Slow-growing Breast Research Articles

Removing the Breast from the Body, Cryoectomy or Cryopreservation of Tumors Preserve Breast Size, Reduce the Risk of Infection and Prevent Scarring

Unprecedented studies have shown that slow-growing breast cancers can be treated with highly targeted tumor cryopreservation technology without the need for surgery. Experiments show that this method is effective in women with low-risk breast cancer over the age of 60. Cryoablation is a solution that eliminates breast tumors safely, quickly and painlessly or without the need for surgery. Takes. This method exposes the patient's tissues to severe cold to remove them without the need for anesthesia in the clinic. The new study, which involved about 200 women, found that after eliminating low-risk breast cancer, patients were left without cancer for three years. This treatment can be used to treat cancers of the bone, kidney, prostate and other types. Unlike lumpectomy or mastectomy, which involves removing the breast from the body, cryoectomy or cryopreservation of tumors preserve breast size, reduce the risk of infection and prevent scarring, and allow patients to function normally quickly, the researchers said. Resume yourself. Keywords: Cancer; Cells; Tissues; Tumors; Prevention; Prognosis; Diagnosis; Imaging; Screening, Treatment; Management

Cryoablation and Cryolocalization in the Prevention, Prognosis, Diagnosis, Imaging, Screening, Treatment and Management of Breast Cancer

Unprecedented studies have shown that slow-growing breast cancers can be treated with highly targeted tumor cryopreservation technology without the need for surgery. Experiments show that this method is effective in women with low-risk breast cancer over the age of 60. Cryoablation is a solution that eliminates breast tumors safely, quickly and painlessly or without the need for surgery. Takes. This method exposes the patient's tissues to severe cold to remove them without the need for anesthesia in the clinic. The new study, which involved about 200 women, found that after eliminating low-risk breast cancer, patients were left without cancer for three years. This treatment can be used to treat cancers of the bone, kidney, prostate and other types. Unlike lumpectomy or mastectomy, which involves removing the breast from the body, cryoectomy or cryopreservation of tumors preserve breast size, reduce the risk of infection and prevent scarring, and allow patients to function normally quickly, the researchers said. Resume yourself. Keywords: Cancer; Cells; Tissues, Tumors; Prevention, Prognosis; Diagnosis; Imaging; Screening; Treatment; Management

Breast Hamartoma: Clinical, Radiological, and Histopathological Evaluation.

Breast hamartomas are rare, benign, and slow-growing breast tumors that can be definitively diagnosed by combining the results of clinical, radiological, and histopathological examination. This study aimed to evaluate the clinical, radiological, and histopathological features of hamartomas and summarize our clinical approach to hamartomas. Patients diagnosed with breast hamartoma between 2010 and 2020 in our clinic were retrospectively analyzed. Demographic information, clinical examination, radiological findings, histopathological features, changes during follow-up, and follow-up data were obtained and analyzed. Of the 1,429 patients operated on in our clinic for benign breast diseases between January 2010 and March 2020, 39 (2.7%) were diagnosed with breast hamartomas with histopathological examination. All patients were women with a median age of 37 (19-62) years. Most of the patients (64%) were in the premenopausal period. Radiological examinations were conducted using mammography (66%), breast ultrasonography (100%), and breast magnetic resonance imaging (48%). Biopsy was performed in 14 preoperative patients, and nine (64%) patients were diagnosed with hamartoma. All patients were operated on; 37 patients underwent a lumpectomy, and two had a mastectomy. No patients had hamartoma recurrence during an average follow-up period of 39 months. Hamartomas are similar to other benign breast pathologies. Definitive diagnosis can be achieved by combining the results of clinical, radiological, and histopathological examination. Given its similar composition to normal breast tissue, hamartoma has a low rate of malignancy. Definitive diagnosis and appropriate surgical treatment are required.

Cellular heterogeneity profiling by hyaluronan probes reveals an invasive but slow-growing breast tumor subset.

Tumor heterogeneity confounds cancer diagnosis and the outcome of therapy, necessitating analysis of tumor cell subsets within the tumor mass. Elevated expression of hyaluronan (HA) and HA receptors, receptor for HA-mediated motility (RHAMM)/HA-mediated motility receptor and cluster designation 44 (CD44), in breast tumors correlates with poor outcome. We hypothesized that a probe for detecting HA-HA receptor interactions may reveal breast cancer (BCa) cell heterogeneity relevant to tumor progression. A fluorescent HA (F-HA) probe containing a mixture of polymer sizes typical of tumor microenvironments (10-480 kDa), multiplexed profiling, and flow cytometry were used to monitor HA binding to BCa cell lines of different molecular subtypes. Formulae were developed to quantify binding heterogeneity and to measure invasion in vivo. Two subsets exhibiting differential binding (HA(-/low) vs. HA(high)) were isolated and characterized for morphology, growth, and invasion in culture and as xenografts in vivo. F-HA-binding amounts and degree of heterogeneity varied with BCa subtype, were highest in the malignant basal-like cell lines, and decreased upon reversion to a nonmalignant phenotype. Binding amounts correlated with CD44 and RHAMM displayed but binding heterogeneity appeared to arise from a differential ability of HA receptor-positive subpopulations to interact with F-HA. HA(high) subpopulations exhibited significantly higher local invasion and lung micrometastases but, unexpectedly, lower proliferation than either unsorted parental cells or the HA(-/low) subpopulation. Querying F-HA binding to aggressive tumor cells reveals a previously undetected form of heterogeneity that predicts invasive/metastatic behavior and that may aid both early identification of cancer patients susceptible to metastasis, and detection/therapy of invasive BCa subpopulations.

Time Course of Paclitaxel-Induced Apoptosis in an Experimental Model of Virus-Induced Breast Cancer

Early assessment of the efficacy of treatment is important in patients with breast cancer, whose routine adjuvant regimen frequently includes chemotherapy. Irrespective of the exact mechanisms involved in induction, the common early phenotypic marker of apoptosis is the expression on the outer cell membrane surface of phosphatidylserine, which avidly binds annexin V. (99m)Tc-labeled annexin V has been proposed for in vivo scintigraphic detection of apoptosis, albeit with contradicting results. This study was performed to define the time course of apoptosis induced by the chemotherapeutic agent paclitaxel in a model of virus-induced murine breast cancer. The RIII virus induces an estrogen-dependent, slow-growing breast cancer; BALB-c/cRIII female mice with breast tumors averaging 10 mm were studied, both in baseline conditions and at various times after the intravenous administration of paclitaxel (equivalent to a human dose of 20 mg/70 kg of body weight). The biodistribution of (99m)Tc-annexin V was evaluated at baseline and then at 1, 3, 6, and 24 h after paclitaxel administration. Apoptotic and antiapoptotic markers were also evaluated in tumor samples obtained at the same time points: DNA breaks (terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling [TUNEL]), active caspase-3, apoptosis-inducing factor, and Bcl-2 protein. Baseline uptake of (99m)Tc-annexin V in breast tumors was about 2-fold higher than the uptake in normal breast tissue (demonstrating some ongoing apoptosis); tracer uptake increased at 1 and 3 h after paclitaxel administration (to almost double the baseline value) and then declined to levels even lower than baseline. Although no activation of the apoptosis-inducing factor mechanism was detected, a peak in TUNEL-positive tumor cells was reached 3 h after paclitaxel administration (to more than 6-fold the baseline level). The antiapoptotic marker Bcl-2 exhibited a biphasic pattern, with a maximum drop at 3 h, followed by return toward baseline levels at 6 h. These results define the time course of various biologic events taking place in this model of murine breast cancer after a proapoptotic insult (single-dose paclitaxel). Although confirming that in vivo uptake of (99m)Tc-annexin V reflects the degree of apoptosis, the study also suggests that the apoptotic response to antitumor therapy may differ from tumor type to tumor type. Therefore, contradicting results previously reported may depend on an inadequate time window chosen for imaging with (99m)Tc-annexin V.

Influence of genotype and feeding on chemical composition of organic chicken meat

The aim of this study was to evaluate the effects of different genotypes and of feeding on meat chemical composition, including fatty acid profile, of chickens reared under organic conditions. Two meat–type fast-growing (FG) and medium-growing (MG), and one egg-type slow-growing (SG) strains were assigned to 2 different diets differing for the protein source: soybean (SB) and faba bean (FB) in partial substitution of soybean. Genotype markedly affected the meat chemical composition. SG breast and thigh meat showed lower content of lipids (P<0.01) than FG. The highest proportions of polyunsaturated fatty acids (PUFA) n-6 and n-3 and the lowest proportion of monounsaturated (MUFA) (P<0.01), as well as the lowest ratio of PUFA n6/n3 (P<0.01) were found in SG breast and thigh meat. MG showed always intermediate values. As for feeding, FB treatment produced only a slight increment of protein in breast and a decrease of fat and ash in thigh meat. Total PUFA and PUFA n-6 resulted lower in both thigh and breast meat of FB groups compared to SB (P<0.01).

11C] Acetoacetate Utilization by Breast and Prostate Tumors: a PET and Biodistribution Study in Mice

A significant positive correlation has been observed between ketone body availability and their uptake by tumor cells. Our objective was to evaluate [11C]acetoacetate as a potential tracer of ketone body utilization by breast and prostate tumors and to compare it with [11C]acetate. Biodistribution studies were performed with [11C]acetoacetate and [11C]acetate in mice bearing breast or prostate tumors. The percentage of the injected dose accumulated per gram of tissue was determined. These results were complemented by dynamic positron emission tomography (PET) imaging of the radiotracer uptake and dosimetry calculations. [11C]Acetoacetate uptake was optimal between 5 and 30 min, with maximal uptake of 2.72, 2.42, 2.54, and 2.19% injected dose (%ID)/g for MC7-L1, MC4-L2, PC3, and LN-CaP tumors respectively. Tumor retention for [11C]acetoacetate tended to be higher than [11C]acetate, but this did not reach statistical significance. [11C]Acetate uptake was reached within 15 min with optimal uptake of 1.25, 2.30, and 0.96%ID/g for MC7-L1, MC4-L2, and PC-3 tumors, respectively. We observed a moderate uptake of [11C]acetoacetate in breast and prostate tumors with low background activity due to rapid elimination of this tracer. Further studies are warranted to determine if this tracer can detect slow-growing breast and prostate cancers in the clinical setting.

A simple model of breast carcinoma growth may provide explanations for observations of apparently complex phenomena.

There has been great debate regarding the importance of ductal carcinoma in situ (DCIS) in the breast. Autopsy results that demonstrate a much greater number of these lesions compared with the number of invasive carcinomas, and the numbers of deaths from breast carcinoma each year have been cited as evidence that DCIS rarely leads to invasion and death. These analyses have overlooked the fact that, to sustain a rate of detection each year, there would have to be a reservoir of undetected breast carcinomas growing in the population. The authors developed a simple model that makes this clear. In addition, complex phenomena have been suggested to explain why invasive breast disease may grow more rapidly among very young women and more slowly among the very old. A simple model provides some insight that may simplify the explanation of these observations. The simple model of breast carcinoma growth assumes that there are three types of breast carcinoma that begin each year in a cohort of women. It assumes that all breast carcinomas begin as DCIS and take 9 years to go from a single cell to an invasive lesion for the slowest growing lesions, 6 years for intermediate growing DCIS lesions, and 3 years for fast-growing DCIS lesions. Furthermore, once an invasive clone forms, the model assumes that it will double in 60 days for fast-growing lesions, 120 days for intermediate growing lesions, and 180 days for slow-growing lesions. Three new tumors begin to grow in each successive year (one of each type). The model uses simple vectors that are defined by the size of the tumors and the time since tumor initiation, and it assumes that all tumors are detected when they reach 2 cm in greatest dimension. The model can be used to show graphically how many undetected tumors (DCIS as well as invasive carcinomas) there may be in the population to sustain the detection of three invasive tumors each year. Using the assumptions described above, the model showed that, by the time the first slow-growing breast carcinoma reaches 2 cm in greatest dimension, there will be 29 other slow-growing tumors that have not reached that size (9 DCIS and 20 smaller invasive carcinomas), 19 moderately growing tumors (6 DCIS and 13 smaller invasive carcinomas), and 9 fast-growing tumors (3 DCIS and 6 smaller invasive carcinomas). This means that, for every three breast tumors that reach 2 cm, the model predicted that there would be another 57 tumors (39 smaller invasive carcinomas and 18 DCIS) that would be undetected "below the surface". The model showed clearly that faster growing tumors would be expected to predominate among the youngest women, because they are the first to "reach the surface"; and, if the number of newly initiated tumors decreases with age, then there will be more of the slowest growing tumors that are left to reach the surface among the oldest women in the population. Even if the authors' assumptions are incorrect, their model made it clear that, to diagnose several breast carcinomas per 1000 women each year means that there have to be many more undetected carcinomas in the population to sustain the rate of detection. Although the model did not prove that DCIS may become potentially invasive and lethal, it did demonstrate that, even if all of these in situ lesions become invasive and lethal, many more DCIS lesions would have to be expected in the population than the number of invasive carcinomas detected each year and the number of deaths from breast carcinoma each year. Furthermore, the model provided a simple, purely mechanical illustration that may explain the preponderance of faster growing breast carcinomas among very young women and the preponderance of slower growing tumors among elderly women.