[32] The peak age of Wilms' tumor is 3 to 4 years and most cases occur before the age of 10 years. This first-of-its-kind assistance program is designed for caregivers of a child or adult diagnosed with a rare disorder. 19-65 years. Also, a stage V tumor is not necessarily worse than, but nevertheless comparable in prognosis to a stage IV tumor. 10.1038/nature04632. 2018;233(4):2882-2888. Matthay KK, Seeger RC, Brodeur GM, Maris JM. https://rarediseases.org/living-with-a-rare-disease/find-clinical-trials/, For information about clinical trials sponsored by private sources, contact: The FLI protein controls the growth and development of some cell types by regulating the transcription of certain genes. Sometimes these gene changes are passed on from a parent to a child, but most Wilms tumors dont seem to be caused by inherited gene mutations. No involvement of extrarenal or renal sinus lymph-vascular spaces. About 20 percent of cases of Beckwith-Wiedemann syndrome are caused by a genetic change known as paternal uniparental disomy (UPD). In almost all affected people, the deletion includes the tip of chromosome 11. 2012;59(1):247-67. When tumor suppressor genes are deleted, cancer can occur. Before phenotype: case report and review of the literature. People normally inherit one copy of chromosome 11 from each parent. Current Management for Pediatric Urologic Oncology. Expert Rev Mol Med. The American Cancer Society medical and editorial content team. Research shows early detection leads to improved outcomes, because cancers are often smaller and easier to remove surgically. In addition to cancer surveillance, patients with WT1-related Wilms tumor syndromes may require multidisciplinary care provided by pediatric subspecialists: Children should also continue to have regular check-ups by their physicians. The genes are located close together in a region designated 11p15.5 near one end of the chromosome. Translocations disrupting constitutional t(11;22). Early removal tends to promote positive outcomes. There are no known lifestyle-related or environmental causes of Wilms tumors, so it's important to know that there is nothing these children or their parents could have done to prevent these cancers. If we dont have a program for you now, please continue to check back with us. To use the sharing features on this page, please enable JavaScript. Clear cell renal sarcoma is also a renal tumor that affects children; however, the tumor metastasizes to bones and other organs. In addition, tumor that is spilled from the mass, either by biopsy or tumor rupture is also included in stage III. Irminger JC, Schoenle EJ, Briner J, Humbel RE. Like the other genetic changes responsible for Beckwith-Wiedemann syndrome, these changes disrupt the normal regulation of genes in this part of chromosome 11. chromosome 11 is the most frequent genetic alteration in Wilms tumors, indicating that one or more tumor suppressor genes that map to this chromosomal region are involved in the development. Riggi N, Stamenkovic I. Researchers now understand some of the gene changes that can occur in Wilms tumors, but its still not clear what causes these changes. The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Disclaimer. [5] [6] [7] [8] Function [ edit] This gene encodes a transcription factor that contains four zinc finger motifs at the C-terminus and a proline / glutamine -rich DNA-binding domain at the N-terminus. It contains cancerous fibroblastic cells which are connective tissue cells that may spread to nearby tissue. Hum Genet. Researchers do not yet know exactly why some children get Wilms tumors, but they have made great progress in understanding how normal kidneys develop, as well as how this process can go wrong, leading to a Wilms tumor. [citation needed], In case of relapse of Wilms' tumor, the 4-year survival rate for children with a standard-risk has been estimated to be 80%. A translocation involving chromosome 11 can cause a type of cancerous tumor known as Ewing sarcoma. Some gene changes can be inherited, but most Wilms tumors are not the result of known inherited syndromes. We also demonstrate that abnormalities of chromosome #1, previously unrecognized in this tumor, are frequently present. Wilms' tumor or nephroblastoma is a kidney cancer that generally affects children, and very rarely adults. Abdominal ultrasounds are safe and painless, and they do not involve the use of radiation. Guo C, White PS, Weiss MJ, Hogarty MD, Thompson PM, Stram DO, Gerbing R, [5] [6] It is named after Max Wilms, the German surgeon (1867-1918) who first described it. Wilms tumor is typically found in children younger than five years old. PMC As general cancer prevention measures, children should be encouraged to lead as healthy a lifestyle as possible. Although both disorders can be caused by abnormal regulation of these genes, the changes that cause Russell-Silver syndrome lead to slow growth and short stature instead of overgrowth. 65+ years. Two copies of chromosome 11, one copy inherited from each parent, form one of the pairs. Children with bilateral Wilms tumor will be given doxorubicin, vincristine and dactinomycin prior to surgery in hopes to shrink the tumor and preserve as much renal tissue as possible. Some of these conditions include: Patients with these conditions have a greater risk of developing a malignant tumor of the kidney known as Wilms tumor (WT), or nephroblastoma. Changes in chromosome 11 have been identified in other types of cancer. If an individual is infertile, there should be no chance of passing on the WT1 mutation to future children. These findings suggest that changes in the short arm of chromosome No. The doctor will then perform a physical examination. [31], Wilms' tumor affects approximately one person per 10,000 worldwide before the age of 15 years. In: Pizzo PA, Poplack DG, eds. Aniridia (complete or partial absence of the iris, the colored part the eye): All people with WAGR syndrome have this; it is due to the loss of one copy of a gene known as. High-resolution studies in patients with aniridia-Wilms tumor association, Wilms tumor or related congenital abnormalities. See our, URL of this page: https://medlineplus.gov/genetics/chromosome/11/. Most cases do not have mutations in any of these genes.[15]. {currentyear} American Cancer Society, Inc. All rights reserved. Introduction. Researchers have determined that changes in genomic imprinting disrupt the regulation of several genes located at 11p15.5, including CDKN1C, H19, IGF2, and KCNQ1OT1. Eur J Hum Genet. Epub 2007 Dec 21. In Beckwith-Wiedemann syndrome, paternal UPD usually occurs early in embryonic development and affects only some of the body's cells. Stage IV of the disease is considered to be metastatic meaning the cancer has spread throughout the patients body, most often to the lungs. To expand the knowledge on the biological role of WT1 in other uterine cancers, we focused on its detection in endometrial carcinoma. The stroma may include striated muscle, cartilage, bone, fat tissue, and fibrous tissue. Loss of heterozygosity (LOH) on the short arm of chromosome 11 is the most frequent genetic alteration in Wilms tumors, indicating that one or more tumor suppressor genes that map to this. Girls are slightly more likely than boys to develop Wilms tumor and African Americans are also at a higher risk. Changes in certain genes in early kidney cells can lead to problems as the kidneys develop. 7th ed. Reproductive options exist for an individual with an alteration in the WT1 gene who does not wish to pass this alteration onto future children: Before one can proceed with prenatal testing or PGD, a WT1 mutation must be identified in a parent. N Eichler E, FitzGerald MG, Jaffe DB, LaButti K, Nicol R, Park HS, Seaman C, Reviewed December 2014. https://ghr.nlm.nih.gov/condition/wagr-syndrome Accessed May 4, 2019. Wilms tumor affects approximately 1 in 10,000 children with the median age of onset being 3.5 years. All related syndromes that increase the probability of a child getting Wilms tumor also have some alteration of the WT1 gene as well. The specific WT1-related condition that a person may develop is related to the type of mutation on one copy of the WT1 gene: With the exception of egg and sperm cells, each cell of the body normally has two working copies of the WT1 gene. First, a blood or saliva sample is obtained from an affected individual. The American Cancer Society is a qualified 501(c)(3) tax-exempt organization. Extensive tumor involvement of renal sinus soft tissue. https://www.cancer.net/cancer-types/wilms-tumor-childhood/statistics Accessed May 4, 2019. FOIA The majority of people with Wilms' tumor present with an asymptomatic abdominal mass which is noticed by a family member or healthcare professional. Principles and Practice of Pediatric Oncology. U.S. National Library of Medicine. Reviewed March 2013. https://ghr.nlm.nih.gov/condition/frasier-syndrome Accessed May 4, 2019. Cytogenetics and molecular genetics of Wilms' tumor of childhood. Hum Genet. . [citation needed], The mesenchymal component may include cells showing rhabdomyoid differentiation or malignancy (rhabdomyosarcomatous Wilms). 1985 Jan 1;14(1-2):95-109. doi: 10.1016/0165-4608(85)90220-1. Frasier syndrome. government site. WAGR syndrome is a rare genetic condition caused by a deletion of a group of genes located on chromosome number 11. This is the most common stage of Wilms tumor accounting for 40% to 45% of all Wilms tumors. [19], Once Wilms' tumor is suspected, an ultrasound scan is usually done first to confirm the presence of an intrarenal mass. Genes are packaged in chromosomes (long strands of DNA). Or ask us how you can get involved and support the fight against cancer. Individuals with such a deletion have signs and symptoms of both Potocki-Shaffer syndrome and WAGR syndrome. [citation needed], Wilms' tumors may be separated into two prognostic groups based on pathologic characteristics:[citation needed]. This group of disorders includes: In addition to the WT1-related Wilms tumor syndromes, there are a number of other genetic conditions associated with the development of WT. The 11q23 deletion can occur in the body's cells after conception, which is called a somatic mutation, or it can be inherited from a parent. Am J Med Genet C Semin Med Genet. These parent-specific differences in gene expression are caused by a phenomenon called genomic imprinting. JOURNAL ARTICLES Adv Pediatr. doi: [1][2] It is also the most common pediatric abdominal cancer and the fourth most common pediatric cancer overall. Approximately 50% of children with WAGR syndrome will develop Wilms tumor. Engl J Med. End-stage renal (kidney) disease: Patients may develop renal failure, often in association with a condition known as focal segmental glomerulosclerosis. Stage III indicates that the tumor has spread beyond the kidney. Would you like email updates of new search results? NIH. Learn more about the cancer today and see how our team of physicians can help. Treatment in North America is nephrectomy or in Europe chemotherapy followed by nephrectomy. 02/2018. [22][23] According to the extent of tumor tissue at the time of initial diagnosis, four stages are considered, with a fifth classification for bilateral involvement. Presentation, diagnosis, and staging of Wilms tumor. September 10, 2019 MeSH It is responsible for 95% of all malignant kidney tumors in patients under the age of 15 years old. Deletion of the WT1 gene is responsible for the genitourinary abnormalities and the increased risk of Wilms tumor in affected individuals. Abnormal external genitals: These features are often seen in boys, and may include undescended testicles, inguinal hernias or hypospadias (a birth defect characterized by abnormal placement of the urinary opening). LOH for these chromosomal regions can now be used as an independent prognostic factor together with disease stage to target intensity of treatment to risk of treatment failure. American Cancer Society. http://www.centerwatch.com/, For information about clinical trials conducted in Europe, contact: Dysfunction is caused when the tumor compresses the normal kidney parenchyma. 2012 Jul 13;91(1):56-72. An earlier diagnosis may also reduce the need for chemotherapy and lower the dose of or eliminate the need for radiation treatment. Hum Genet. [20], Staging is a standard way to describe the extent of spread of Wilms' tumors[21] and to determine prognosis and treatments. For other genes, only the copy inherited from a person's mother (the maternally inherited copy) is expressed. The estimated risks for developing Wilms tumor depend upon the type of WT1 mutation that is present. Characterized by kidney diseases since birth leading to early-onset kidney failure, ambiguous genitalia (intersex disorders). Chintagumpala M, Muscal JA. Parents should watch for symptoms of illness and have their children evaluated promptly if these occur. TTY: (866) 411-1010 Epub 2007 Jan 23. Cancer Genet Cytogenet. Orphanet J Rare Dis. Interestingly, the tumor from the patient was later described by pathology as an intralobar nephroblastomatosis (ILNR), not Wilms tumor. Featured: Have cancer and want to quit smoking? Wilms' tumor or Wilms tumor, [3] also known as nephroblastoma, is a cancer of the kidneys that typically occurs in children (rarely in adults ), [4] and occurs most commonly as a renal tumor in child patients. Email: [emailprotected], Some current clinical trials also are posted on the following page on the NORD website: Neurologic issues: Nervous center issues include seizures, brain malformations, or muscle weakness/tightness. Neuroblastoma is a type of cancerous tumor composed of immature nerve cells (neuroblasts). All cancer screening should be performed in consultation with a pediatric oncologist, and radiology studies should be reviewed by a radiologist with pediatric expertise. 2015 Mar 1;29(5):467-82. doi: 10.1101/gad.256396.114. Clear cell renal sarcoma and Wilms tumor may be hard to differentiate. [32] People of African descent may have slightly higher rates of Wilms' tumor. Below are diseases that may impact the ability to appropriately diagnose Wilms tumor in a patient. [9] Most nephroblastomas are on one side of the body only and are found on both sides in less than 5% of cases, although people with Denys-Drash syndrome mostly have bilateral or multiple tumors. Tumor extends beyond the kidney but is completely excised. Another condition called WAGR syndrome (described below) is caused by a deletion of genetic material from the short arm of chromosome 11 at a position described as 11p13. Learn more about the causes, types, risk factors, symptoms, diagnosis, and treatment. Researchers are working to determine which genes are included on the der(22) chromosome and what role these genes play in development. 2007 May;61(5 Pt 2):43R-47R. We usually look like our parents because they are the source of our DNA. Seattle (WA): University of Washington, Seattle; 1993-2019. Some of the topics we can assist with include: For medical questions, we encourage you to review our information with your doctor. Chromosome 11 likely contains 1,300 to 1,400 genes that provide instructions for making proteins. Eur J Hum Genet. Hall CR, Wu Y, Shaffer LG, Hecht JT. Characterization of Our 24/7 cancer helpline provides support for people dealing with cancer. 1999 Dec;65(6):1595-607. doi: 10.1086/302666. As a result, patients with the WAGR syndrome often have a variety of issues, including: People with Denys-Drash syndrome may develop the following clinical features: People with Frasier syndrome may develop the following clinical features: Individuals with GU anomalies syndrome may develop the following clinical features: WT1-related Wilms tumor syndromes are caused by alterations, or mutations," at a specific area in an individuals genetic information. Wilms tumor. For reprint requests, please see our Content Usage Policy. 11p14-p12 deletion in WAGR syndrome by array CGH for identifying genes Bilateral Wilms' tumors are as a whole placed in Stage V. The overall 5-year survival is estimated to be approximately 90%,[24][25] but for individuals the prognosis is highly dependent on individual staging and treatment. INTERNET 1983 Oct;10(2):191-7. doi: 10.1016/0165-4608(83)90124-3. Cancer.Net. WAGR syndrome is linked to the loss or inactivation of the WT1 gene on chromosome 11, which is a gene that usually controls cell growth and suppresses the growth of tumors. 10.1017/S1462399406000020. It is usually found before birth by ultrasound or within the first 3 months of life. Two copies of chromosome 11, one copy inherited from each parent, form one of the pairs. Science 366(6470):1247-1251. Chapter 29: Renal Tumors. Accessed May 4, 2019. Adolescent . Unless otherwise specified in boxes, then reference is: Nephroblastoma in childhood: current possibilities for an early radiographic diagnosis, Italian Journal of Surgery 1969, "Wilms Tumor and Other Childhood Kidney Tumors Treatment", "Patient-specific hydrogel phantoms for the preoperative simulation of nephron-sparing surgery in Wilms' tumor patients: A feasibility study", "Rationale for the treatment of Wilms tumour in the UMBRELLA SIOPRTSG 2016 protocol", "Wilms Tumor and Other Childhood Kidney Tumors Treatment (PDQ): Health Professional Version", 10.1002/(SICI)1096-8628(19981002)79:4<260::AID-AJMG6>3.0.CO;2-Q, "Frequent association of beta-catenin and WT1 mutations in Wilms tumors", "Wilms tumor genetics: mutations in WT1, WTX, and CTNNB1 account for only about one-third of tumors", "Advances in Wilms Tumor Treatment and Biology: Progress Through International Collaboration", "Presentation, diagnosis, and staging of Wilms tumor", "Wilms' tumor: biology, diagnosis and treatment", "Treatment by type and stage of Wilms tumor", "Defective chromosome segregation and telomere dysfunction in aggressive Wilms' tumors", "Surveillance Recommendations for Children with Overgrowth Syndromes and Predisposition to Wilms Tumors and Hepatoblastoma", "Age distributions, birth weights, nephrogenic rests, and heterogeneity in the pathogenesis of Wilms tumor", GeneReviews/NCBI/NIH/UW entry on Wilms' Tumor Overview, Multiple cutaneous and uterine leiomyomatosis syndrome, https://en.wikipedia.org/w/index.php?title=Wilms%27_tumor&oldid=1155370892, Short description is different from Wikidata, Articles with unsourced statements from April 2021, Articles with unsourced statements from June 2020, All articles with specifically marked weasel-worded phrases, Articles with specifically marked weasel-worded phrases from November 2018, Creative Commons Attribution-ShareAlike License 3.0, ~500 new diagnoses per year (United States). Pathology The tumor typically arises from mesodermal precursors of the renal parenchyma (metanephros). D, Baumann C, Benzacken B, Verloes A. Chromosome 11 spans about 135 million DNA building blocks (base pairs) and represents between 4 and 4.5 percent of the total DNA in cells. . The process of genetic testing can be performed to assess whether an affected individual has an alteration in theWT1 gene: Note: WAGR syndrome is typically diagnosed by observing a large deletion of genetic material through chromosome studies or specific deletion testing. Changes involving chromosome 11 include an extra piece of the chromosome in each cell (partial trisomy 11), a missing segment of the chromosome in each cell (partial monosomy 11), and a circular structure called a ring chromosome 11. 1984;67(3):245-8. doi: 10.1007/BF00291349. [2], Typical signs and symptoms of Wilms' tumor include the following:[citation needed], Wilms' tumor has many causes, which can broadly be categorized as syndromic and non-syndromic. There is a specific gene known as WT1, located on chromosome 11 at position p13, which is altered in patients with the WT1-related WT syndromes. The parent carries a chromosomal rearrangement between chromosomes 11 and 22 called a balanced translocation. These individuals have two normal copies of chromosome 11, two normal copies of chromosome 22, and extra genetic material from the der(22) chromosome. Tumor suppressor genes usually suppress the growth . The tumor has spread through the blood to organs such as the lungs, liver, brain, or bones. Fischbach BV, Trout KL, Lewis J, Luis CA, Sika M. WAGR syndrome: a clinical About 1 percent of all people with Beckwith-Wiedemann syndrome have a chromosomal abnormality such as a rearrangement (translocation) involving 11p15.5 or abnormal copying (duplication) or deletion of genetic material in this region. Trout K. W. Wilms Tumor. U.S. Department of Health and Human Services. Because gene alterations in WT1 may cause abnormal formation of the reproductive organs in individuals with either DDS or FS, these individuals may be infertile. However, if the tumor is found to have LOH of both chromosomes 1p and 16q, more aggressive therapy may be indicated. Please note that NORD provides this information for the benefit of the rare disease community. 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[ 1 - 3] For children younger than 20 years with Wilms tumor (also known as nephroblastoma), the 5-year relative survival rate is 93%. 10.1038/sj.ejhg.5201163. Phone: 203-744-0100 Bremond-Gignac D, Crolla JA, Copin H, Guichet A, Bonneau D, Taine L, Lacombe Both tumors had a diploid chromosome range. Because researchers use different approaches to predict the number of genes on each chromosome, the estimated number of genes varies. 11p13 (WT1 locus) and 11p15.5 (WT2 locus) are known to have genetic or epigenetic aberrations in these tumours. Differential diagnosis is the process of differentiating between two or more conditions with similar signs or symptoms. Unauthorized use of these marks is strictly prohibited. Description Collapse Section Humans normally have 46 chromosomes in each cell, divided into 23 pairs. Sankar S, Lessnick SL. The tumor was named after Dr. Max Wilms (1867-1918). Phone: 617-249-7300, Danbury, CT office Epub 2008 Dec 18. https://www.dana-farber.org/rhabdoid-tumor/ Accessed May 4, 2019. These chromosomal changes are somatic, which means they are acquired during a person's lifetime and are present only in certain cells. Higher risk of developing Wilms tumor: The risk of developing Wilms tumor varies, depending upon the. Promiscuous partnerships in Ewing's sarcoma. GeneReviews [Internet]. Wilms tumor can be cured with proper treatment. Xu S, Han JC, Morales A, Menzie CM, Williams K, Fan YS. Oncogene. Accessed at www.cancer.gov/types/kidney/hp/wilms-treatment-pdq on August 22, 2018. Cancer Genet Cytogenet. These lesions are Wilms tumor precursors. WT1 is located on the short arm of human chromosome 11 and consists of 10 coding exons. Children who inherit the altered gene copy are at risk to develop the features of a WT1-related Wilms tumor syndrome over the course of their lives. The overlap between these 21 constitutionally mutated predisposition genes and 20 genes somatically mutated in Wilms tumour is limited . It is helpful for checking whether a cancer has grown into nearby veins or has spread to organs beyond the kidney. [30] There are a number of rare genetic syndromes that have been linked to an increased risk of developing Wilms Tumor. Wilms tumor. Specifically, Russell-Silver syndrome has been associated with changes in genomic imprinting that affect the regulation of the H19 and IGF2 genes on chromosome 11. [2] The majority of cases occur in children with no associated genetic syndromes; however, a minority of children with Wilms' tumor have a congenital abnormality. Stage IV tumors are those that have spread through the vascular system. . One of the first effects seen with WAGR syndrome is on the eye. Wilms' tumor or Wilms tumor,[3] also known as nephroblastoma, is a cancer of the kidneys that typically occurs in children (rarely in adults),[4] and occurs most commonly as a renal tumor in child patients. The kidneys develop very early as a fetus grows in the womb. deletion within the Potocki-Shaffer syndrome interval on chromosome 11p11.2 Therapy depends on the stage of the tumor as well as if the patient has a family history of Wilms tumor. Epub 2012 Dec 13. Chromosome 1p and 11q deletions and outcome in neuroblastoma. Attiyeh EF, London WB, Mosse YP, Wang Q, Winter C, Khazi D, McGrady PW, Seeger
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