI on the regulation of macrophage polarization could completely reverse the immunosuppressive microenvironment, and activate the initiation of T cell‐mediated immune response. Therefore, this three‐pronged CalNI showed a huge promise to be an alternative to conventional oncology therapy, which presents a more satisfactory therapeutic efficiency than any kind of single induction mode. [ABSTRACT FROM AUTHOR]

Biomineralization is a phenomenon that involves the deposition of inorganic ions onto organic substrates, resulting in the formation of hard tissue materials. Tumor mineralization, on the other hand, encompasses two key aspects: tumor calcification and tumor iron mineralization. The occurrence of spontaneous tumor calcification and regional lymph node calcification in colorectal cancer, lung cancer, and glioblastoma has been established as a favorable prognostic factor in clinical settings. Building upon this understanding, we propose the concept and advance the development of a compound that artificially induces bionic mineralization around the surface of cancer cells. This process has demonstrated exceptional efficacy in inhibiting the growth and metastasis of cervical, breast, and lung tumors. Moreover, it has exhibited outstanding performance in the early-stage diagnosis of cancer. Consequently, we anticipate that this concept holds significant potential for cancer-targeted mineralization therapy and diagnosis, offering a novel avenue for the development of anticancer drugs.

Abstract As the indispensable second cellular messenger, calcium signaling is involved in the regulation of almost all physiological processes by activating specific target proteins. The importance of calcium ions (Ca2+) makes its “Janus nature” strictly regulated by its concentration. Abnormal regulation of calcium signals may cause some diseases; however, artificial regulation of calcium homeostasis in local lesions may also play a therapeutic role. “Calcium overload,” for example, is characterized by excessive enrichment of intracellular Ca2+, which irreversibly switches calcium signaling from “positive regulation” to “reverse destruction,” leading to cell death. However, this undesirable death could be defined as “calcicoptosis” to offer a novel approach for cancer treatment. Indeed, Ca2+ is involved in various cancer diagnostic and therapeutic events, including calcium overload-induced calcium homeostasis disorder, calcium channels dysregulation, mitochondrial dysfunction, calcium-associated immunoregulation, cell/vascular/tumor calcification, and calcification-mediated CT imaging. In parallel, the development of multifunctional calcium-based nanomaterials (e.g., calcium phosphate, calcium carbonate, calcium peroxide, and hydroxyapatite) is becoming abundantly available. This review will highlight the latest insights of the calcium-based nanomaterials, explain their application, and provide novel perspective. Identifying and characterizing new patterns of calcium-dependent signaling and exploiting the disease element linkage offer additional translational opportunities for cancer theranostics.

Highlights: Recent progress of the calcium-based nanomaterials-mediated cancer diagnosis and therapy were summarized. Main challenges and clinical translation prospects of calcium-based nanomaterials were discussed.As the indispensable second cellular messenger, calcium signaling is involved in the regulation of almost all physiological processes by activating specific target proteins. The importance of calcium ions (Ca2+) makes its “Janus nature” strictly regulated by its concentration. Abnormal regulation of calcium signals may cause some diseases; however, artificial regulation of calcium homeostasis in local lesions may also play a therapeutic role. “Calcium overload,” for example, is characterized by excessive enrichment of intracellular Ca2+, which irreversibly switches calcium signaling from “positive regulation” to “reverse destruction,” leading to cell death. However, this undesirable death could be defined as “calcicoptosis” to offer a novel approach for cancer treatment. Indeed, Ca2+ is involved in various cancer diagnostic and therapeutic events, including calcium overload-induced calcium homeostasis disorder, calcium channels dysregulation, mitochondrial dysfunction, calcium-associated immunoregulation, cell/vascular/tumor calcification, and calcification-mediated CT imaging. In parallel, the development of multifunctional calcium-based nanomaterials (e.g., calcium phosphate, calcium carbonate, calcium peroxide, and hydroxyapatite) is becoming abundantly available. This review will highlight the latest insights of the calcium-based nanomaterials, explain their application, and provide novel perspective. Identifying and characterizing new patterns of calcium-dependent signaling and exploiting the disease element linkage offer additional translational opportunities for cancer theranostics. [ABSTRACT FROM AUTHOR]

Extraosseous calcifications correspond to ubiquitous deposits of intra-tissue calcium salts leading to dysfunction of the affected tissue or organ. There are two types: metastatic calcifications and dystrophic calcifications. Their formation mechanism is by mimicking the physiological mineralization process with an "osteoblast-like" cell. The cause of extra-osseous calcification is variable and depends on risk factors. If the subject is young, you will have to think about a genetic syndrome!, (Copyright © 2024. Published by Elsevier Masson SAS.)

Aims: The purpose was to investigate the correlation between calcification and outcome in metastatic colorectal cancer (mCRC) patients who received bevacizumab plus chemotherapy as the first-line treatment. Methods: A single retrospective cohort study was conducted with all diagnosed mCRC cases who received bevacizumab and chemotherapy as the first-line therapy. Results: Among all enrolled patients (n = 159), 31 had tumor calcification. The median overall survival and progression-free survival were significantly better in patients with tumor calcification than in those without calcification. A higher objective overall response rate was also observed in the tumor calcification group. On multivariate analysis, tumor calcification was independently associated with overall survival and progression-free survival. Conclusions: Tumor calcification was independently associated with improved survival in mCRC patients treated with bevacizumab plus chemotherapy. Colorectal cancer is one of the most commonly diagnosed malignancies globally and nearly half of these patients develop metastatic colorectal cancer (mCRC). The current standard treatment for mCRC includes 5-fluorouracil-based chemotherapy with or without bevacizumab. Nevertheless, a predictive biomarker of efficacy for bevacizumab has not yet been firmly established. This retrospective study aimed to investigate the correlation between tumor calcification and prognosis in mCRC patients who received bevacizumab plus chemotherapy as the first-line treatment. The authors found that tumor calcification was independently associated with improved survival in mCRC patients treated with bevacizumab plus chemotherapy. [ABSTRACT FROM AUTHOR]

Objectives: Sialolithiasis is the most common cause of calcifications detected with ultrasound in patients with chronic inflammatory symptoms and swellings of the salivary glands. Other differential diagnoses of calcifications are extremely rare and mostly benign. Methods: Case report and literature review. Results: Two rare cases of malignant parotid gland tumors with calcifications in a localization typical for sialolithiasis, which were mistaken for salivary calculi based on image findings, are presented. Conclusions: This report intends to highlight the pitfalls in the imaging of parotid gland diseases. Even if malignant tumors of the parotid gland with calcifications are extremely rare, in ambiguous cases, differential diagnoses should be considered carefully. A high suspicion index of the need for further diagnostics in cases with calcifications is practical and could include missing periprandial symptoms, no obstruction signs in the proximal duct, and missing evidence of sialolithiasis in sialendoscopy. [ABSTRACT FROM AUTHOR]

Tumor calcification is found to be associated with the benign prognostic, and which shows considerable promise as a somewhat predictive index of the tumor response clinically. However, calcification is still a missing area in clinical cancer treatment. A specific strategy is proposed for inducing tumor calcification through the synergy of calcium peroxide (CaO 2 )-based microspheres and transcatheter arterial embolization for the treatment of hepatocellular carcinoma (HCC). The persistent calcium stress in situ specifically leads to powerful tumor calcioptosis, resulting in diffuse calcification and a high-density shadow on computed tomography that enables clear localization of the in vivo tumor site and partial delineation of tumor margins in an orthotopic HCC rabbit model. This osmotic calcification can facilitate tumor clinical diagnosis, which is of great significance in differentiating tumor response during early follow-up periods. Proteome and phosphoproteome analysis identify that calreticulin (CALR) is a crucial target protein involved in tumor calcioptosis. Further fluorescence molecular imaging analysis also indicates that CALR can be used as a prodromal marker of calcification to predict tumor response at an earlier stage in different preclinical rodent models. These findings suggest that upregulated CALR in association with tumor calcification, which may be broadly useful for quick visualization of tumor response., (© 2024 Wiley‐VCH GmbH.)

Introduction: Myxoid/round-cell liposarcoma (MRCL) is a specific histological subtype that accounts for 30-35% of liposarcomas and whose virulence depends on the quantity of round-cells within the tumor. MRCL is associated with specific chromosomal translocations resulting in the formation of CHOP/FUS and CHOP/EWS fusion proteins. A high sensitivity of MRCL to trabectedin was reported. Case Report: We report the case of a 63-year-old woman with a bulky and metastatic MRCL, treated with trabectedin 1.5 mg/m2 as a first-line treatment. She experienced a long-lasting clinical benefit. The patients received 14 cycles of trabectedin and achieved a durable partial response to the metastases and a stable disease of the primary tumor, which is a very favorable safety profile. Also noteworthy is that we have observed a calcification of the primary tumor and the metastasis. The response, which lasted 30 months, led to a symptomatic improvement, associated with an excellent general condition and an absence of pain. Conclusion: To the best of our knowledge, this is the first report of a MRCL treated with trabectedin that resulted in a calcification of the primary tumor and the metastases, associated with an outstandingly long response. This case suggests that trabectedin may represent a feasible first-line therapeutic option for patients with MRCL, with meaningful clinical benefits and an acceptable safety profile.

Objective: The objective of this paper was to describe the volumetric natural history of meningiomas in patients with neurofibromatosis type 2 (NF2)., Methods: The authors performed a retrospective descriptive study by reviewing NF2 patients with meningiomas at their institution between 2000 and 2019. Demographic data were collected from the electronic medical records. Tumor volume was collected using volumetric segmentation software. Imaging characteristics including peritumoral brain edema (PTBE) and tumor calcification were collected for each patient from their first to most recent MRI at the authors' institution. An increase of 15% or more per year from original tumor size was used as the cutoff to define growth., Results: A total of 137 meningiomas from 48 patients were included in the analysis. The average number of tumors per person was 2.9. Ninety-nine (72.3%) tumors were in female patients. The median length of follow-up from first imaging to last imaging was 32 months (IQR 10.9, 68.3 months). Most tumors were located in the cerebral convexity (24.8%), followed by the falcine region (18.2%) and spine (10.2%). The median tumor growth was 0.12 cm3/yr (IQR 0.03, 0.52 cm3/yr). At the time of first imaging, 21.9% of tumors had calcifications, while 13.9% of meningiomas had PTBE. Of 137 tumors, 52 showed growth. Characteristics associated with tumor growth included PTBE (OR 9.12, 95% CI 1.48-56.4), tumor volume (per cm3) at first imaging (OR 0.91, 95% CI 0.83-0.99), and 10-year increased age at first imaging (OR 0.57, 95% CI 0.43-0.74). PTBE had the shortest median time to growth at 9.2 months., Conclusions: Although the majority of NF2-associated meningiomas do not grow in the short term, a wide range of growth patterns can be seen. Younger age at first imaging and presence of PTBE are associated with growth. Patients with these characteristics likely benefit from closer follow-up.

Copyright of Neurosurgical Review is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background/aim: Tumoral calcification after chemotherapy or radiation therapy has been reported in various cancer patients, but not after radioembolization. The purpose of this study was to evaluate the prognostic value of radioembolization-induced tumor calcification of hepatocellular carcinoma (HCC) treated by radioembolization., Patients and Methods: This retrospective study comprised patients with single nodular HCC who underwent yttrium-90 radioembolization between November 2015 and April 2019. The presence of tumoral calcification was visually assessed on a follow-up computed tomography (CT) scan., Results: Fifty-five patients (64.8±11.8 years, 43 men) were evaluated. Tumoral calcification was present in 21 (38.2%) of 55 patients in the one-month CT scan (calcification group). The complete response rate for the primary index tumor was 72.7% (40 of 55) in the total study population, and 100% (21 of 21) in the calcification group, respectively. The calcification group had a longer local progression-free survival rate than the non-calcification group (p=0.017)., Conclusion: Radioembolization-induced tumoral calcification is relatively common and can be used as an early surrogate marker of complete response., (Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)