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The purpose of this work is to develop a medical system that optimizes the sensitivity of the bone scintigraphy in the diagnosis to patients with bone cancer problems, bone disease, infections, bone wear, or malignancies like bone metastasis which will monitor the deterioration of the bones caused by the disease in case. In this work the sensitivity of bone scintigraphy was improved to help in their interpretation and therefore we aid in the radiological digitization, which consists of a process that allows to obtain a digitalized image from an analogue image. Which means it is susceptible to being stored in the form of a number representing the position of a pixel point, elementary surface unit. This can be done using the means of digitization and digital image processing (PDI), in addition to the enhancement tools offered by various processes, a greater sensitivity is projected in the radiological images, to evaluate the results potential gain in the diagnostic probability offered by this digitization process. The picture formats that can be used are JPG, BMP or DICOM. To have an improvement in the radiological diagnostic sensitivity, a conversion of a grayscale image to the color map in RGB (Red, Green and Blue) must be done, representing the values of the pixels of the grayscale image as follows: (1) The lowest values will be displayed in shades of blue, (2) Intermediate values are represented in shades of green, and (3) The lowest values will be displayed in shades of red. When using this color map, the image will be different tones by the combination of the above-mentioned colors.

Objectives. We present an extremely rare case of breast cancer with metastasis to the bone marrow, which was also simultaneously diagnosed with chronic lymphocytic leukemia (CLL). Case Presentation. A 56-year-old female with a history of routine blood transfusions presented with chronic fatigue and recurrent right upper quadrant abdominal pain due to cholecystitis. Additionally, nodules were palpable in both breasts, which were subsequently detected as suspicious calcified lesions on ultrasound. Leukocytosis and bi-cytopenia were found. Cholecystectomy was performed and biopsies from some tissues were conducted. Gall bladder and subcutaneous tissue from the umbilical area showed neoplastic cells suggestive of breast carcinoma. Bone marrow biopsy showed CLL and non-hematopoietic cells identical to the previously detected neoplastic cells. Immunohistochemistry revealed that the breast carcinoma was ER-positive, PR-positive, and HER2negative. Outcome. After a thorough investigation, the bone marrow depression was proven to result from a metastatic bone marrow lesion from breast cancer diagnosed concurrently with CLL. Conclusions. This circumstance obliged clinicians to be more considerate of the diagnostic approach and treatment of patients with neoplasm presenting with cytopenia. It is to avoid underdiagnosis and ensure that every pathology in the bone marrow is investigated and managed accordingly.

Background: Breast cancer is one of the most common gynecologic malignancies in women and the main cause of death in 25% of all cases. The main cause of death from breast cancer is metastases, it is estimated that 5-10% of breast cancers have metastasized at the time of early diagnosis with an advanced stage. Purpose: To analyze the risk factors that influence the incidence of metastases in patients with advanced breast cancer. Methods: This study is an analytic observational study with a cross-sectional design, the number of samples in the study was 120 patients. The inclusion criteria of the study sample were breast cancer patients with advanced stages III and IV in the last five years. Exclusion criteria were incomplete patient medical records. The sampling technique in this study was consecutive sampling. This research was conducted at Ibnu Sina Hospital, Makassar City. The variables analyzed in this study were type 2 diabetes mellitus, anemia, and hypertension which were tested with the chi-square test. Results: The results of this study showed that diabetes mellitus type 2 (p=0.00; Prevalence Rate [PR]=1.79; 95% CI=1.32-2.42) and anemia (p=0.03; Prevalence Rate [PR] = 1.82; 95% CI = 1.61-2.86) is a risk factor that affects the incidence of metastases in patients with advanced breast cancer. While the risk factor that has no effect is hypertension. Conclusion: Type 2 diabetes mellitus and anemia are risk factors that influence the incidence of metastases in breast cancer patients.

Objectives. We present an extremely rare case of breast cancer with metastasis to the bone marrow, which was also simultaneously diagnosed with chronic lymphocytic leukemia (CLL). Case Presentation. A 56-year-old female with a history of routine blood transfusions presented with chronic fatigue and recurrent right upper quadrant abdominal pain due to cholecystitis. Additionally, nodules were palpable in both breasts, which were subsequently detected as suspicious calcified lesions on ultrasound. Leukocytosis and bi-cytopenia were found. Cholecystectomy was performed and biopsies from some tissues were conducted. Gall bladder and subcutaneous tissue from the umbilical area showed neoplastic cells suggestive of breast carcinoma. Bone marrow biopsy showed CLL and non-hematopoietic cells identical to the previously detected neoplastic cells. Immunohistochemistry revealed that the breast carcinoma was ER-positive, PR-positive, and HER2negative. Outcome. After a thorough investigation, the bone marrow depression was proven to result from a metastatic bone marrow lesion from breast cancer diagnosed concurrently with CLL. Conclusions. This circumstance obliged clinicians to be more considerate of the diagnostic approach and treatment of patients with neoplasm presenting with cytopenia. It is to avoid underdiagnosis and ensure that every pathology in the bone marrow is investigated and managed accordingly. [ABSTRACT FROM AUTHOR]

The incidence of secondary neoplasms of the testis has been reported at 0.02%–2.5%. The testis is a rare metastasis site for prostatic adenocarcinoma. A 62-year-old gentleman presented with neck swelling and testicular swelling. On evaluation, he was found to have metastatic carcinoma of prostate on 68-Gallium prostate-specific membrane antigen study with disseminated metastasis along with right testicular metastases. The patient underwent bilateral orchidectomy as part of the hormonal treatment, and the histopathological examination revealed the metastatic deposits on both the testis with the left testis showing only micrometastasis. Only few cases of bilateral testes metastases from the prostatic carcinoma are reported in the literature.

We report here a color-coded imaging model in which metastatic niches in the lung and liver of breast cancer can be identified. The transgenic green fluorescent protein (GFP)-expressing nude mouse was used as the host. The GFP nude mouse expresses GFP in all organs. However, GFP expression is dim in the liver parenchymal cells. Mouse mammary tumor cells (MMT 060562) (MMT), expressing red fluorescent protein (RFP), were injected in the tail vein of GFP nude mice to produce experimental lung metastasis and in the spleen of GFP nude mice to establish a liver metastasis model. Niche formation in the lung and liver metastasis was observed using very high resolution imaging systems. In the lung, GFP host-mouse cells accumulated around as few as a single MMT-RFP cell. In addition, GFP host cells were observed to form circle-shaped niches in the lung even without RFP cancer cells, which was possibly a niche in which future metastasis could be formed. In the liver, as with the lung, GFP host cells could form circle-shaped niches. Liver and lung metastases were removed surgically and cultured in vitro. MMT-RFP cells and GFP host cells resembling cancer-associated fibroblasts (CAFs) were observed interacting, suggesting that CAFs could serve as a metastatic niche.

The incidence of secondary neoplasms of the testis has been reported at 0.02%–2.5%. The testis is a rare metastasis site for prostatic adenocarcinoma. A 62-year-old gentleman presented with neck swelling and testicular swelling. On evaluation, he was found to have metastatic carcinoma of prostate on 68-Gallium prostate-specific membrane antigen study with disseminated metastasis along with right testicular metastases. The patient underwent bilateral orchidectomy as part of the hormonal treatment, and the histopathological examination revealed the metastatic deposits on both the testis with the left testis showing only micrometastasis. Only few cases of bilateral testes metastases from the prostatic carcinoma are reported in the literature. [ABSTRACT FROM AUTHOR]

A 61-year-old man presented to the oncology clinic with Gleason 9 (4 + 5) prostate cancer. Staging CT showed multiple nodules in both lungs. Since the lung lesions were too small for biopsy, he was started on anti-androgen therapy for suspected metastatic, hormone-sensitive prostate cancer. While his prostate-specific antigen decreased from 32 to <0.1 ng/ml, the multiple lung lesions showed no response on subsequent imaging. The patient presented during follow-up with severe right leg pain, at which time magnetic resonance imaging revealed a large, hyperintense mass in the femur. The mass was resected along with two lung nodules, with pathology demonstrating metastatic alveolar soft part sarcoma. This serves as an important reminder that lesions suspicious for metastases may be due to cancers of multiple primary origins, particularly if the pattern of metastasis is atypical or there is varied response to therapy. [ABSTRACT FROM AUTHOR]

Benign Metastasizing Leiomyoma (BML) is a rare disease which represents with multiple leiomyomatous lesions in many tissues and organs especially in lungs. These patients have been operated for leiomyoma of the uterus. Here we report a case of a 41-year-old woman who was evaluated in a thoracic surgery hospital for dyspnea and bilateral nodules in chest roentgenogram. She had no history of neoplasm, only myomectomy history of uterine leiomyoma 10 years ago. Biopsy and histopathological examination were consistent with pulmonary leiomyoma. The patient was reffered to our clinic and we performed a total abdominal hysterectomy for her multiple uterine leiomyomas. The final diagnosis was ‘benign pulmonary metastasizing leiomyoma’. After this diagnosis, surgical castration was performed but two years later, repeat imaging showed progression in pulmonary lesions and progesterone therapy was administered to the patient. Patient has continued on this hormonal therapy to date and during the 5-years follow-up, the persisting lesions in both lungs regressed.

Neutrophils are being increasingly recognized as an important element in tumor progression. They have been shown to exert important effects at nearly every stage of tumor progression with a number of studies demonstrating that their presence is critical to tumor development. Novel aspects of neutrophil biology have recently been elucidated and its contribution to tumorigenesis is only beginning to be appreciated. Neutrophil extracellular traps (NETs) are neutrophil-derived structures composed of DNA decorated with antimicrobial peptides. They have been shown to trap and kill microorganisms, playing a critical role in host defense. However, their contribution to tumor development and metastasis has recently been demonstrated in a number of studies highlighting NETs as a potentially important therapeutic target. Here, studies implicating NETs as facilitators of tumor progression and metastasis are reviewed. In addition, potential mechanisms by which NETs may exert these effects are explored. Finally, the ability to target NETs therapeutically in human neoplastic disease is highlighted. [ABSTRACT FROM AUTHOR]

Complex carbohydrates, which are major components of the cell membrane, perform important functions in cell-cell and cell-extracellular matrix interactions, as well as in signal transduction. They comprise three kinds of biomolecules: glycoproteins, proteoglycans and glycosphingolipids. Recent studies have also shown that glycan changes in malignant cells take a variety of forms and mediate key pathophysiological events during the various stages of tumour progression. Glycosylation changes are universal hallmarks of malignant transformation and tumour progression in human cancer, which take place on the whole cells or some specific molecules. Accordingly, those changes make them prominent candidates for cancer biomarkers in the meantime. This review mainly focuses on the correlation between glycosylation and the metastasis potential of tumour cells from comprehensive aspects to further address the vital roles of glycans in oncogenesising. Moreover, utilizing these glycosylation changes to ward off tumour metastasis by means of anti-adhesion approach or devising anti-cancer vaccine is one of promising targets of future study. [ABSTRACT FROM AUTHOR]

Benign Metastasizing Leiomyoma (BML) is a rare disease which represents with multiple leiomyomatous lesions in many tissues and organs especially in lungs. These patients have been operated for leiomyoma of the uterus. Here we report a case of a 41-year-old woman who was evaluated in a thoracic surgery hospital for dyspnea and bilateral nodules in chest roentgenogram. She had no history of neoplasm, only myomectomy history of uterine leiomyoma 10 years ago. Biopsy and histopathological examination were consistent with pulmonary leiomyoma. The patient was reffered to our clinic and we performed a total abdominal hysterectomy for her multiple uterine leiomyomas. The final diagnosis was 'benign pulmonary metastasizing leiomyoma'. After this diagnosis, surgical castration was performed but two years later, repeat imaging showed progression in pulmonary lesions and progesterone therapy was administered to the patient. Patient has continued on this hormonal therapy to date and during the 5-years follow-up, the persisting lesions in both lungs regressed. [ABSTRACT FROM AUTHOR]

Although cancer of the prostate (CaP) is the most commonly occurring cancer in males, there are major limitations in its diagnosis and long-term cure. Consequently, understanding the molecular mechanisms involved in the progression of CaP is of particular importance for production of pharmacological and biological agents to manage the disease. The development of the normal prostate is regulated by stromal–epithelial interactions via endocrine and paracrine factors, such as androgens and growth factors, which act as precise homeostatic regulators of cellular proliferation. Importantly, after a period of hormonal therapy, CaP shifts from an androgen-dependent to an androgen-independent state with a concomitant switch from paracrine to autocrine growth factor stimulation and subsequent upregulation of growth factor expression. Thus, growth factors and their receptors have a pivotal role in CaP. This is emphasized by current evidence obtained from clinical specimens as well as several in vitro and in vivo models strongly suggesting that epidermal growth factor and the neurotrophins (nerve growth factor, brain derived neurotrophin factor, neurotrophin-3 and neurotrophin-4/5) together with their tyrosine kinase receptors could play a very significant role in CaP progression. [Copyright &y& Elsevier]

Metastasis remains one of the major challenges before hepatocellular carcinoma (HCC) is finally conquered. This paper summarized a decade's studies on HCC metastasis at the Liver Cancer Institute of Fudan University. We have established a stepwise metastatic human HCC model system, which included a metastatic HCC model in nude mice (LCI-D20), a HCC cell line with high metastatic potential (MHCC97), a relatively low metastatic potential cell clone (MHCC97L) and several stepwise high metastatic potential cell clones (MHCC97H, HCCLM3, and HCCLM6) from their parent MHCC97 cell. Endeavors have been made for searching human HCC metastasis-related chromosomes/ proteins/genes. Monogene-based studies revealed that HCC invasion/metastasis was similar to that of other solid tumors, and the biological characteristics of small HCC were only slightly better than that of large HCC. Using comparative genomic hybridization (CGH), fluorescence in situ hybridization (FISH), genotyping, cDNA microarray, and 2-dimensional gel electrophoresis, we obtained some interesting results. In particular, in collaboration with the National Institute of Health (NIH) in the United States, we generated a molecular signature that can classify metastatic HCC patients, identified osteopontin as a lead gene in the signature, and found that genes favoring metastasis progression were initiated in the primary tumors. We also found that chromosome 8p deletion, particularly in the region of 8p23, was associated with HCC metastasis. Cytokeratin 19 was identified as one of the proteins, which was found in MHCC97H, but not in MHCC97L cells. Experimental interventions using the high metastatic nude mice model have provided clues for the prevention of HCC metastasis. Translation from workbench to bedside demonstrated that serum VEGF, microvessel density, and p53 scoring may be of value for the prediction of postoperative metastatic recurrence. Interferon alpha proved effective for the prevention of recurrence both experimentally and clinically. In conclusion, HCC metastasis that probably initiated in the primary tumor is a multigene-involved, multistep, and changing process. The further elucidation of the mechanism underlying HCC metastasis will provide a more solid basis for the prediction and prevention of the metastatic recurrence of HCC. [ABSTRACT FROM AUTHOR]

Rho GTPases are signaling molecules known to control cell motility. Several recent studies have suggested a role for Rho proteins in mediating tumor metastasis independent of their affects on cell proliferation. As Rho proteins require post-translational modification with a geranlygeranyl moiety for full activity, we tested the affect of blocking geranylation on localization, downstream signaling, and stimulation of invasion. Expression of a constitutively active Rho construct in A375 melanoma cells dramatically stimulated invasion through Matrigel membranes; however, a constitutively active RhoA mutated so that it cannot be geranylated, failed to stimulate invasion. Moreover, expression of epitope or GFP tagged modifications of this nongeranylatable constitutively active Rho demonstrated that geranylation is necessary for correct cellular localization of Rho. Geranylation was also found to be necessary for full downstream activation of serum response factor mediated transcription. Pharmacologic inhibition of Rho geranylation produced similar inhibition of Rho localization, signaling, and invasion. Our results suggest that inhibition of Rho geranylation may be an attractive pharmacologic target for inhibiting melanoma metastasis. [ABSTRACT FROM AUTHOR]

The management of wound complications following metastatic spine tumor surgery (MSTS) remains a formidable task. Plastic coverage procedures after MSTS are challenging due to unhealthy donor sites following previous radiotherapy and prolonged nonambulation. Negative pressure wound therapy (NPWT) is usually not recommended after MSTS due to fear of tumor seeding and excessive blood loss. However, in certain patients post-MSTS, who may be considered as receiving palliative treatment, NPWT can be effective in managing wound complications. We describe our initial experience with the use of NPWT in a 57-year-old lady diagnosed with multiple lumbar and cervicothoracic vertebral metastases secondary to non-small cell lung carcinoma. She underwent 2 cycles of preoperative radiotherapy followed by decompression and posterior instrumentation of lumbosacral and cervicothoracic regions succeeded by another cycle of radiotherapy. The patient developed wound dehiscence and poly-microbial surgical site infection that was not responsive to regular debridements and antibiotics. Hence, we applied NPWT as an alternative treatment to plastic surgical procedures. The patient clinically improved with a reduced quantity of wound discharge, increased granulation tissue, and a downward trend in the inflammatory markers. Subsequently, wound was secondarily closed after 14 days. The patient was discharged after a total hospital stay of 41 days. The intravenous antibiotics (piperacillin/tazobactam) were changed to oral (ciprofloxacin) after 6 weeks and continued for 4 months. The patient survived for 3 years without any wound complications. Our case report suggests that NPWT can be a potential treatment option for managing wound complications following MSTS., Competing Interests: Disclosures and COI: The authors received no funding for this study and report no conflicts of interest., (©International Society for the Advancement of Spine Surgery 2019.)

The article presents the medical case of a 76-year-old asymptomatic woman with small bowel carcinoid. The patient's medical history is described. The article points out the possibility that the patient could develop malignant carcinoid syndrome in the future. It suggests that inoperable metastatic disease may be treated by hepatic artery ligation or hyperthermic liver perfusion.

While chemotherapy strongly restricts or reverses tumor growth, the response of host tissue to therapy can counteract its anti-tumor activity by promoting tumor re-growth and/or metastases, thus limiting therapeutic efficacy. Here, we show that vascular endothelial growth factor receptor 3 (VEGFR3)-expressing macrophages infiltrating chemotherapy-treated tumors play a significant role in metastasis. They do so in part by inducing lymphangiogenesis as a result of cathepsin release, leading to VEGF-C upregulation by heparanase. We found that macrophages from chemotherapy-treated mice are sufficient to trigger lymphatic vessel activity and structure in naive tumors in a VEGFR3-dependent manner. Blocking VEGF-C/VEGFR3 axis inhibits the activity of chemotherapy-educated macrophages, leading to reduced lymphangiogenesis in treated tumors. Overall, our results suggest that disrupting the VEGF-C/VEGFR3 axis not only directly inhibits lymphangiogenesis but also blocks the pro-metastatic activity of macrophages in chemotherapy-treated mice., (Copyright © 2016 The Author(s). Published by Elsevier Inc. All rights reserved.)