Correlation between vitamin D deficiency and metastatic breast carcinoma in a predominantly Hispanic population: A retrospective study.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e12553-e12553
Author(s):  
Saurabh Deepak Chitnis ◽  
Andrea M. Popescu-Martinez
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Metastatic Breast Cancer ◽  
Relative Risk ◽  
Vitamin D Deficiency ◽  
Active Form ◽  
Metastatic Breast ◽  
Breast Cancer Cell Lines ◽  
Vitamin D Levels

e12553 Background: There have been numerous studies conducted linking Vitamin D deficiency to various cancers, including cancers of the breast. Studies associating Vitamin D deficiency and Breast cancer have shown mixed results in patients with no clear consensus. Recently published in vitro studies have shown that the active form of Vitamin D can inhibit the metastatic capability of breast cancer cell lines to bone. Based on this we aimed to elucidate whether there exists any correlation between Vitamin D deficiency at diagnosis and Metastatic breast cancer. Methods: Retrospective analysis of the EMR for women diagnosed with breast cancer and enrolled in Oncology database seen at NYMC-Metropolitan Hospital Center from 2010-2016 was done. Patients were grouped into either breast cancer with metastases or without metastases and their Vitamin D levels at diagnosis were reviewed. Patients with 25- Hydroxy Vitamin D levels measured within one year of diagnosis of breast cancer were included for the study. Study was planned from 2010-2016 specifically as Vitamin D levels for patients were not monitored as frequently prior to 2010. Results: From total of 102 patients who started follow up with Oncology clinic during the study time period, 2 were referred to our center for further management with diagnosis made prior to 2010 and were not included in the study. Out of the 100 patients considered, 58 patients had Vitamin D levels measured within a year of diagnosis of breast cancer and were included in the study. 70% of the population was Latino/Hispanic. The table represents the results of the study. Odds ratio for a patient with Vit D deficiency to develop metastatic breast cancer was 0.92 and relative risk was calculated to be 0.93. Conclusions: Based on above results, the outcome was similar in both groups. The odd’s ratio and the relative risk imply that there was no difference evidenced between both groups. These findings signify that there was no direct correlation between Metastatic breast cancer and Vitamin D deficiency at time of diagnosis in the population seen at our center. [Table: see text]

Hypocalcemia induced by bisphophonates in cancer patients with vitamin D deficiency

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 19644-19644
Author(s):  
C. F. Yazbeck ◽  
A. M. Gonzalez-Angulo ◽  
S. A. Shaw ◽  
S. G. Waguespack ◽  
R. Vassilopoulou-Sellin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Metastatic Breast Cancer ◽  
Vitamin D Deficiency ◽  
Cancer Patients ◽  
Metastatic Breast ◽  
Zolendronic Acid ◽  
Vitamin D Levels ◽  
Symptomatic Hypocalcemia ◽  
Normal Albumin

19644 Background: The use of bisphosphonates for treatment of hypercalcemia, bone pain and reduction of skeletal morbidity in metastatic breast cancer is increasing. Moreover, vitamin D deficiency is commonly associated with cancer. Hypocalcemia has been reported following IV bisphosphonate use. Methods: We present the clinical and lab findings in 6 cases of bisphosphonate-induced hypocalcemia, caused by unmasked vitamin D deficiency. Results: Our 1st patient was diagnosed with breast cancer and developed metastases 6yrs later. She was given Zolendronic acid 4 mg IV with a baseline calcium level (Ca) of 9.7 mg/dl, normal albumin, and elevated alkaline phosphatase. 3 days later, she developed symptomatic severe hypocalcemia with tetany: Ca dropped to 6.1 mg/dl with recovery. After her 2nd dose of Zolendronic acid, Ca dropped again to 6 mg/dl with normal albumin, intact parathyroid hormone (PTH) of 637 pg/ml (range 10–65) and 25-hydroxy vitamin D levels (25-OHD) of 4 ng/ml (range 20–100). Our 2nd patient presented with metastatic breast cancer and was treated with Zolendronic acid for hypercalcemia with a baseline Ca of 13 mg/dl, PTH-related protein of 2.8 pmol/l (range <1.8) and PTH of 7 pg/ml. She then developed hypocalcemia with corrected Ca of 7.7 mg/dl and 25-OHD of 13 ng/ml. Our 3rd patient with breast cancer was also treated with Zolendronic acid for bone metastases and hypercalcemia. She then presented with symptomatic hypocalcemia: ionized Ca level of 1.09 mmol/l (range 1.13–1.32), PTH of 211 pg/ml and 25-OHD of 13 ng/ml. Our other 3 cases had similar presentations to the above and will be discussed in detail. All 6 cases were treated with ergocalciferol and long-term oral calcium and vitamin D therapy. All of our cases presented with symptomatic hypocalcemia with vitamin D levels less than 30ng/mL. Conclusions: Since bisphosphonate use is increasing in cancer patients and vitamin D deficiency is not an uncommon finding in this population, consideration should be given to routine checking of 25-OHD levels before initiating treatment with bisphosphonates and supplementing with calcium and vitamin D when necessary (<30ng/mL). This could potentially prevent further morbidity. Further prospective studies would be needed for early replacement with vitamin D and calcium in those with vitamin D deficiency. No significant financial relationships to disclose.

Associations Between Cholecalciferol Supplementation and Self-Reported Symptoms Among Women With Metastatic Breast Cancer and Vitamin D Deficiency: A Pilot Study

2021 ◽  
Vol 48 (3) ◽  
pp. 352-360
Author(s):  
Patricia Maureen Sheean ◽  
Patricia Robinson ◽  
Mary Beth Bartolotta ◽  
Cara Joyce ◽  
William Adams ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Metastatic Breast Cancer ◽  
Pilot Study ◽  
Vitamin D Deficiency ◽  
Metastatic Breast ◽  
Cholecalciferol Supplementation

An in vitro hyaluronic acid hydrogel based platform to model dormancy in brain metastatic breast cancer cells

2020 ◽  
Vol 107 ◽  
pp. 65-77 ◽  
Author(s):  
Akshay A. Narkhede ◽  
James H. Crenshaw ◽  
David K. Crossman ◽  
Lalita A. Shevde ◽  
Shreyas S. Rao
Keyword(s):  
Breast Cancer ◽  
Hyaluronic Acid ◽  
Metastatic Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Metastatic Breast ◽  
Hyaluronic Acid Hydrogel

Rapid in vitro assay for predicting response to fluorouracil in patients with metastatic breast cancer.

1995 ◽  
Vol 13 (2) ◽  
pp. 419-423 ◽  
Author(s):  
R M Elledge ◽  
G M Clark ◽  
J Hon ◽  
M Thant ◽  
R Belt ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Clinical Response ◽  
Tumor Cells ◽  
Predictive Value ◽  
Metastatic Breast ◽  
In Vitro Assay ◽  
Vitro Assay ◽  
Biopsy Specimens

PURPOSE To determine if a rapid 3H-uridine uptake assay using breast tumor cells from biopsy specimens could predict clinical response to fluorouracil (5FU) in patients with metastatic breast cancer. PATIENTS AND METHODS A double-blind prospective study was conducted of 60 patients with measurable, metastatic breast cancer who had failed to respond to at least one prior chemotherapy regimen. Patients received 5FU 300 mg/m2/d by continuous infusion and were monitored for response. Tumor cells from biopsy specimens were grown in microwells and exposed for 3 days to 0.1, 1.0, 10.0, and 100.00 micrograms/mL of 5FU on strips coated with drug and extracellular matrix. Cells were pulsed with 3H-uridine overnight. Incorporated radioactivity was compared for wells with and without drug. Results were available 4 days from specimen submission. RESULTS Of 45 eligible patients, 11 (24%) were not assessable in vitro. Nine patients were assessable in vitro, but not clinically. Of the remaining 25 patients, who were assessable both clinically and in vitro, there was one complete response (CR), five partial responses (PRs), five cases of stable disease, and 14 cases of progressive disease, for an objective response rate of 24%. Response in vitro was significantly correlated with clinical response (P = .002). Of six clinical responders, five also responded in vitro, for an assay sensitivity of 83%. Of 19 nonresponders, 17 were nonresponders in vitro, for a specificity of 89%. The positive predictive value of the test was 71% (five of seven), and the negative predictive value was 94% (17 of 18). CONCLUSION Results of an in vitro assay were significantly correlated with clinical response in patients with metastatic breast cancer treated with continuous infusion 5FU.

scholarly journals High concentration calcitriol induces endoplasmic reticulum stress related gene profile in breast cancer cells

2017 ◽  
Vol 95 (2) ◽  
pp. 289-294 ◽  
Author(s):  
Ali Burak Ozkaya ◽  
Handan Ak ◽  
Hikmet Hakan Aydin
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Survival Function ◽  
Active Form ◽  
Breast Cancer Cell Lines ◽  
Transcriptomic Profile

Calcitriol, the active form of vitamin D, is known for its anticancer properties including induction of apoptosis as well as the inhibition of angiogenesis and metastasis. Understanding the mechanisms of action for calcitriol will help with the development of novel treatment strategies. Since vitamin D exerts its cellular actions via binding to its receptor and by altering expressions of a set of genes, we aimed to evaluate the effect of calcitriol on transcriptomic profile of breast cancer cells. We previously demonstrated that calcitriol alters endoplasmic reticulum (ER) stress markers, therefore in this study we have focused on ER-stress-related genes to reveal calcitriols action on these genes in particular. We have treated breast cancer cell lines MCF-7 and MDA-MB-231 with previously determined IC50 concentrations of calcitriol and evaluated the transcriptomic alterations via microarray. During analysis, only genes altered by at least 2-fold with a P value < 0.05 were taken into consideration. Our findings revealed an ER-stress-associated transcriptomic profile induced by calcitriol. Induced genes include genes with a pro-survival function (NUPR1, DNAJB9, HMOX1, LCN2, and LAMP3) and with a pro-death function (CHOP (DDIT3), DDIT4, NDGR1, NOXA, and CLGN). These results suggest that calcitriol induces an ER-stress-like response inducing both pro-survival and pro-death transcripts in the process.

Reversal of the glycolytic phenotype by dichloroacetate inhibits metastatic breast cancer cell growth in vitro and in vivo

2009 ◽  
Vol 120 (1) ◽  
pp. 253-260 ◽  
Author(s):  
Ramon C. Sun ◽  
Mitali Fadia ◽  
Jane E. Dahlstrom ◽  
Christopher R. Parish ◽  
Philip G. Board ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Metastatic Breast ◽  
Cancer Cell Growth ◽  
Breast Cancer Cell Growth

Phase I crossover study of paclitaxel with r-verapamil in patients with metastatic breast cancer.

1996 ◽  
Vol 14 (4) ◽  
pp. 1173-1184 ◽  
Author(s):  
A W Tolcher ◽  
K H Cowan ◽  
D Solomon ◽  
F Ognibene ◽  
B Goldspiel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Phase I ◽  
Crossover Study ◽  
Cardiac Toxicity ◽  
Metastatic Breast ◽  
Pharmacokinetic Analysis ◽  
Hematologic Toxicity ◽  
Outpatient Therapy

PURPOSE We conducted a phase I crossover study of escalating doses of both paclitaxel (Taxol; Bristol-Myers, Squibb, Princeton, NJ) and r-verapamil, the less cardiotoxic stereoisomer, in heavily pretreated patients with metastatic breast cancer. PATIENTS AND METHODS Twenty-nine patients refractory to paclitaxel by 3-hour infusion were treated orally with r-verapamil every 4 hours starting 24 hours before the same-dose 3-hour paclitaxel infusion and continuing for a total of 12 doses. Once the maximum-tolerated dose (MTD) of the combination was determined, seven additional patients who had not been treated with either drug were evaluated to determine whether the addition of r-verapamil altered the pharmacokinetics of paclitaxel. Consenting patients had tumor biopsies for P-glycoprotein (Pgp) expression before receiving paclitaxel and after becoming refractory to paclitaxel therapy. RESULTS The MTD of the combination was 225 mg/m2 of r-verapamil every 4 hours with paclitaxel 200 mg/m2 by 3-hour infusion. Dose-limiting hypotension and bradycardia were observed in three of five patients treated at 250 mg/m2 r-verapamil. Fourteen patients received 32 cycles of r-verapamil at the MTD as outpatient therapy without developing cardiac toxicity. The median peak and trough serum verapamil concentrations at the MTD were 5.1 micromol/L (range, 1.9 to 6.3), respectively, which are within the range necessary for in vitro modulation of Pgp-mediated multidrug resistance (MDR). Increased serum verapamil concentrations and cardiac toxicity were observed more frequently in patients with elevated hepatic transaminases and bilirubin levels. Hematologic toxicity from combined paclitaxel and r-verapamil was significantly worse compared with the previous cycle of paclitxel without r-verapamil. In the pharmacokinetic analysis, r-verapamil delayed mean paclitaxel clearance and increased mean peak paclitaxel concentrations. CONCLUSION r-Verapamil at 225 mg/m2 orally every 4 hours can be given safely with paclitaxel 200 mg/m2 by 3-hour infusion as outpatient therapy and is associated with serum levels considered active for Pgp inhibition. The addition of r-verapamil significantly alters the toxicity and pharmacokinetics of paclitaxel.

scholarly journals ADAM22/LGI1 complex as a new actionable target for breast cancer brain metastasis

BMC Medicine ◽  
2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Sara Charmsaz ◽  
Ben Doherty ◽  
Sinéad Cocchiglia ◽  
Damir Varešlija ◽  
Attilio Marino ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Brain Metastasis ◽  
In Silico ◽  
Ex Vivo ◽  
Metastatic Breast ◽  
Peptide Mimetic ◽  
Breast Cancer Brain Metastasis

Abstract Background Metastatic breast cancer is a major cause of cancer-related deaths in woman. Brain metastasis is a common and devastating site of relapse for several breast cancer molecular subtypes, including oestrogen receptor-positive disease, with life expectancy of less than a year. While efforts have been devoted to developing therapeutics for extra-cranial metastasis, drug penetration of blood–brain barrier (BBB) remains a major clinical challenge. Defining molecular alterations in breast cancer brain metastasis enables the identification of novel actionable targets. Methods Global transcriptomic analysis of matched primary and metastatic patient tumours (n = 35 patients, 70 tumour samples) identified a putative new actionable target for advanced breast cancer which was further validated in vivo and in breast cancer patient tumour tissue (n = 843 patients). A peptide mimetic of the target’s natural ligand was designed in silico and its efficacy assessed in in vitro, ex vivo and in vivo models of breast cancer metastasis. Results Bioinformatic analysis of over-represented pathways in metastatic breast cancer identified ADAM22 as a top ranked member of the ECM-related druggable genome specific to brain metastases. ADAM22 was validated as an actionable target in in vitro, ex vivo and in patient tumour tissue (n = 843 patients). A peptide mimetic of the ADAM22 ligand LGI1, LGI1MIM, was designed in silico. The efficacy of LGI1MIM and its ability to penetrate the BBB were assessed in vitro, ex vivo and in brain metastasis BBB 3D biometric biohybrid models, respectively. Treatment with LGI1MIM in vivo inhibited disease progression, in particular the development of brain metastasis. Conclusion ADAM22 expression in advanced breast cancer supports development of breast cancer brain metastasis. Targeting ADAM22 with a peptide mimetic LGI1MIM represents a new therapeutic option to treat metastatic brain disease.

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